Oxidative stress induced by tert-butylhydroperoxide interferes with the placental transport of glucose: in vitro studies with BeWo cells
Increased oxidative stress is implicated in the onset and progression of prevalent pregnancy disorders (e.g. gestational diabetes and fetal growth restriction), and in programming the fetus to develop metabolic diseases later in life. Since the molecular mechanisms underlying these effects of oxidat...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Araújo, João R. [verfasserIn] |
|---|
| Format: |
E-Artikel |
|---|---|
| Sprache: |
Englisch |
| Erschienen: |
2013transfer abstract |
|---|
| Schlagwörter: |
|---|
| Umfang: |
9 |
|---|
| Übergeordnetes Werk: |
Enthalten in: Mexican student-teachers’ “English” language praxicum: Decolonizing attempts - López-Gopar, Mario E. ELSEVIER, 2022, EJP, New York, NY [u.a.] |
|---|---|
| Übergeordnetes Werk: |
volume:720 ; year:2013 ; number:1 ; day:15 ; month:11 ; pages:218-226 ; extent:9 |
| Links: |
|---|
| DOI / URN: |
10.1016/j.ejphar.2013.10.023 |
|---|
| Katalog-ID: |
ELV02224302X |
|---|
| LEADER | 01000caa a22002652 4500 | ||
|---|---|---|---|
| 001 | ELV02224302X | ||
| 003 | DE-627 | ||
| 005 | 20230625135116.0 | ||
| 007 | cr uuu---uuuuu | ||
| 008 | 180603s2013 xx |||||o 00| ||eng c | ||
| 024 | 7 | |a 10.1016/j.ejphar.2013.10.023 |2 doi | |
| 028 | 5 | 2 | |a GBVA2013020000017.pica |
| 035 | |a (DE-627)ELV02224302X | ||
| 035 | |a (ELSEVIER)S0014-2999(13)00779-6 | ||
| 040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
| 041 | |a eng | ||
| 082 | 0 | |a 610 | |
| 082 | 0 | 4 | |a 610 |q DE-600 |
| 082 | 0 | 4 | |a 370 |q VZ |
| 084 | |a 5,3 |2 ssgn | ||
| 100 | 1 | |a Araújo, João R. |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Oxidative stress induced by tert-butylhydroperoxide interferes with the placental transport of glucose: in vitro studies with BeWo cells |
| 264 | 1 | |c 2013transfer abstract | |
| 300 | |a 9 | ||
| 336 | |a nicht spezifiziert |b zzz |2 rdacontent | ||
| 337 | |a nicht spezifiziert |b z |2 rdamedia | ||
| 338 | |a nicht spezifiziert |b zu |2 rdacarrier | ||
| 520 | |a Increased oxidative stress is implicated in the onset and progression of prevalent pregnancy disorders (e.g. gestational diabetes and fetal growth restriction), and in programming the fetus to develop metabolic diseases later in life. Since the molecular mechanisms underlying these effects of oxidative stress are largely unexplored, we aimed to investigate if the placental transport of glucose – the main energetic substrate for the fetus and placenta – is altered by oxidative stress. In a human syncytiotrophoblast (STB) cell model, the BeWo cell line, oxidative stress was induced by treatment with 100µM tert-butylhydroperoxide (tert-BOOH) for 24h. Tert-BOOH decreased the steady-state intracellular accumulation (A max) of [3H]2-deoxyglucose ([3H]DG) mediated by both facilitative (GLUT) and non-facilitative (non-GLUT) glucose transporters. These effects were not associated with a change in the mRNA expression level of GLUT1, the major placental glucose transporter. Also, they seemed to be independent from phosphoinositide 3-kinase and protein kinase C signaling pathways and were unchanged either by inhibitors of free radical-generating enzymes or by free radical scavengers. In contrast, the dietary polyphenols quercetin, epigallocatechin-3-gallate and resveratrol completely reversed the inhibitory effect of tert-BOOH upon [3H]DG accumulation through a specific effect on GLUT-mediated transport. Finally, tert-BOOH induced an increase in the transepithelial permeability to [3H]DG in the apical-to-basal direction, apparently related to an increase in its paracellular transport. In conclusion, tert-BOOH-induced oxidative stress reduces STB accumulation of glucose associated with an increase in its transepithelial permeability. This effect may contribute to the deleterious consequences of pregnancy disorders associated with oxidative stress. | ||
| 520 | |a Increased oxidative stress is implicated in the onset and progression of prevalent pregnancy disorders (e.g. gestational diabetes and fetal growth restriction), and in programming the fetus to develop metabolic diseases later in life. Since the molecular mechanisms underlying these effects of oxidative stress are largely unexplored, we aimed to investigate if the placental transport of glucose – the main energetic substrate for the fetus and placenta – is altered by oxidative stress. In a human syncytiotrophoblast (STB) cell model, the BeWo cell line, oxidative stress was induced by treatment with 100µM tert-butylhydroperoxide (tert-BOOH) for 24h. Tert-BOOH decreased the steady-state intracellular accumulation (A max) of [3H]2-deoxyglucose ([3H]DG) mediated by both facilitative (GLUT) and non-facilitative (non-GLUT) glucose transporters. These effects were not associated with a change in the mRNA expression level of GLUT1, the major placental glucose transporter. Also, they seemed to be independent from phosphoinositide 3-kinase and protein kinase C signaling pathways and were unchanged either by inhibitors of free radical-generating enzymes or by free radical scavengers. In contrast, the dietary polyphenols quercetin, epigallocatechin-3-gallate and resveratrol completely reversed the inhibitory effect of tert-BOOH upon [3H]DG accumulation through a specific effect on GLUT-mediated transport. Finally, tert-BOOH induced an increase in the transepithelial permeability to [3H]DG in the apical-to-basal direction, apparently related to an increase in its paracellular transport. In conclusion, tert-BOOH-induced oxidative stress reduces STB accumulation of glucose associated with an increase in its transepithelial permeability. This effect may contribute to the deleterious consequences of pregnancy disorders associated with oxidative stress. | ||
| 650 | 7 | |a Oxidative stress |2 Elsevier | |
| 650 | 7 | |a Placenta |2 Elsevier | |
| 650 | 7 | |a Glucose |2 Elsevier | |
| 650 | 7 | |a Transport |2 Elsevier | |
| 700 | 1 | |a Pereira, Ana C. |4 oth | |
| 700 | 1 | |a Correia-Branco, Ana |4 oth | |
| 700 | 1 | |a Keating, Elisa |4 oth | |
| 700 | 1 | |a Martel, Fátima |4 oth | |
| 773 | 0 | 8 | |i Enthalten in |n Elsevier |a López-Gopar, Mario E. ELSEVIER |t Mexican student-teachers’ “English” language praxicum: Decolonizing attempts |d 2022 |d EJP |g New York, NY [u.a.] |w (DE-627)ELV008405875 |
| 773 | 1 | 8 | |g volume:720 |g year:2013 |g number:1 |g day:15 |g month:11 |g pages:218-226 |g extent:9 |
| 856 | 4 | 0 | |u https://doi.org/10.1016/j.ejphar.2013.10.023 |3 Volltext |
| 912 | |a GBV_USEFLAG_U | ||
| 912 | |a GBV_ELV | ||
| 912 | |a SYSFLAG_U | ||
| 951 | |a AR | ||
| 952 | |d 720 |j 2013 |e 1 |b 15 |c 1115 |h 218-226 |g 9 | ||
| 953 | |2 045F |a 610 | ||
| author_variant |
j r a jr jra |
|---|---|
| matchkey_str |
arajojoorpereiraanaccorreiabrancoanakeat:2013----:xdtvsrsidcdyetuyhdoeoienefrsihhpaetlrnprogu |
