Prevention of phosphine-induced cytotoxicity by nutrients in HepG2 cells
Background & objectives: Phosphides used as an insecticide and rodenticide, produce phosphine (PH3) which causes accidental and intentional poisoning cases and deaths. There is no specific treatment or antidote available for PH3poisoning. It is suggested that PH3-induced toxicity is associated w...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Marzieh Rashedinia [verfasserIn] Akram Jamshidzadeh [verfasserIn] Abbas Rezaiean Mehrabadi [verfasserIn] Hossein Niknahad [verfasserIn] |
|---|
| Format: |
E-Artikel |
|---|---|
| Sprache: |
Englisch |
| Erschienen: |
2016 |
|---|
| Schlagwörter: |
Dihydroxyacetone - fructose - glyceraldehyde - phosphine - α-ketoglutarate |
|---|
| Übergeordnetes Werk: |
In: Indian Journal of Medical Research - Wolters Kluwer Medknow Publications, 2005, 144(2016), 4, Seite 560-565 |
|---|---|
| Übergeordnetes Werk: |
volume:144 ; year:2016 ; number:4 ; pages:560-565 |
| Links: |
|---|
| DOI / URN: |
10.4103/0971-5916.200896 |
|---|
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DOAJ04567101X |
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| 520 | |a Background & objectives: Phosphides used as an insecticide and rodenticide, produce phosphine (PH3) which causes accidental and intentional poisoning cases and deaths. There is no specific treatment or antidote available for PH3poisoning. It is suggested that PH3-induced toxicity is associated with adenosine triphosphate (ATP) depletion; therefore, in this study the effect of some nutrients was evaluated on PH3cytotoxicity in a cell culture model. Methods: PH3was generated from reaction of zinc phosphide (10 mM) with water in the closed culture medium of HepG2 cells, and cytotoxicity was measured after one and three hours of incubation. ATP, glutathione (GSH) and lipid peroxidation were also assessed at one or three hours post-incubation. ATP suppliers including dihydroxyacetone, glyceraldehyde and fructose were added to the culture medium 10 min before PH3generation to prevent or reduce phosphine-induced cytotoxicity. Results: Phosphine caused about 30 and 66 per cent cell death at one and three hours of incubation, respectively. ATP content of the cells was depleted to 14.7 per cent of control at one hour of incubation. ATP suppliers were able to prevent cytotoxicity and ATP depletion induced by PH3. Dihydroxyacetone, α-ketoglutarate, fructose and mannitol restored the ATP content of the cells from 14.7 per cent to about 40 , 34 , 32 and 30 per cent, respectively. Lipid peroxidation and GSH depletion were not significantly induced by zinc phosphide in this study. Interpretation & conclusions: The results supported the hypothesis that phosphine-induced cytotoxicity was due to decrease of ATP levels. ATP suppliers could prevent its toxicity by generating ATP through glycolysis. α-keto compounds such as dihydroxyacetone and α-ketoglutarate may bind to phosphine and restore mitochondrial respiration. | ||
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10.4103/0971-5916.200896 doi (DE-627)DOAJ04567101X (DE-599)DOAJ18d2e174e09d47f8ac28938d4e7019aa DE-627 ger DE-627 rakwb eng Marzieh Rashedinia verfasserin aut Prevention of phosphine-induced cytotoxicity by nutrients in HepG2 cells 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background & objectives: Phosphides used as an insecticide and rodenticide, produce phosphine (PH3) which causes accidental and intentional poisoning cases and deaths. There is no specific treatment or antidote available for PH3poisoning. It is suggested that PH3-induced toxicity is associated with adenosine triphosphate (ATP) depletion; therefore, in this study the effect of some nutrients was evaluated on PH3cytotoxicity in a cell culture model. Methods: PH3was generated from reaction of zinc phosphide (10 mM) with water in the closed culture medium of HepG2 cells, and cytotoxicity was measured after one and three hours of incubation. ATP, glutathione (GSH) and lipid peroxidation were also assessed at one or three