DNA methylation and RASSF4 expression are involved in T-2 toxin-induced hepatotoxicity
T-2 toxin is a secondary metabolite produced by Fusarium species and commonly contaminates food and animal feed. T-2 toxin can induce hepatotoxicity through apoptosis and oxidative stress; however, the underlying mechanism is not clear. Recent studies indicated that RASSF4, a member of the RASSF fam...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Liu, Aimei [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2019transfer abstract |
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| Schlagwörter: |
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| Übergeordnetes Werk: |
Enthalten in: Too late or too little? Potential for Alzheimer's disease passive immunotherapy via targeted intracerebroventricular delivery - 2013, an international journal concerned with the effects of chemicals on living systems and immunotoxicology, Amsterdam [u.a.] |
|---|---|
| Übergeordnetes Werk: |
volume:425 ; year:2019 ; day:1 ; month:09 ; pages:0 |
| Links: |
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| DOI / URN: |
10.1016/j.tox.2019.152246 |
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ELV047697911 |
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| 245 | 1 | 0 | |a DNA methylation and RASSF4 expression are involved in T-2 toxin-induced hepatotoxicity |
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| 520 | |a T-2 toxin is a secondary metabolite produced by Fusarium species and commonly contaminates food and animal feed. T-2 toxin can induce hepatotoxicity through apoptosis and oxidative stress; however, the underlying mechanism is not clear. Recent studies indicated that RASSF4, a member of the RASSF family, participates in cell apoptosis and some cancers due to its inactivation via DNA hypermethylation. However, its role in T-2 toxin-induced liver toxicity is poorly understood. Therefore, in this study, female Wistar rats were given a single dose of T-2 toxin at 2 mg/kg b.w. and were sacrificed at 1, 3 and 7 days post-exposure. A normal rat liver cell line (BRL) was exposed to different concentrations of T-2 toxin (10, 20, 40 nM) for 4, 8, 12 h, respectively. Histopathological analysis revealed with apoptosis in some liver cells and clear proliferation under T-2 toxin exposure. Expression analysis by immunohistochemical assays, quantitative real-time PCR (qPCR) and western blot demonstrated that T-2 toxin activated PI3K-Akt/Caspase/NF-κB signaling pathways. Additionally, DNA methylation assays revealed that the expression of RASSF4 was silenced by promoter hypermethylation after exposure to T-2 toxin for 1 and 3 days as compared to the control group. Moreover, joint treatment of 5-Aza-2′-deoxycytidine (DAC) (5 μM) and T-2 toxin (40 nM) increased expression of RASSF4 and PI3K-Akt/caspase/NF-κB signaling pathways-related genes, inducing cell apoptosis. These findings for the first time demonstrated that DNA methylation regulated the RASSF4 expression under T-2 toxin, along with the activation of its downstream pathways, resulting in apoptosis. | ||
| 520 | |a T-2 toxin is a secondary metabolite produced by Fusarium species and commonly contaminates food and animal feed. T-2 toxin can induce hepatotoxicity through apoptosis and oxidative stress; however, the underlying mechanism is not clear. Recent studies indicated that RASSF4, a member of the RASSF family, participates in cell apoptosis and some cancers due to its inactivation via DNA hypermethylation. However, its role in T-2 toxin-induced liver toxicity is poorly understood. Therefore, in this study, female Wistar rats were given a single dose of T-2 toxin at 2 mg/kg b.w. and were sacrificed at 1, 3 and 7 days post-exposure. A normal rat liver cell line (BRL) was exposed to different concentrations of T-2 toxin (10, 20, 40 nM) for 4, 8, 12 h, respectively. Histopathological analysis revealed with apoptosis