| hierarchy_sort_str |
2013transfer abstract |
| publishDate |
2013 |
| allfields |
10.1016/j.ejphar.2013.10.023 doi GBVA2013020000017.pica (DE-627)ELV02224302X (ELSEVIER)S0014-2999(13)00779-6 DE-627 ger DE-627 rakwb eng 610 610 DE-600 370 VZ 5,3 ssgn Araújo, João R. verfasserin aut Oxidative stress induced by tert-butylhydroperoxide interferes with the placental transport of glucose: in vitro studies with BeWo cells 2013transfer abstract 9 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Increased oxidative stress is implicated in the onset and progression of prevalent pregnancy disorders (e.g. gestational diabetes and fetal growth restriction), and in programming the fetus to develop metabolic diseases later in life. Since the molecular mechanisms underlying these effects of oxidative stress are largely unexplored, we aimed to investigate if the placental transport of glucose – the main energetic substrate for the fetus and placenta – is altered by oxidative stress. In a human syncytiotrophoblast (STB) cell model, the BeWo cell line, oxidative stress was induced by treatment with 100µM tert-butylhydroperoxide (tert-BOOH) for 24h. Tert-BOOH decreased the steady-state intracellular accumulation (A max) of [3H]2-deoxyglucose ([3H]DG) mediated by both facilitative (GLUT) and non-facilitative (non-GLUT) glucose transporters. These effects were not associated with a change in the mRNA expression level of GLUT1, the major placental glucose transporter. Also, they seemed to be independent from phosphoinositide 3-kinase and protein kinase C signaling pathways and were unchanged either by inhibitors of free radical-generating enzymes or by free radical scavengers. In contrast, the dietary polyphenols quercetin, epigallocatechin-3-gallate and resveratrol completely reversed the inhibitory effect of tert-BOOH upon [3H]DG accumulation through a specific effect on GLUT-mediated transport. Finally, tert-BOOH induced an increase in the transepithelial permeability to [3H]DG in the apical-to-basal direction, apparently related to an increase in its paracellular transport. In conclusion, tert-BOOH-induced oxidative stress reduces STB accumulation of glucose associated with an increase in its transepithelial permeability. This effect may contribute to the deleterious consequences of pregnancy disorders associated with oxidative stress. Increased oxidative stress is implicated in the onset and progression of prevalent pregnancy disorders (e.g. gestational diabetes and fetal growth restriction), and in programming the fetus to develop metabolic diseases later in life. Since the molecular mechanisms underlying these effects of oxidative stress are largely unexplored, we aimed to investigate if the placental transport of glucose – the main energetic substrate for the fetus and placenta – is altered by oxidative stress. In a human syncytiotrophoblast (STB) cell model, the BeWo cell line, oxidative stress was induced by treatment with 100µM tert-butylhydroperoxide (tert-BOOH) for 24h. Tert-BOOH decreased the steady-state intracellular accumulation (A max) of [3H]2-deoxyglucose ([3H]DG) mediated by both facilitative (GLUT) and non-facilitative (non-GLUT) glucose transporters. These effects were not associated with a change in the mRNA expression level of GLUT1, the major placental glucose transporter. Also, they seemed to be independent from phosphoinositide 3-kinase and protein kinase C signaling pathways and were unchanged either by inhibitors of free radical-generating enzymes or by free radical scavengers. In contrast, the dietary polyphenols quercetin, epigallocatechin-3-gallate and resveratrol completely reversed the inhibitory effect of tert-BOOH upon [3H]DG accumulation through a specific effect on GLUT-mediated transport. Finally, tert-BOOH induced an increase in the transepithelial permeability to [3H]DG in the apical-to-basal direction, apparently related to an increase in its paracellular transport. In conclusion, tert-BOOH-induced oxidative stress reduces STB accumulation of glucose associated with an increase in its transepithelial permeability. This effect may contribute to the deleterious consequences of pregnancy disorders associated with oxidative stress. Oxidative stress Elsevier Placenta Elsevier Glucose Elsevier Transport Elsevier Pereira, Ana C. oth Correia-Branco, Ana oth Keating, Elisa oth Martel, Fátima oth Enthalten in Elsevier López-Gopar, Mario E. ELSEVIER Mexican student-teachers’ “English” language praxicum: Decolonizing attempts 2022 EJP New York, NY [u.a.] (DE-627)ELV008405875 volume:720 year:2013 number:1 day:15 month:11 pages:218-226 extent:9 https://doi.org/10.1016/j.ejphar.2013.10.023 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U AR 720 2013 1 15 1115 218-226 9 045F 610 |
| spelling |
10.1016/j.ejphar.2013.10.023 doi GBVA2013020000017.pica (DE-627)ELV02224302X (ELSEVIER)S0014-2999(13)00779-6 DE-627 ger DE-627 rakwb eng 610 610 DE-600 370 VZ 5,3 ssgn Araújo, João R. verfasserin aut Oxidative stress induced by tert-butylhydroperoxide interferes with the placental transport of glucose: in vitro studies with BeWo cells 2013transfer abstract 9 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Increased oxidative stress is implicated in the onset and progression of prevalent pregnancy disorders (e.g. gestational diabetes and fetal growth restriction), and in programming the fetus to develop metabolic diseases later in life. Since the molecular mechanisms underlying these effects of oxidative stress are largely unexplored, we aimed to investigate if the placental transport of glucose – the main energetic substrate for the fetus and placenta – is altered by oxidative stress. In a human syncytiotrophoblast (STB) cell model, the BeWo cell line, oxidative stress was induced by treatment with 100µM tert-butylhydroperoxide (tert-BOOH) for 24h. Tert-BOOH decreased the steady-state intracellular accumulation (A max) of [3H]2-deoxyglucose ([3H]DG) mediated by both facilitative (GLUT) and non-facilitative (non-GLUT) glucose transporters. These effects were not associated with a change in the mRNA expression level of GLUT1, the major placental glucose transporter. Also, they seemed to be independent from phosphoinositide 3-kinase and protein kinase C signaling pathways and were unchanged either by inhibitors of free radical-generating enzymes or by free radical scavengers. In contrast, the dietary polyphenols quercetin, epigallocatechin-3-gallate and resveratrol completely reversed the inhibitory effect of tert-BOOH upon [3H]DG accumulation through a specific effect on GLUT-mediated transport. Finally, tert-BOOH induced an increase in the transepithelial permeability to [3H]DG in the apical-to-basal direction, apparently related to an increase in its paracellular transport. In conclusion, tert-BOOH-induced oxidative stress reduces STB accumulation of glucose associated with an increase