hours post-incubation. ATP suppliers including dihydroxyacetone, glyceraldehyde and fructose were added to the culture medium 10 min before PH3generation to prevent or reduce phosphine-induced cytotoxicity. Results: Phosphine caused about 30 and 66 per cent cell death at one and three hours of incubation, respectively. ATP content of the cells was depleted to 14.7 per cent of control at one hour of incubation. ATP suppliers were able to prevent cytotoxicity and ATP depletion induced by PH3. Dihydroxyacetone, α-ketoglutarate, fructose and mannitol restored the ATP content of the cells from 14.7 per cent to about 40 , 34 , 32 and 30 per cent, respectively. Lipid peroxidation and GSH depletion were not significantly induced by zinc phosphide in this study. Interpretation & conclusions: The results supported the hypothesis that phosphine-induced cytotoxicity was due to decrease of ATP levels. ATP suppliers could prevent its toxicity by generating ATP through glycolysis. α-keto compounds such as dihydroxyacetone and α-ketoglutarate may bind to phosphine and restore mitochondrial respiration. Dihydroxyacetone - fructose - glyceraldehyde - phosphine - α-ketoglutarate Medicine R Akram Jamshidzadeh verfasserin aut Abbas Rezaiean Mehrabadi verfasserin aut Hossein Niknahad verfasserin aut In Indian Journal of Medical Research Wolters Kluwer Medknow Publications, 2005 144(2016), 4, Seite 560-565 (DE-627)DOAJ000026956 09715916 nnns volume:144 year:2016 number:4 pages:560-565 https://doi.org/10.4103/0971-5916.200896 kostenfrei https://doaj.org/article/18d2e174e09d47f8ac28938d4e7019aa kostenfrei http://www.ijmr.org.in/article.asp?issn=0971-5916;year=2016;volume=144;issue=4;spage=560;epage=565;aulast=Rashedinia kostenfrei https://doaj.org/toc/0971-5916 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA AR 144 2016 4 560-565 |
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10.4103/0971-5916.200896 doi (DE-627)DOAJ04567101X (DE-599)DOAJ18d2e174e09d47f8ac28938d4e7019aa DE-627 ger DE-627 rakwb eng Marzieh Rashedinia verfasserin aut Prevention of phosphine-induced cytotoxicity by nutrients in HepG2 cells 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background & objectives: Phosphides used as an insecticide and rodenticide, produce phosphine (PH3) which causes accidental and intentional poisoning cases and deaths. There is no specific treatment or antidote available for PH3poisoning. It is suggested that PH3-induced toxicity is associated with adenosine triphosphate (ATP) depletion; therefore, in this study the effect of some nutrients was evaluated on PH3cytotoxicity in a cell culture model. Methods: PH3was generated from reaction of zinc phosphide (10 mM) with water in the closed culture medium of HepG2 cells, and cytotoxicity was measured after one and three hours of incubation. ATP, glutathione (GSH) and lipid peroxidation were also assessed at one or three hours post-incubation. ATP suppliers including dihydroxyacetone, glyceraldehyde and fructose were added to the culture medium 10 min before PH3generation to prevent or reduce phosphine-induced cytotoxicity. Results: Phosphine caused about 30 and 66 per cent cell death at one and three hours of incubation, respectively. ATP content of the cells was depleted to 14.7 per cent of control at one hour of incubation. ATP suppliers were able to prevent cytotoxicity and ATP depletion induced by PH3. Dihydroxyacetone, α-ketoglutarate, fructose and mannitol restored the ATP content of the cells from 14.7 per cent to about 40 , 34 , 32 and 30 per cent, respectively. Lipid peroxidation and GSH depletion were not significantly induced by zinc phosphide in this study. Interpretation & conclusions: The results supported the hypothesis that phosphine-induced cytotoxicity was due to decrease of ATP levels. ATP suppliers could prevent its toxicity by generating ATP through glycolysis. α-keto compounds such as dihydroxyacetone and α-ketoglutarate may bind to phosphine and restore mitochondrial respiration. Dihydroxyacetone - fructose - glyceraldehyde - phosphine - α-ketoglutarate