in some liver cells and clear proliferation under T-2 toxin exposure. Expression analysis by immunohistochemical assays, quantitative real-time PCR (qPCR) and western blot demonstrated that T-2 toxin activated PI3K-Akt/Caspase/NF-κB signaling pathways. Additionally, DNA methylation assays revealed that the expression of RASSF4 was silenced by promoter hypermethylation after exposure to T-2 toxin for 1 and 3 days as compared to the control group. Moreover, joint treatment of 5-Aza-2′-deoxycytidine (DAC) (5 μM) and T-2 toxin (40 nM) increased expression of RASSF4 and PI3K-Akt/caspase/NF-κB signaling pathways-related genes, inducing cell apoptosis. These findings for the first time demonstrated that DNA methylation regulated the RASSF4 expression under T-2 toxin, along with the activation of its downstream pathways, resulting in apoptosis. | ||
| 650 | 7 | |a APS |2 Elsevier | |
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| 700 | 1 | |a Chen, Dongmei |4 oth | |
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| 700 | 1 | |a Wang, Xu |4 oth | |
| 700 | 1 | |a Wu, Qinghua |4 oth | |
| 700 | 1 | |a Yuan, Zonghui |4 oth | |
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10.1016/j.tox.2019.152246 doi GBV00000000000726.pica (DE-627)ELV047697911 (ELSEVIER)S0300-483X(19)30202-1 DE-627 ger DE-627 rakwb eng 610 VZ 530 VZ 52.56 bkl Liu, Aimei verfasserin aut DNA methylation and RASSF4 expression are involved in T-2 toxin-induced hepatotoxicity 2019transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier T-2 toxin is a secondary metabolite produced by Fusarium species and commonly contaminates food and animal feed. T-2 toxin can induce hepatotoxicity through apoptosis and oxidative stress; however, the underlying mechanism is not clear. Recent studies indicated that RASSF4, a member of the RASSF family, participates in cell apoptosis and some cancers due to its inactivation via DNA hypermethylation. However, its role in T-2 toxin-induced liver toxicity is poorly understood. Therefore, in this study, female Wistar rats were given a single dose of T-2 toxin at 2 mg/kg b.w. and were sacrificed at 1, 3 and 7 days post-exposure. A normal rat liver cell line (BRL) was exposed to different concentrations of T-2 toxin (10, 20, 40 nM) for 4, 8, 12 h, respectively. Histopathological analysis revealed with apoptosis in some liver cells and clear proliferation under T-2 toxin exposure. Expression analysis by immunohistochemical assays, quantitative real-time PCR (qPCR) and western blot demonstrated that T-2 toxin activated PI3K-Akt/Caspase/NF-κB signaling pathways. Additionally, DNA methylation assays revealed that the expression of RASSF4 was silenced by promoter hypermethylation after exposure to T-2 toxin for 1 and 3 days as compared to the control group. Moreover, joint treatment of 5-Aza-2′-deoxycytidine (DAC) (5 μM) and T-2 toxin (40 nM) increased expression of RASSF4 and PI3K-Akt/caspase/NF-κB signaling pathways-related genes, inducing cell apoptosis. These findings for the first time demonstrated that DNA methylation regulated the RASSF4 expression under T-2 toxin, along with the activation of its downstream pathways, resulting in apoptosis. T-2 toxin is a secondary metabolite produced by Fusarium species and commonly contaminates food and animal feed. T-2 toxin can induce hepatotoxicity through apoptosis and oxidative stress; however, the underlying mechanism is not clear. Recent studies indicated that RASSF4, a member of the RASSF family, participates in cell apoptosis and some cancers due to its inactivation via DNA hypermethylation. However, its role in T-2 toxin-induced liver toxicity is poorly understood. Therefore, in this study, female Wistar rats were given a single dose of T-2 toxin at 2 mg/kg b.w. and were sacrificed at 1, 3 and 7 days post-exposure. A normal rat liver cell line (BRL) was exposed to different concentrations of T-2 toxin (10, 20, 