in its transepithelial permeability. This effect may contribute to the deleterious consequences of pregnancy disorders associated with oxidative stress. Increased oxidative stress is implicated in the onset and progression of prevalent pregnancy disorders (e.g. gestational diabetes and fetal growth restriction), and in programming the fetus to develop metabolic diseases later in life. Since the molecular mechanisms underlying these effects of oxidative stress are largely unexplored, we aimed to investigate if the placental transport of glucose – the main energetic substrate for the fetus and placenta – is altered by oxidative stress. In a human syncytiotrophoblast (STB) cell model, the BeWo cell line, oxidative stress was induced by treatment with 100µM tert-butylhydroperoxide (tert-BOOH) for 24h. Tert-BOOH decreased the steady-state intracellular accumulation (A max) of [3H]2-deoxyglucose ([3H]DG) mediated by both facilitative (GLUT) and non-facilitative (non-GLUT) glucose transporters. These effects were not associated with a change in the mRNA expression level of GLUT1, the major placental glucose transporter. Also, they seemed to be independent from phosphoinositide 3-kinase and protein kinase C signaling pathways and were unchanged either by inhibitors of free radical-generating enzymes or by free radical scavengers. In contrast, the dietary polyphenols quercetin, epigallocatechin-3-gallate and resveratrol completely reversed the inhibitory effect of tert-BOOH upon [3H]DG accumulation through a specific effect on GLUT-mediated transport. Finally, tert-BOOH induced an increase in the transepithelial permeability to [3H]DG in the apical-to-basal direction, apparently related to an increase in its paracellular transport. In conclusion, tert-BOOH-induced oxidative stress reduces STB accumulation of glucose associated with an increase in its transepithelial permeability. This effect may contribute to the deleterious consequences of pregnancy disorders associated with oxidative stress. Oxidative stress Elsevier Placenta Elsevier Glucose Elsevier Transport Elsevier Pereira, Ana C. oth Correia-Branco, Ana oth Keating, Elisa oth Martel, Fátima oth Enthalten in Elsevier López-Gopar, Mario E. ELSEVIER Mexican student-teachers’ “English” language praxicum: Decolonizing attempts 2022 EJP New York, NY [u.a.] (DE-627)ELV008405875 volume:720 year:2013 number:1 day:15 month:11 pages:218-226 extent:9 https://doi.org/10.1016/j.ejphar.2013.10.023 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U AR 720 2013 1 15 1115 218-226 9 045F 610 |
| allfields_unstemmed |
10.1016/j.ejphar.2013.10.023 doi GBVA2013020000017.pica (DE-627)ELV02224302X (ELSEVIER)S0014-2999(13)00779-6 DE-627 ger DE-627 rakwb eng 610 610 DE-600 370 VZ 5,3 ssgn Araújo, João R. verfasserin aut Oxidative stress induced by tert-butylhydroperoxide interferes with the placental transport of glucose: in vitro studies with BeWo cells 2013transfer abstract 9 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Increased oxidative stress is implicated in the onset and progression of prevalent pregnancy disorders (e.g. gestational diabetes and fetal growth restriction), and in programming the fetus to develop metabolic diseases later in life. Since the molecular mechanisms underlying these effects of oxidative stress are largely unexplored, we aimed to investigate if the placental transport of glucose – the main energetic substrate for the fetus and placenta – is altered by oxidative stress. In a human syncytiotrophoblast (STB) cell model, the BeWo cell line, oxidative stress was induced by treatment with 100µM tert-butylhydroperoxide (tert-BOOH) for 24h. Tert-BOOH decreased the steady-state intracellular accumulation (A max) of [3H]2-deoxyglucose ([3H]DG) mediated by both facilitative (GLUT) and non-facilitative (non-GLUT) glucose transporters. These effects were not associated with a change in the mRNA expression level of GLUT1, the major placental glucose transporter. Also, they seemed to be independent from phosphoinositide 3-kinase and protein kinase C signaling pathways and were unchanged either by inhibitors of free radical-generating enzymes or by free radical scavengers. In contrast, the dietary polyphenols quercetin, epigallocatechin-3-gallate and resveratrol completely reversed the inhibitory effect of tert-BOOH upon [3H]DG accumulation through a specific effect on GLUT-mediated transport. Finally, tert-BOOH induced an increase in the transepithelial permeability to [3H]DG in the apical-to-basal direction, apparently related to an increase in its paracellular transport. In conclusion, tert-BOOH-induced oxidative stress reduces STB accumulation of glucose associated with an increase in its transepithelial permeability. This effect may contribute to the deleterious consequences of pregnancy disorders associated with oxidative stress. Increased oxidative stress is implicated in the onset and progression of prevalent pregnancy disorders (e.g. gestational diabetes and fetal growth restriction), and in programming the fetus to develop metabolic diseases later in life. Since the molecular mechanisms underlying these effects of oxidative stress are largely unexplored, we aimed to investigate if the placental transport of glucose – the main energetic substrate for the fetus and placenta – is altered by oxidative stress. In a human syncytiotrophoblast (STB) cell model, the BeWo cell line, oxidative stress was induced by treatment with 100µM tert-butylhydroperoxide (tert-BOOH) for 24h. Tert-BOOH decreased the steady-state intracellular accumulation (A max) of [3H]2-deoxyglucose ([3H]DG) mediated by both facilitative (GLUT) and non-facilitative (non-GLUT) glucose transporters. These effects were not associated with a change in the mRNA expression level of GLUT1, the major placental glucose transporter. Also, they seemed to be independent from phosphoinositide 3-kinase and protein kinase C signaling pathways and were unchanged either by inhibitors of free radical-generating enzymes or by free radical scavengers. In contrast, the dietary polyphenols quercetin, epigallocatechin-3-gallate and resveratrol completely reversed the inhibitory effect of tert-BOOH upon [3H]DG accumulation through a specific effect on GLUT-mediated transport. Finally, tert-BOOH induced an increase in the transepithelial permeability to [3H]DG in the apical-to-basal direction, apparently related to an increase in its paracellular transport. In conclusion, tert-BOOH-induced oxidative stress reduces STB accumulation of glucose associated with an increase in its transepithelial permeability. This effect may contribute to the deleterious consequences of pregnancy disorders associated with oxidative stress. Oxidative stress Elsevier Placenta Elsevier Glucose Elsevier Transport Elsevier Pereira, Ana C. oth Correia-Branco, Ana oth Keating, Elisa oth Martel, Fátima oth Enthalten in Elsevier López-Gopar, Mario E. ELSEVIER Mexican student-teachers’ “English” language praxicum: Decolonizing attempts 2022 EJP New York, NY [u.a.] (DE-627)ELV008405875 volume:720 year:2013 number:1 day:15 month:11 pages:218-226 extent:9 https://doi.org/10.1016/j.ejphar.2013.10.023 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U AR 720 2013 1 15 1115 218-226 9 045F 610 |