Medicine R Akram Jamshidzadeh verfasserin aut Abbas Rezaiean Mehrabadi verfasserin aut Hossein Niknahad verfasserin aut In Indian Journal of Medical Research Wolters Kluwer Medknow Publications, 2005 144(2016), 4, Seite 560-565 (DE-627)DOAJ000026956 09715916 nnns volume:144 year:2016 number:4 pages:560-565 https://doi.org/10.4103/0971-5916.200896 kostenfrei https://doaj.org/article/18d2e174e09d47f8ac28938d4e7019aa kostenfrei http://www.ijmr.org.in/article.asp?issn=0971-5916;year=2016;volume=144;issue=4;spage=560;epage=565;aulast=Rashedinia kostenfrei https://doaj.org/toc/0971-5916 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA AR 144 2016 4 560-565 |
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10.4103/0971-5916.200896 doi (DE-627)DOAJ04567101X (DE-599)DOAJ18d2e174e09d47f8ac28938d4e7019aa DE-627 ger DE-627 rakwb eng Marzieh Rashedinia verfasserin aut Prevention of phosphine-induced cytotoxicity by nutrients in HepG2 cells 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background & objectives: Phosphides used as an insecticide and rodenticide, produce phosphine (PH3) which causes accidental and intentional poisoning cases and deaths. There is no specific treatment or antidote available for PH3poisoning. It is suggested that PH3-induced toxicity is associated with adenosine triphosphate (ATP) depletion; therefore, in this study the effect of some nutrients was evaluated on PH3cytotoxicity in a cell culture model. Methods: PH3was generated from reaction of zinc phosphide (10 mM) with water in the closed culture medium of HepG2 cells, and cytotoxicity was measured after one and three hours of incubation. ATP, glutathione (GSH) and lipid peroxidation were also assessed at one or three hours post-incubation. ATP suppliers including dihydroxyacetone, glyceraldehyde and fructose were added to the culture medium 10 min before PH3generation to prevent or reduce phosphine-induced cytotoxicity. Results: Phosphine caused about 30 and 66 per cent cell death at one and three hours of incubation, respectively. ATP content of the cells was depleted to 14.7 per cent of control at one hour of incubation. ATP suppliers were able to prevent cytotoxicity and ATP depletion induced by PH3. Dihydroxyacetone, α-ketoglutarate, fructose and mannitol restored the ATP content of the cells from 14.7 per cent to about 40 , 34 , 32 and 30 per cent, respectively. Lipid peroxidation and GSH depletion were not significantly induced by zinc phosphide in this study. Interpretation & conclusions: The results supported the hypothesis that phosphine-induced cytotoxicity was due to decrease of ATP levels. ATP suppliers could prevent its toxicity by generating ATP through glycolysis. α-keto compounds such as dihydroxyacetone and α-ketoglutarate may bind to phosphine and restore mitochondrial respiration. Dihydroxyacetone - fructose - glyceraldehyde - phosphine - α-ketoglutarate Medicine R Akram Jamshidzadeh verfasserin aut Abbas Rezaiean Mehrabadi verfasserin aut Hossein Niknahad verfasserin aut In Indian Journal of Medical Research Wolters Kluwer Medknow Publications, 2005 144(2016), 4, Seite 560-565 (DE-627)DOAJ000026956 09715916 nnns volume:144 year:2016 number:4 pages:560-565 https://doi.org/10.4103/0971-5916.200896 kostenfrei https://doaj.org/article/18d2e174e09d47f8ac28938d4e7019aa kostenfrei http://www.ijmr.org.in/article.asp?issn=0971-5916;year=2016;volume=144;issue=4;spage=560;epage=565;aulast=Rashedinia kostenfrei https://doaj.org/toc/0971-5916 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA AR 144 2016 4 560-565 |