40 nM) for 4, 8, 12 h, respectively. Histopathological analysis revealed with apoptosis in some liver cells and clear proliferation under T-2 toxin exposure. Expression analysis by immunohistochemical assays, quantitative real-time PCR (qPCR) and western blot demonstrated that T-2 toxin activated PI3K-Akt/Caspase/NF-κB signaling pathways. Additionally, DNA methylation assays revealed that the expression of RASSF4 was silenced by promoter hypermethylation after exposure to T-2 toxin for 1 and 3 days as compared to the control group. Moreover, joint treatment of 5-Aza-2′-deoxycytidine (DAC) (5 μM) and T-2 toxin (40 nM) increased expression of RASSF4 and PI3K-Akt/caspase/NF-κB signaling pathways-related genes, inducing cell apoptosis. These findings for the first time demonstrated that DNA methylation regulated the RASSF4 expression under T-2 toxin, along with the activation of its downstream pathways, resulting in apoptosis. APS Elsevier DMSO Elsevier DTT Elsevier Bcl-x Elsevier JNK Elsevier MTT Elsevier Caspase-3 Elsevier RIPA Elsevier BSA Elsevier NF-κB Elsevier p38 Elsevier PI3K Elsevier ANOVA Elsevier OD Elsevier RASSF4 Elsevier FBS Elsevier Akt1 Elsevier qPCR Elsevier BSP Elsevier QUMA Elsevier PBS Elsevier BCA Elsevier SDS Elsevier DAB Elsevier DAC Elsevier MST1 Elsevier LD<ce:inf loc="post">50</ce:inf> Elsevier T-2 toxin Elsevier PAGE Elsevier MSP Elsevier P53 Elsevier p-Akt Elsevier STAT Elsevier JAK Elsevier PMSF Elsevier Caspase-9 Elsevier Bax Elsevier MDM2 Elsevier Fas Elsevier BRL Elsevier HE Elsevier C-jun Elsevier Xu, Xiaoqing oth Hou, Ren oth Badawy, Sara oth Tao, Yanfei oth Chen, Dongmei oth Ihsan, Awais oth Wang, Xu oth Wu, Qinghua oth Yuan, Zonghui oth Enthalten in Elsevier Science Too late or too little? Potential for Alzheimer's disease passive immunotherapy via targeted intracerebroventricular delivery 2013 an international journal concerned with the effects of chemicals on living systems and immunotoxicology Amsterdam [u.a.] (DE-627)ELV011413085 volume:425 year:2019 day:1 month:09 pages:0 https://doi.org/10.1016/j.tox.2019.152246 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U GBV_ILN_22 GBV_ILN_40 GBV_ILN_105 52.56 Regenerative Energieformen alternative Energieformen VZ AR 425 2019 1 0901 0 |
| spelling |
10.1016/j.tox.2019.152246 doi GBV00000000000726.pica (DE-627)ELV047697911 (ELSEVIER)S0300-483X(19)30202-1 DE-627 ger DE-627 rakwb eng 610 VZ 530 VZ 52.56 bkl Liu, Aimei verfasserin aut DNA methylation and RASSF4 expression are involved in T-2 toxin-induced hepatotoxicity 2019transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier T-2 toxin is a secondary metabolite produced by Fusarium species and commonly contaminates food and animal feed. T-2 toxin can induce hepatotoxicity through apoptosis and oxidative stress; however, the underlying mechanism is not clear. Recent studies indicated that RASSF4, a member of the RASSF family, participates in cell apoptosis and some cancers due to its inactivation via DNA hypermethylation. However, its role in T-2 toxin-induced liver toxicity is poorly understood. Therefore, in this study, female Wistar rats were given a single dose of T-2 toxin at 2 mg/kg b.w. and were sacrificed at 1, 3 and 7 days post-exposure. A normal rat liver cell line (BRL) was exposed to different concentrations of T-2 toxin (10, 20, 40 nM) for 4, 8, 12 h, respectively. Histopathological analysis revealed with apoptosis in some liver cells and clear proliferation under T-2 toxin exposure. Expression analysis by immunohistochemical assays, quantitative real-time PCR (qPCR) and western blot demonstrated that T-2 toxin activated PI3K-Akt/Caspase/NF-κB signaling pathways. Additionally, DNA methylation assays revealed that the expression of RASSF4 was silenced by promoter hypermethylation after exposure to T-2 toxin for 1 and 3 days as compared to the control group. Moreover, joint treatment of 5-Aza-2′-deoxycytidine (DAC) (5 