| allfieldsGer |
10.1016/j.ejphar.2013.10.023 doi GBVA2013020000017.pica (DE-627)ELV02224302X (ELSEVIER)S0014-2999(13)00779-6 DE-627 ger DE-627 rakwb eng 610 610 DE-600 370 VZ 5,3 ssgn Araújo, João R. verfasserin aut Oxidative stress induced by tert-butylhydroperoxide interferes with the placental transport of glucose: in vitro studies with BeWo cells 2013transfer abstract 9 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Increased oxidative stress is implicated in the onset and progression of prevalent pregnancy disorders (e.g. gestational diabetes and fetal growth restriction), and in programming the fetus to develop metabolic diseases later in life. Since the molecular mechanisms underlying these effects of oxidative stress are largely unexplored, we aimed to investigate if the placental transport of glucose – the main energetic substrate for the fetus and placenta – is altered by oxidative stress. In a human syncytiotrophoblast (STB) cell model, the BeWo cell line, oxidative stress was induced by treatment with 100µM tert-butylhydroperoxide (tert-BOOH) for 24h. Tert-BOOH decreased the steady-state intracellular accumulation (A max) of [3H]2-deoxyglucose ([3H]DG) mediated by both facilitative (GLUT) and non-facilitative (non-GLUT) glucose transporters. These effects were not associated with a change in the mRNA expression level of GLUT1, the major placental glucose transporter. Also, they seemed to be independent from phosphoinositide 3-kinase and protein kinase C signaling pathways and were unchanged either by inhibitors of free radical-generating enzymes or by free radical scavengers. In contrast, the dietary polyphenols quercetin, epigallocatechin-3-gallate and resveratrol completely reversed the inhibitory effect of tert-BOOH upon [3H]DG accumulation through a specific effect on GLUT-mediated transport. Finally, tert-BOOH induced an increase in the transepithelial permeability to [3H]DG in the apical-to-basal direction, apparently related to an increase in its paracellular transport. In conclusion, tert-BOOH-induced oxidative stress reduces STB accumulation of glucose associated with an increase in its transepithelial permeability. This effect may contribute to the deleterious consequences of pregnancy disorders associated with oxidative stress. Increased oxidative stress is implicated in the onset and progression of prevalent pregnancy disorders (e.g. gestational diabetes and fetal growth restriction), and in programming the fetus to develop metabolic diseases later in life. Since the molecular mechanisms underlying these effects of oxidative stress are largely unexplored, we aimed to investigate if the placental transport of glucose – the main energetic substrate for the fetus and placenta – is altered by oxidative stress. In a human syncytiotrophoblast (STB) cell model, the BeWo cell line, oxidative stress was induced by treatment with 100µM tert-butylhydroperoxide (tert-BOOH) for 24h. Tert-BOOH decreased the steady-state intracellular accumulation (A max) of [3H]2-deoxyglucose ([3H]DG) mediated by both facilitative (GLUT) and non-facilitative (non-GLUT) glucose transporters. These effects were not associated with a change in the mRNA expression level of GLUT1, the major placental glucose transporter. Also, they seemed to be independent from phosphoinositide 3-kinase and protein kinase C signaling pathways and were unchanged either by inhibitors of free radical-generating enzymes or by free radical scavengers. In contrast, the dietary polyphenols quercetin, epigallocatechin-3-gallate and resveratrol completely reversed the inhibitory effect of tert-BOOH upon [3H]DG accumulation through a specific effect on GLUT-mediated transport. Finally, tert-BOOH induced an increase in the transepithelial permeability to [3H]DG in the apical-to-basal direction, apparently related to an increase in its paracellular transport. In conclusion, tert-BOOH-induced oxidative stress reduces STB accumulation of glucose associated with an increase in its transepithelial permeability. This effect may contribute to the deleterious consequences of pregnancy disorders associated with oxidative stress. Oxidative stress Elsevier Placenta Elsevier Glucose Elsevier Transport Elsevier Pereira, Ana C. oth Correia-Branco, Ana oth Keating, Elisa oth Martel, Fátima oth Enthalten in Elsevier López-Gopar, Mario E. ELSEVIER Mexican student-teachers’ “English” language praxicum: Decolonizing attempts 2022 EJP New York, NY [u.a.] (DE-627)ELV008405875 volume:720 year:2013 number:1 day:15 month:11 pages:218-226 extent:9 https://doi.org/10.1016/j.ejphar.2013.10.023 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U AR 720 2013 1 15 1115 218-226 9 045F 610 |
| allfieldsSound |
10.1016/j.ejphar.2013.10.023 doi GBVA2013020000017.pica (DE-627)ELV02224302X (ELSEVIER)S0014-2999(13)00779-6 DE-627 ger DE-627 rakwb eng 610 610 DE-600 370 VZ 5,3 ssgn Araújo, João R. verfasserin aut Oxidative stress induced by tert-butylhydroperoxide interferes with the placental transport of glucose: in vitro studies with BeWo cells 2013transfer abstract 9 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Increased oxidative stress is implicated in the onset and progression of prevalent pregnancy disorders (e.g. gestational diabetes and fetal growth restriction), and in programming the fetus to develop metabolic diseases later in life. Since the molecular mechanisms underlying these effects of oxidative stress are largely unexplored, we aimed to investigate if the placental transport of glucose – the main energetic substrate for the fetus and placenta – is altered by oxidative stress. In a human syncytiotrophoblast (STB) cell model, the BeWo cell line, oxidative stress was induced by treatment with 100µM tert-butylhydroperoxide (tert-BOOH) for 24h. Tert-BOOH decreased the steady-state intracellular accumulation (A max) of [3H]2-deoxyglucose ([3H]DG) mediated by both facilitative (GLUT) and non-facilitative (non-GLUT) glucose transporters. These effects were not associated with a change in the mRNA expression level of GLUT1, the major placental glucose transporter. Also, they seemed to be independent from phosphoinositide 3-kinase and protein kinase C signaling pathways and were unchanged either by inhibitors of free radical-generating enzymes or by free radical scavengers. In contrast, the dietary polyphenols quercetin, epigallocatechin-3-gallate and resveratrol completely reversed the inhibitory effect of tert-BOOH upon [3H]DG accumulation through a specific effect on GLUT-mediated transport. Finally, tert-BOOH induced an