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10.4103/0971-5916.200896 doi (DE-627)DOAJ04567101X (DE-599)DOAJ18d2e174e09d47f8ac28938d4e7019aa DE-627 ger DE-627 rakwb eng Marzieh Rashedinia verfasserin aut Prevention of phosphine-induced cytotoxicity by nutrients in HepG2 cells 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background & objectives: Phosphides used as an insecticide and rodenticide, produce phosphine (PH3) which causes accidental and intentional poisoning cases and deaths. There is no specific treatment or antidote available for PH3poisoning. It is suggested that PH3-induced toxicity is associated with adenosine triphosphate (ATP) depletion; therefore, in this study the effect of some nutrients was evaluated on PH3cytotoxicity in a cell culture model. Methods: PH3was generated from reaction of zinc phosphide (10 mM) with water in the closed culture medium of HepG2 cells, and cytotoxicity was measured after one and three hours of incubation. ATP, glutathione (GSH) and lipid peroxidation were also assessed at one or three hours post-incubation. ATP suppliers including dihydroxyacetone, glyceraldehyde and fructose were added to the culture medium 10 min before PH3generation to prevent or reduce phosphine-induced cytotoxicity. Results: Phosphine caused about 30 and 66 per cent cell death at one and three hours of incubation, respectively. ATP content of the cells was depleted to 14.7 per cent of control at one hour of incubation. ATP suppliers were able to prevent cytotoxicity and ATP depletion induced by PH3. Dihydroxyacetone, α-ketoglutarate, fructose and mannitol restored the ATP content of the cells from 14.7 per cent to about 40 , 34 , 32 and 30 per cent, respectively. Lipid peroxidation and GSH depletion were not significantly induced by zinc phosphide in this study. Interpretation & conclusions: The results supported the hypothesis that phosphine-induced cytotoxicity was due to decrease of ATP levels. ATP suppliers could prevent its toxicity by generating ATP through glycolysis. α-keto compounds such as dihydroxyacetone and α-ketoglutarate may bind to phosphine and restore mitochondrial respiration. Dihydroxyacetone - fructose - glyceraldehyde - phosphine - α-ketoglutarate Medicine R Akram Jamshidzadeh verfasserin aut Abbas Rezaiean Mehrabadi verfasserin aut Hossein Niknahad verfasserin aut In Indian Journal of Medical Research Wolters Kluwer Medknow Publications, 2005 144(2016), 4, Seite 560-565 (DE-627)DOAJ000026956 09715916 nnns volume:144 year:2016 number:4 pages:560-565 https://doi.org/10.4103/0971-5916.200896 kostenfrei https://doaj.org/article/18d2e174e09d47f8ac28938d4e7019aa kostenfrei http://www.ijmr.org.in/article.asp?issn=0971-5916;year=2016;volume=144;issue=4;spage=560;epage=565;aulast=Rashedinia kostenfrei https://doaj.org/toc/0971-5916 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA AR 144 2016 4 560-565 |
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10.4103/0971-5916.200896 doi (DE-627)DOAJ04567101X (DE-599)DOAJ18d2e174e09d47f8ac28938d4e7019aa DE-627 ger DE-627 rakwb eng Marzieh Rashedinia verfasserin aut Prevention of phosphine-induced cytotoxicity by nutrients in HepG2 cells 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background & objectives: Phosphides used as an insecticide and rodenticide, produce phosphine (PH3) which causes accidental and intentional poisoning cases and deaths. There is no specific treatment or antidote available for PH3poisoning. It is suggested that PH3-induced toxicity is associated with adenosine triphosphate (ATP) depletion; therefore, in this study the effect of some nutrients was evaluated on PH3cytotoxicity in a cell culture model. Methods: PH3was generated from reaction of zinc phosphide (10 mM) with water in the closed culture medium of HepG2 cells, and cytotoxicity was measured after one and three hours of incubation. ATP, glutathione (GSH) and lipid peroxidation were also assessed at one or three hours post-incubation. ATP suppliers including dihydroxyacetone, glyceraldehyde and fructose were added to the culture medium 10 min before PH3generation to prevent or reduce phosphine-induced cytotoxicity. Results: Phosphine caused about 30 and 66 per cent cell death at one and three hours of incubation, respectively. ATP content of the cells was depleted to 14.7 per cent of control at one hour of incubation. ATP suppliers were able to prevent cytotoxicity and ATP depletion induced by PH3. Dihydroxyacetone, α-ketoglutarate, fructose and mannitol restored the ATP content of the cells from 14.7 per cent