μM) and T-2 toxin (40 nM) increased expression of RASSF4 and PI3K-Akt/caspase/NF-κB signaling pathways-related genes, inducing cell apoptosis. These findings for the first time demonstrated that DNA methylation regulated the RASSF4 expression under T-2 toxin, along with the activation of its downstream pathways, resulting in apoptosis. T-2 toxin is a secondary metabolite produced by Fusarium species and commonly contaminates food and animal feed. T-2 toxin can induce hepatotoxicity through apoptosis and oxidative stress; however, the underlying mechanism is not clear. Recent studies indicated that RASSF4, a member of the RASSF family, participates in cell apoptosis and some cancers due to its inactivation via DNA hypermethylation. However, its role in T-2 toxin-induced liver toxicity is poorly understood. Therefore, in this study, female Wistar rats were given a single dose of T-2 toxin at 2 mg/kg b.w. and were sacrificed at 1, 3 and 7 days post-exposure. A normal rat liver cell line (BRL) was exposed to different concentrations of T-2 toxin (10, 20, 40 nM) for 4, 8, 12 h, respectively. Histopathological analysis revealed with apoptosis in some liver cells and clear proliferation under T-2 toxin exposure. Expression analysis by immunohistochemical assays, quantitative real-time PCR (qPCR) and western blot demonstrated that T-2 toxin activated PI3K-Akt/Caspase/NF-κB signaling pathways. Additionally, DNA methylation assays revealed that the expression of RASSF4 was silenced by promoter hypermethylation after exposure to T-2 toxin for 1 and 3 days as compared to the control group. Moreover, joint treatment of 5-Aza-2′-deoxycytidine (DAC) (5 μM) and T-2 toxin (40 nM) increased expression of RASSF4 and PI3K-Akt/caspase/NF-κB signaling pathways-related genes, inducing cell apoptosis. These findings for the first time demonstrated that DNA methylation regulated the RASSF4 expression under T-2 toxin, along with the activation of its downstream pathways, resulting in apoptosis. APS Elsevier DMSO Elsevier DTT Elsevier Bcl-x Elsevier JNK Elsevier MTT Elsevier Caspase-3 Elsevier RIPA Elsevier BSA Elsevier NF-κB Elsevier p38 Elsevier PI3K Elsevier ANOVA Elsevier OD Elsevier RASSF4 Elsevier FBS Elsevier Akt1 Elsevier qPCR Elsevier BSP Elsevier QUMA Elsevier PBS Elsevier BCA Elsevier SDS Elsevier DAB Elsevier DAC Elsevier MST1 Elsevier LD<ce:inf loc="post">50</ce:inf> Elsevier T-2 toxin Elsevier PAGE Elsevier MSP Elsevier P53 Elsevier p-Akt Elsevier STAT Elsevier JAK Elsevier PMSF Elsevier Caspase-9 Elsevier Bax Elsevier MDM2 Elsevier Fas Elsevier BRL Elsevier HE Elsevier C-jun Elsevier Xu, Xiaoqing oth Hou, Ren oth Badawy, Sara oth Tao, Yanfei oth Chen, Dongmei oth Ihsan, Awais oth Wang, Xu oth Wu, Qinghua oth Yuan, Zonghui oth Enthalten in Elsevier Science Too late or too little? Potential for Alzheimer's disease passive immunotherapy via targeted intracerebroventricular delivery 2013 an international journal concerned with the effects of chemicals on living systems and immunotoxicology Amsterdam [u.a.] (DE-627)ELV011413085 volume:425 year:2019 day:1 month:09 pages:0 https://doi.org/10.1016/j.tox.2019.152246 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U GBV_ILN_22 GBV_ILN_40 GBV_ILN_105 52.56 Regenerative Energieformen alternative Energieformen VZ AR 425 2019 1 0901 0 |
| allfields_unstemmed |