increase in the transepithelial permeability to [3H]DG in the apical-to-basal direction, apparently related to an increase in its paracellular transport. In conclusion, tert-BOOH-induced oxidative stress reduces STB accumulation of glucose associated with an increase in its transepithelial permeability. This effect may contribute to the deleterious consequences of pregnancy disorders associated with oxidative stress. Increased oxidative stress is implicated in the onset and progression of prevalent pregnancy disorders (e.g. gestational diabetes and fetal growth restriction), and in programming the fetus to develop metabolic diseases later in life. Since the molecular mechanisms underlying these effects of oxidative stress are largely unexplored, we aimed to investigate if the placental transport of glucose – the main energetic substrate for the fetus and placenta – is altered by oxidative stress. In a human syncytiotrophoblast (STB) cell model, the BeWo cell line, oxidative stress was induced by treatment with 100µM tert-butylhydroperoxide (tert-BOOH) for 24h. Tert-BOOH decreased the steady-state intracellular accumulation (A max) of [3H]2-deoxyglucose ([3H]DG) mediated by both facilitative (GLUT) and non-facilitative (non-GLUT) glucose transporters. These effects were not associated with a change in the mRNA expression level of GLUT1, the major placental glucose transporter. Also, they seemed to be independent from phosphoinositide 3-kinase and protein kinase C signaling pathways and were unchanged either by inhibitors of free radical-generating enzymes or by free radical scavengers. In contrast, the dietary polyphenols quercetin, epigallocatechin-3-gallate and resveratrol completely reversed the inhibitory effect of tert-BOOH upon [3H]DG accumulation through a specific effect on GLUT-mediated transport. Finally, tert-BOOH induced an increase in the transepithelial permeability to [3H]DG in the apical-to-basal direction, apparently related to an increase in its paracellular transport. In conclusion, tert-BOOH-induced oxidative stress reduces STB accumulation of glucose associated with an increase in its transepithelial permeability. This effect may contribute to the deleterious consequences of pregnancy disorders associated with oxidative stress. Oxidative stress Elsevier Placenta Elsevier Glucose Elsevier Transport Elsevier Pereira, Ana C. oth Correia-Branco, Ana oth Keating, Elisa oth Martel, Fátima oth Enthalten in Elsevier López-Gopar, Mario E. ELSEVIER Mexican student-teachers’ “English” language praxicum: Decolonizing attempts 2022 EJP New York, NY [u.a.] (DE-627)ELV008405875 volume:720 year:2013 number:1 day:15 month:11 pages:218-226 extent:9 https://doi.org/10.1016/j.ejphar.2013.10.023 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U AR 720 2013 1 15 1115 218-226 9 045F 610 |
| language |
English |
| source |
Enthalten in Mexican student-teachers’ “English” language praxicum: Decolonizing attempts New York, NY [u.a.] volume:720 year:2013 number:1 day:15 month:11 pages:218-226 extent:9 |
| sourceStr |
Enthalten in Mexican student-teachers’ “English” language praxicum: Decolonizing attempts New York, NY [u.a.] volume:720 year:2013 number:1 day:15 month:11 pages:218-226 extent:9 |
| format_phy_str_mv |
Article |
| institution |
findex.gbv.de |
| topic_facet |
Oxidative stress Placenta Glucose Transport |
| dewey-raw |
610 |
| isfreeaccess_bool |
false |
| container_title |
Mexican student-teachers’ “English” language praxicum: Decolonizing attempts |
| authorswithroles_txt_mv |
Araújo, João R. @@aut@@ Pereira, Ana C. @@oth@@ Correia-Branco, Ana @@oth@@ Keating, Elisa @@oth@@ Martel, Fátima @@oth@@ |
| publishDateDaySort_date |
2013-01-15T00:00:00Z |
| hierarchy_top_id |
ELV008405875 |
| dewey-sort |
3610 |
| id |
ELV02224302X |
| language_de |
englisch |
| fullrecord |
<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">ELV02224302X</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230625135116.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">180603s2013 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1016/j.ejphar.2013.10.023</subfield><subfield code="2">doi</subfield></datafield><datafield tag="028" ind1="5" ind2="2"><subfield code="a">GBVA2013020000017.pica</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)ELV02224302X</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(ELSEVIER)S0014-2999(13)00779-6</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="082" ind1="0" ind2=" "><subfield code="a">610</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">DE-600</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">370</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">5,3</subfield><subfield code="2">ssgn</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Araújo, João R.</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Oxidative stress induced by tert-butylhydroperoxide interferes with the placental transport of glucose: in vitro studies with BeWo cells</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2013transfer abstract</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">9</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zzz</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">z</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zu</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Increased oxidative stress is implicated in the onset and progression of prevalent pregnancy disorders (e.g. gestational diabetes and fetal growth restriction), and in programming the fetus to develop metabolic diseases later in life. Since the molecular mechanisms underlying these effects of oxidative stress are largely unexplored, we aimed to investigate if the placental transport of glucose – the main energetic substrate for the fetus and placenta – is altered by oxidative stress. In a human syncytiotrophoblast (STB) cell model, the BeWo cell line, oxidative stress was induced by treatment with 100µM tert-butylhydroperoxide (tert-BOOH) for 24h. Tert-BOOH decreased the steady-state intracellular accumulation (A max) of [3H]2-deoxyglucose ([3H]DG) mediated by both facilitative (GLUT) and non-facilitative (non-GLUT) glucose transporters. These effects were not associated with a change in the mRNA expression level of GLUT1, the major placental glucose transporter. Also, they seemed to be independent from phosphoinositide 3-kinase and protein kinase C signaling pathways and were unchanged either by inhibitors of free radical-generating enzymes or by free radical scavengers. In contrast, the dietary polyphenols quercetin, epigallocatechin-3-gallate and resveratrol completely reversed the inhibitory effect of tert-BOOH upon [3H]DG accumulation through a specific effect on GLUT-mediated transport. Finally, tert-BOOH induced an increase in the transepithelial permeability to [3H]DG in the apical-to-basal direction, apparently related to an increase in its paracellular transport. In conclusion, tert-BOOH-induced oxidative stress reduces STB accumulation of glucose associated with an increase in its transepithelial permeability. This effect may contribute to the deleterious consequences of pregnancy disorders associated with oxidative stress.