to about 40 , 34 , 32 and 30 per cent, respectively. Lipid peroxidation and GSH depletion were not significantly induced by zinc phosphide in this study. Interpretation & conclusions: The results supported the hypothesis that phosphine-induced cytotoxicity was due to decrease of ATP levels. ATP suppliers could prevent its toxicity by generating ATP through glycolysis. α-keto compounds such as dihydroxyacetone and α-ketoglutarate may bind to phosphine and restore mitochondrial respiration. Dihydroxyacetone - fructose - glyceraldehyde - phosphine - α-ketoglutarate Medicine R Akram Jamshidzadeh verfasserin aut Abbas Rezaiean Mehrabadi verfasserin aut Hossein Niknahad verfasserin aut In Indian Journal of Medical Research Wolters Kluwer Medknow Publications, 2005 144(2016), 4, Seite 560-565 (DE-627)DOAJ000026956 09715916 nnns volume:144 year:2016 number:4 pages:560-565 https://doi.org/10.4103/0971-5916.200896 kostenfrei https://doaj.org/article/18d2e174e09d47f8ac28938d4e7019aa kostenfrei http://www.ijmr.org.in/article.asp?issn=0971-5916;year=2016;volume=144;issue=4;spage=560;epage=565;aulast=Rashedinia kostenfrei https://doaj.org/toc/0971-5916 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA AR 144 2016 4 560-565 |
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|
| author |
Marzieh Rashedinia |
| spellingShingle |
Marzieh Rashedinia misc Dihydroxyacetone - fructose - glyceraldehyde - phosphine - α-ketoglutarate misc Medicine misc R Prevention of phosphine-induced cytotoxicity by nutrients in HepG2 cells |
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Prevention of phosphine-induced cytotoxicity by nutrients in HepG2 cells Dihydroxyacetone - fructose - glyceraldehyde - phosphine - α-ketoglutarate |
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Prevention of phosphine-induced cytotoxicity by nutrients in HepG2 cells |
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Marzieh Rashedinia Akram Jamshidzadeh Abbas Rezaiean Mehrabadi Hossein Niknahad |
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prevention of phosphine-induced cytotoxicity by nutrients in hepg2 cells |
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Prevention of phosphine-induced cytotoxicity by nutrients in HepG2 cells |
| abstract |
Background & objectives: Phosphides used as an insecticide and rodenticide, produce phosphine (PH3) which causes accidental and intentional poisoning cases and deaths. There is no specific treatment or antidote available for PH3poisoning. It is suggested that PH3-induced toxicity is associated with adenosine triphosphate (ATP) depletion; therefore, in this study the effect of some nutrients was evaluated on PH3cytotoxicity in a cell culture model. Methods: PH3was generated from reaction of zinc phosphide (10 mM) with water in the closed culture medium of HepG2 cells, and cytotoxicity was measured after one and three hours of incubation. ATP, glutathione (GSH) and lipid peroxidation were also assessed at one or three hours post-incubation. ATP suppliers including dihydroxyacetone, glyceraldehyde and fructose were added to the culture medium 10 min before PH3generation to prevent or reduce phosphine-induced cytotoxicity. Results: Phosphine caused about 30 and 66 per cent cell death at one and three hours of incubation, respectively. ATP content of the cells was depleted to 14.7 per cent of control at one hour of incubation. ATP suppliers were able to prevent cytotoxicity and ATP depletion induced by PH3. Dihydroxyacetone, α-ketoglutarate, fructose and mannitol restored the ATP content of the cells from 14.7 per cent to about 40 , 34 , 32 and 30 per cent, respectively. Lipid peroxidation and GSH depletion were not significantly induced by zinc phosphide in this study. Interpretation & conclusions: The results supported the hypothesis that phosphine-induced cytotoxicity was due to decrease of ATP levels. ATP suppliers could prevent its toxicity by generating ATP through glycolysis. α-keto compounds such as dihydroxyacetone and α-ketoglutarate may bind to phosphine and restore mitochondrial respiration. |
| abstractGer |
Background & objectives: Phosphides used as an insecticide and rodenticide, produce phosphine (PH3) which causes accidental and intentional poisoning cases and deaths. There is no specific treatment or antidote available for PH3poisoning. It is suggested that PH3-induced toxicity is associated with adenosine triphosphate (ATP) depletion; therefore, in this study the effect of some nutrients was evaluated on PH3cytotoxicity in a cell culture model. Methods: PH3was generated from reaction of zinc phosphide (10 mM) with water in the closed culture medium of HepG2 cells, and cytotoxicity was measured after one and three hours of incubation. ATP, glutathione (GSH) and lipid peroxidation were also assessed at one or three hours post-incubation. ATP suppliers including dihydroxyacetone, glyceraldehyde and fructose were added to the culture medium 10 min before PH3generation to prevent or reduce phosphine-induced cytotoxicity. Results: Phosphine caused about 30 and 66 per cent cell death at one and three hours of incubation, respectively. ATP content of the cells was depleted to 14.7 per cent of control at one hour of incubation. ATP suppliers were able to prevent cytotoxicity and ATP depletion induced by PH3. Dihydroxyacetone, α-ketoglutarate, fructose and mannitol restored the ATP content of the cells from 14.7 per cent to about 40 , 34 , 32 and 30 per cent, respectively. Lipid peroxidation and GSH depletion were not significantly induced by zinc phosphide in this study. Interpretation & conclusions: The results supported the hypothesis that phosphine-induced cytotoxicity was due to decrease of ATP levels. ATP suppliers could prevent its toxicity by generating ATP through glycolysis. α-keto compounds such as dihydroxyacetone and α-ketoglutarate may bind to phosphine and restore mitochondrial respiration. |
| abstract_unstemmed |
Background & objectives: Phosphides used as an insecticide and rodenticide, produce phosphine (PH3) which causes accidental and intentional poisoning cases and deaths. There is no specific treatment or antidote available for PH3poisoning. It is suggested that PH3-induced toxicity is associated with adenosine triphosphate (ATP) depletion; therefore, in this study the effect of some nutrients was evaluated on PH3cytotoxicity in a cell culture model. Methods: PH3was generated from reaction of zinc phosphide (10 mM) with water in the closed culture medium of HepG2 cells, and cytotoxicity was measured after one and three hours of incubation. ATP, glutathione (GSH) and lipid peroxidation were also assessed at one or three hours post-incubation. ATP suppliers including dihydroxyacetone, glyceraldehyde and fructose were added to the culture medium 10 min before PH3generation to prevent or reduce phosphine-induced cytotoxicity. Results: Phosphine caused about 30 and 66 per cent cell death at one and three hours of incubation, respectively. ATP content of the cells was depleted to 14.7 per cent of control at one hour of incubation. ATP suppliers were able to prevent cytotoxicity and ATP depletion induced by PH3. Dihydroxyacetone, α-ketoglutarate, fructose and mannitol restored the ATP content of the cells from 14.7 per cent to about 40 , 34 , 32 and 30 per cent, respectively. Lipid peroxidation and GSH depletion were not significantly induced by zinc phosphide in this study. Interpretation & conclusions: The results supported the hypothesis that phosphine-induced cytotoxicity was due to decrease of ATP levels. ATP suppliers could prevent its toxicity by generating ATP through glycolysis. α-keto compounds such as dihydroxyacetone and α-ketoglutarate may bind to phosphine and restore mitochondrial respiration. |
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https://doi.org/10.4103/0971-5916.200896 https://doaj.org/article/18d2e174e09d47f8ac28938d4e7019aa http://www.ijmr.org.in/article.asp?issn=0971-5916;year=2016;volume=144;issue=4;spage=560;epage=565;aulast=Rashedinia https://doaj.org/toc/0971-5916 |
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