</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Increased oxidative stress is implicated in the onset and progression of prevalent pregnancy disorders (e.g. gestational diabetes and fetal growth restriction), and in programming the fetus to develop metabolic diseases later in life. Since the molecular mechanisms underlying these effects of oxidative stress are largely unexplored, we aimed to investigate if the placental transport of glucose – the main energetic substrate for the fetus and placenta – is altered by oxidative stress. In a human syncytiotrophoblast (STB) cell model, the BeWo cell line, oxidative stress was induced by treatment with 100µM tert-butylhydroperoxide (tert-BOOH) for 24h. Tert-BOOH decreased the steady-state intracellular accumulation (A max) of [3H]2-deoxyglucose ([3H]DG) mediated by both facilitative (GLUT) and non-facilitative (non-GLUT) glucose transporters. These effects were not associated with a change in the mRNA expression level of GLUT1, the major placental glucose transporter. Also, they seemed to be independent from phosphoinositide 3-kinase and protein kinase C signaling pathways and were unchanged either by inhibitors of free radical-generating enzymes or by free radical scavengers. In contrast, the dietary polyphenols quercetin, epigallocatechin-3-gallate and resveratrol completely reversed the inhibitory effect of tert-BOOH upon [3H]DG accumulation through a specific effect on GLUT-mediated transport. Finally, tert-BOOH induced an increase in the transepithelial permeability to [3H]DG in the apical-to-basal direction, apparently related to an increase in its paracellular transport. In conclusion, tert-BOOH-induced oxidative stress reduces STB accumulation of glucose associated with an increase in its transepithelial permeability. This effect may contribute to the deleterious consequences of pregnancy disorders associated with oxidative stress.</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Oxidative stress</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Placenta</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Glucose</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Transport</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Pereira, Ana C.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Correia-Branco, Ana</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Keating, Elisa</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Martel, Fátima</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="n">Elsevier</subfield><subfield code="a">López-Gopar, Mario E. ELSEVIER</subfield><subfield code="t">Mexican student-teachers’ “English” language praxicum: Decolonizing attempts</subfield><subfield code="d">2022</subfield><subfield code="d">EJP</subfield><subfield code="g">New York, NY [u.a.]</subfield><subfield code="w">(DE-627)ELV008405875</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:720</subfield><subfield code="g">year:2013</subfield><subfield code="g">number:1</subfield><subfield code="g">day:15</subfield><subfield code="g">month:11</subfield><subfield code="g">pages:218-226</subfield><subfield code="g">extent:9</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.1016/j.ejphar.2013.10.023</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ELV</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_U</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">720</subfield><subfield code="j">2013</subfield><subfield code="e">1</subfield><subfield code="b">15</subfield><subfield code="c">1115</subfield><subfield code="h">218-226</subfield><subfield code="g">9</subfield></datafield><datafield tag="953" ind1=" " ind2=" "><subfield code="2">045F</subfield><subfield code="a">610</subfield></datafield></record></collection>
|
| author |
Araújo, João R. |
| spellingShingle |
Araújo, João R. ddc 610 ddc 370 ssgn 5,3 Elsevier Oxidative stress Elsevier Placenta Elsevier Glucose Elsevier Transport Oxidative stress induced by tert-butylhydroperoxide interferes with the placental transport of glucose: in vitro studies with BeWo cells |
| authorStr |
Araújo, João R. |
| ppnlink_with_tag_str_mv |
@@773@@(DE-627)ELV008405875 |
| format |
electronic Article |
| dewey-ones |
610 - Medicine & health 370 - Education |
| delete_txt_mv |
keep |
| author_role |
aut |
| collection |
elsevier |
| remote_str |
true |
| illustrated |
Not Illustrated |
| topic_title |
610 610 DE-600 370 VZ 5,3 ssgn Oxidative stress induced by tert-butylhydroperoxide interferes with the placental transport of glucose: in vitro studies with BeWo cells Oxidative stress Elsevier Placenta Elsevier Glucose Elsevier Transport Elsevier |
| topic |
ddc 610 ddc 370 ssgn 5,3 Elsevier Oxidative stress Elsevier Placenta Elsevier Glucose Elsevier Transport |
| topic_unstemmed |
ddc 610 ddc 370 ssgn 5,3 Elsevier Oxidative stress Elsevier Placenta Elsevier Glucose Elsevier Transport |
| topic_browse |
ddc 610 ddc 370 ssgn 5,3 Elsevier Oxidative stress Elsevier Placenta Elsevier Glucose Elsevier Transport |
| format_facet |
Elektronische Aufsätze Aufsätze Elektronische Ressource |
| format_main_str_mv |
Text Zeitschrift/Artikel |
| carriertype_str_mv |
zu |
| author2_variant |
a c p ac acp a c b acb e k ek f m fm |
| hierarchy_parent_title |
Mexican student-teachers’ “English” language praxicum: Decolonizing attempts |
| hierarchy_parent_id |
ELV008405875 |
| dewey-tens |
610 - Medicine & health 370 - Education |
| hierarchy_top_title |
Mexican student-teachers’ “English” language praxicum: Decolonizing attempts |
| isfreeaccess_txt |
false |
| familylinks_str_mv |
(DE-627)ELV008405875 |
| title |
Oxidative stress induced by tert-butylhydroperoxide interferes with the placental transport of glucose: in vitro studies with BeWo cells |
| ctrlnum |
(DE-627)ELV02224302X (ELSEVIER)S0014-2999(13)00779-6 |
| title_full |
Oxidative stress induced by tert-butylhydroperoxide interferes with the placental transport of glucose: in vitro studies with BeWo cells |
| author_sort |
Araújo, João R. |
| journal |
Mexican student-teachers’ “English” language praxicum: Decolonizing attempts |
| journalStr |
Mexican student-teachers’ “English” language praxicum: Decolonizing attempts |
| lang_code |
eng |
| isOA_bool |
false |
| dewey-hundreds |
600 - Technology 300 - Social sciences |
| recordtype |
marc |
| publishDateSort |
2013 |
| contenttype_str_mv |
zzz |
| container_start_page |
218 |
| author_browse |
Araújo, João R. |
| container_volume |
720 |
| physical |
9 |
| class |
610 610 DE-600 370 VZ 5,3 ssgn |
| format_se |
Elektronische Aufsätze |
| author-letter |
Araújo, João R. |
| doi_str_mv |
10.1016/j.ejphar.2013.10.023 |
| dewey-full |
610 370 |
| title_sort |
oxidative stress induced by tert-butylhydroperoxide interferes with the placental transport of glucose: in vitro studies with bewo cells |
| title_auth |
Oxidative stress induced by tert-butylhydroperoxide interferes with the placental transport of glucose: in vitro studies with BeWo cells |
| abstract |
Increased oxidative stress is implicated in the onset and progression of prevalent pregnancy disorders (e.g. gestational diabetes and fetal growth restriction), and in programming the fetus to develop metabolic diseases later in life. Since the molecular mechanisms underlying these effects of oxidative stress are largely unexplored, we aimed to investigate if the placental transport of glucose – the main energetic substrate for the fetus and placenta – is altered by oxidative stress. In a human syncytiotrophoblast (STB) cell model, the BeWo cell line, oxidative stress was induced by treatment with 100µM tert-butylhydroperoxide (tert-BOOH) for 24h. Tert-BOOH decreased the steady-state intracellular accumulation (A max) of [3H]2-deoxyglucose ([3H]DG) mediated by both facilitative (GLUT) and non-facilitative (non-GLUT) glucose transporters. These effects were not associated with a change in the mRNA expression level of GLUT1, the major placental glucose transporter. Also, they seemed to be independent from phosphoinositide 3-kinase and protein kinase C signaling pathways and were unchanged either by inhibitors of free radical-generating enzymes or by free radical scavengers. In contrast, the dietary polyphenols quercetin, epigallocatechin-3-gallate and resveratrol completely reversed the inhibitory effect of tert-BOOH upon [3H]DG accumulation through a specific effect on GLUT-mediated transport. Finally, tert-BOOH induced an increase in the transepithelial permeability to [3H]DG in the apical-to-basal direction, apparently related to an increase in its paracellular transport. In conclusion, tert-BOOH-induced oxidative stress reduces STB accumulation of glucose associated with an increase in its transepithelial permeability. This effect may contribute to the deleterious consequences of pregnancy disorders associated with oxidative stress. |
| abstractGer |
Increased oxidative stress is implicated in the onset and progression of prevalent pregnancy disorders (e.g. gestational diabetes and fetal growth restriction), and in programming the fetus to develop metabolic diseases later in life. Since the molecular mechanisms underlying these effects of oxidative stress are largely unexplored, we aimed to investigate if the placental transport of glucose – the main energetic substrate for the fetus and placenta – is altered by oxidative stress. In a human syncytiotrophoblast (STB) cell model, the BeWo cell line, oxidative stress was induced by treatment with 100µM tert-butylhydroperoxide (tert-BOOH) for 24h. Tert-BOOH decreased the steady-state intracellular accumulation (A max) of [3H]2-deoxyglucose ([3H]DG) mediated by both facilitative (GLUT) and non-facilitative (non-GLUT) glucose transporters. These effects were not associated with a change in the mRNA expression level of GLUT1, the major placental glucose transporter. Also, they seemed to be independent from phosphoinositide 3-kinase and protein kinase C signaling pathways and were unchanged either by inhibitors of free radical-generating enzymes or by free radical scavengers. In contrast, the dietary polyphenols quercetin, epigallocatechin-3-gallate and resveratrol completely reversed the inhibitory effect of tert-BOOH upon [3H]DG accumulation through a specific effect on GLUT-mediated transport. Finally, tert-BOOH induced an increase in the transepithelial permeability to [3H]DG in the apical-to-basal direction, apparently related to an increase in its paracellular transport. In conclusion, tert-BOOH-induced oxidative stress reduces STB accumulation of glucose associated with an increase in its transepithelial permeability. This effect may contribute to the deleterious consequences of pregnancy disorders associated with oxidative stress. |
| abstract_unstemmed |
Increased oxidative stress is implicated in the onset and progression of prevalent pregnancy disorders (e.g. gestational diabetes and fetal growth restriction), and in programming the fetus to develop metabolic diseases later in life. Since the molecular mechanisms underlying these effects of oxidative stress are largely unexplored, we aimed to investigate if the placental transport of glucose – the main energetic substrate for the fetus and placenta – is altered by oxidative stress. In a human syncytiotrophoblast (STB) cell model, the BeWo cell line, oxidative stress was induced by treatment with 100µM tert-butylhydroperoxide (tert-BOOH) for 24h. Tert-BOOH decreased the steady-state intracellular accumulation (A max) of [3H]2-deoxyglucose ([3H]DG) mediated by both facilitative (GLUT) and non-facilitative (non-GLUT) glucose transporters. These effects were not associated with a change in the mRNA expression level of GLUT1, the major placental glucose transporter. Also, they seemed to be independent from phosphoinositide 3-kinase and protein kinase C signaling pathways and were unchanged either by inhibitors of free radical-generating enzymes or by free radical scavengers. In contrast, the dietary polyphenols quercetin, epigallocatechin-3-gallate and resveratrol completely reversed the inhibitory effect of tert-BOOH upon [3H]DG accumulation through a specific effect on GLUT-mediated transport. Finally, tert-BOOH induced an increase in the transepithelial permeability to [3H]DG in the apical-to-basal direction, apparently related to an increase in its paracellular transport. In conclusion, tert-BOOH-induced oxidative stress reduces STB accumulation of glucose associated with an increase in its transepithelial permeability. This effect may contribute to the deleterious consequences of pregnancy disorders associated with oxidative stress. |
| collection_details |
GBV_USEFLAG_U GBV_ELV SYSFLAG_U |
| container_issue |
1 |
| title_short |
Oxidative stress induced by tert-butylhydroperoxide interferes with the placental transport of glucose: in vitro studies with BeWo cells |
| url |
https://doi.org/10.1016/j.ejphar.2013.10.023 |
| remote_bool |
true |
| author2 |
Pereira, Ana C. Correia-Branco, Ana Keating, Elisa Martel, Fátima |
| author2Str |
Pereira, Ana C. Correia-Branco, Ana Keating, Elisa Martel, Fátima |
| ppnlink |
ELV008405875 |
| mediatype_str_mv |
z |
| isOA_txt |
false |
| hochschulschrift_bool |
false |
| author2_role |
oth oth oth oth |
| doi_str |
10.1016/j.ejphar.2013.10.023 |
| up_date |
2024-07-06T21:30:46.268Z |
| _version_ |
1803866809324011520 |
| fullrecord_marcxml |
<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">ELV02224302X</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230625135116.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">180603s2013 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1016/j.ejphar.2013.10.023</subfield><subfield code="2">doi</subfield></datafield><datafield tag="028" ind1="5" ind2="2"><subfield code="a">GBVA2013020000017.pica</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)ELV02224302X</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(ELSEVIER)S0014-2999(13)00779-6</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="082" ind1="0" ind2=" "><subfield code="a">610</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">DE-600</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">370</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">5,3</subfield><subfield code="2">ssgn</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Araújo, João R.</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Oxidative stress induced by tert-butylhydroperoxide interferes with the placental transport of glucose: in vitro studies with BeWo cells</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2013transfer abstract</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">9</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zzz</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">z</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zu</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Increased oxidative stress is implicated in the onset and progression of prevalent pregnancy disorders (e.g. gestational diabetes and fetal growth restriction), and in programming the fetus to develop metabolic diseases later in life. Since the molecular mechanisms underlying these effects of oxidative stress are largely unexplored, we aimed to investigate if the placental transport of glucose – the main energetic substrate for the fetus and placenta – is altered by oxidative stress. In a human syncytiotrophoblast (STB) cell model, the BeWo cell line, oxidative stress was induced by treatment with 100µM tert-butylhydroperoxide (tert-BOOH) for 24h. Tert-BOOH decreased the steady-state intracellular accumulation (A max) of [3H]2-deoxyglucose ([3H]DG) mediated by both facilitative (GLUT) and non-facilitative (non-GLUT) glucose transporters. These effects were not associated with a change in the mRNA expression level of GLUT1, the major placental glucose transporter. Also, they seemed to be independent from phosphoinositide 3-kinase and protein kinase C signaling pathways and were unchanged either by inhibitors of free radical-generating enzymes or by free radical scavengers. In contrast, the dietary polyphenols quercetin, epigallocatechin-3-gallate and resveratrol completely reversed the inhibitory effect of tert-BOOH upon [3H]DG accumulation through a specific effect on GLUT-mediated transport. Finally, tert-BOOH induced an increase in the transepithelial permeability to [3H]DG in the apical-to-basal direction, apparently related to an increase in its paracellular transport. In conclusion, tert-BOOH-induced oxidative stress reduces STB accumulation of glucose associated with an increase in its transepithelial permeability. This effect may contribute to the deleterious consequences of pregnancy disorders associated with oxidative stress.</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Increased oxidative stress is implicated in the onset and progression of prevalent pregnancy disorders (e.g. gestational diabetes and fetal growth restriction), and in programming the fetus to develop metabolic diseases later in life. Since the molecular mechanisms underlying these effects of oxidative stress are largely unexplored, we aimed to investigate if the placental transport of glucose – the main energetic substrate for the fetus and placenta – is altered by oxidative stress. In a human syncytiotrophoblast (STB) cell model, the BeWo cell line, oxidative stress was induced by treatment with 100µM tert-butylhydroperoxide (tert-BOOH) for 24h. Tert-BOOH decreased the steady-state intracellular accumulation (A max) of [3H]2-deoxyglucose ([3H]DG) mediated by both facilitative (GLUT) and non-facilitative (non-GLUT) glucose transporters. These effects were not associated with a change in the mRNA expression level of GLUT1, the major placental glucose transporter. Also, they seemed to be independent from phosphoinositide 3-kinase and protein kinase C signaling pathways and were unchanged either by inhibitors of free radical-generating enzymes or by free radical scavengers. In contrast, the dietary polyphenols quercetin, epigallocatechin-3-gallate and resveratrol completely reversed the inhibitory effect of tert-BOOH upon [3H]DG accumulation through a specific effect on GLUT-mediated transport. Finally, tert-BOOH induced an increase in the transepithelial permeability to [3H]DG in the apical-to-basal direction, apparently related to an increase in its paracellular transport. In conclusion, tert-BOOH-induced oxidative stress reduces STB accumulation of glucose associated with an increase in its transepithelial permeability. This effect may contribute to the deleterious consequences of pregnancy disorders associated with oxidative stress.</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Oxidative stress</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Placenta</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Glucose</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Transport</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Pereira, Ana C.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Correia-Branco, Ana</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Keating, Elisa</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Martel, Fátima</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="n">Elsevier</subfield><subfield code="a">López-Gopar, Mario E. ELSEVIER</subfield><subfield code="t">Mexican student-teachers’ “English” language praxicum: Decolonizing attempts</subfield><subfield code="d">2022</subfield><subfield code="d">EJP</subfield><subfield code="g">New York, NY [u.a.]</subfield><subfield code="w">(DE-627)ELV008405875</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:720</subfield><subfield code="g">year:2013</subfield><subfield code="g">number:1</subfield><subfield code="g">day:15</subfield><subfield code="g">month:11</subfield><subfield code="g">pages:218-226</subfield><subfield code="g">extent:9</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.1016/j.ejphar.2013.10.023</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ELV</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_U</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">720</subfield><subfield code="j">2013</subfield><subfield code="e">1</subfield><subfield code="b">15</subfield><subfield code="c">1115</subfield><subfield code="h">218-226</subfield><subfield code="g">9</subfield></datafield><datafield tag="953" ind1=" " ind2=" "><subfield code="2">045F</subfield><subfield code="a">610</subfield></datafield></record></collection>
|
| score |
7.4016905 |