10.1016/j.tox.2019.152246 doi GBV00000000000726.pica (DE-627)ELV047697911 (ELSEVIER)S0300-483X(19)30202-1 DE-627 ger DE-627 rakwb eng 610 VZ 530 VZ 52.56 bkl Liu, Aimei verfasserin aut DNA methylation and RASSF4 expression are involved in T-2 toxin-induced hepatotoxicity 2019transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier T-2 toxin is a secondary metabolite produced by Fusarium species and commonly contaminates food and animal feed. T-2 toxin can induce hepatotoxicity through apoptosis and oxidative stress; however, the underlying mechanism is not clear. Recent studies indicated that RASSF4, a member of the RASSF family, participates in cell apoptosis and some cancers due to its inactivation via DNA hypermethylation. However, its role in T-2 toxin-induced liver toxicity is poorly understood. Therefore, in this study, female Wistar rats were given a single dose of T-2 toxin at 2 mg/kg b.w. and were sacrificed at 1, 3 and 7 days post-exposure. A normal rat liver cell line (BRL) was exposed to different concentrations of T-2 toxin (10, 20, 40 nM) for 4, 8, 12 h, respectively. Histopathological analysis revealed with apoptosis in some liver cells and clear proliferation under T-2 toxin exposure. Expression analysis by immunohistochemical assays, quantitative real-time PCR (qPCR) and western blot demonstrated that T-2 toxin activated PI3K-Akt/Caspase/NF-κB signaling pathways. Additionally, DNA methylation assays revealed that the expression of RASSF4 was silenced by promoter hypermethylation after exposure to T-2 toxin for 1 and 3 days as compared to the control group. Moreover, joint treatment of 5-Aza-2′-deoxycytidine (DAC) (5 μM) and T-2 toxin (40 nM) increased expression of RASSF4 and PI3K-Akt/caspase/NF-κB signaling pathways-related genes, inducing cell apoptosis. These findings for the first time demonstrated that DNA methylation regulated the RASSF4 expression under T-2 toxin, along with the activation of its downstream pathways, resulting in apoptosis. T-2 toxin is a secondary metabolite produced by Fusarium species and commonly contaminates food and animal feed. T-2 toxin can induce hepatotoxicity through apoptosis and oxidative stress; however, the underlying mechanism is not clear. Recent studies indicated that RASSF4, a member of the RASSF family, participates in cell apoptosis and some cancers due to its inactivation via DNA hypermethylation. However, its role in T-2 toxin-induced liver toxicity is poorly understood. Therefore, in this study, female Wistar rats were given a single dose of T-2 toxin at 2 mg/kg b.w. and were sacrificed at 1, 3 and 7 days post-exposure. A normal rat liver cell line (BRL) was exposed to different concentrations of T-2 toxin (10, 20, 40 nM) for 4, 8, 12 h, respectively. Histopathological analysis revealed with apoptosis in some liver cells and clear proliferation under T-2 toxin exposure. Expression analysis by immunohistochemical assays, quantitative real-time PCR (qPCR) and western blot demonstrated that T-2 toxin activated PI3K-Akt/Caspase/NF-κB signaling pathways. Additionally, DNA methylation assays revealed that the expression of RASSF4 was silenced by promoter hypermethylation after exposure to T-2 toxin for 1 and 3 days as compared to the control group. Moreover, joint treatment of 5-Aza-2′-deoxycytidine (DAC) (5 μM) and T-2 toxin (40 nM) increased expression of RASSF4 and PI3K-Akt/caspase/NF-κB signaling pathways-related genes, inducing cell apoptosis. These findings for the first time demonstrated that DNA methylation regulated the RASSF4 expression under T-2 toxin, along with the activation of its downstream pathways, resulting in apoptosis. APS Elsevier DMSO Elsevier DTT Elsevier Bcl-x Elsevier JNK Elsevier MTT Elsevier Caspase-3 Elsevier RIPA Elsevier BSA Elsevier NF-κB Elsevier p38 Elsevier PI3K Elsevier ANOVA Elsevier OD Elsevier RASSF4 Elsevier FBS Elsevier Akt1 Elsevier qPCR Elsevier BSP Elsevier QUMA Elsevier PBS Elsevier BCA Elsevier SDS Elsevier DAB Elsevier DAC Elsevier MST1 Elsevier LD<ce:inf loc="post">50</ce:inf> Elsevier T-2 toxin Elsevier PAGE Elsevier MSP Elsevier P53 Elsevier p-Akt Elsevier STAT Elsevier JAK Elsevier PMSF Elsevier Caspase-9 Elsevier Bax Elsevier MDM2 Elsevier Fas Elsevier BRL Elsevier HE Elsevier C-jun Elsevier Xu, Xiaoqing oth Hou, Ren oth Badawy, Sara oth Tao, Yanfei oth Chen, Dongmei oth Ihsan, Awais oth Wang, Xu oth Wu, Qinghua oth Yuan, Zonghui oth Enthalten in Elsevier Science Too late or too little? Potential for Alzheimer's disease passive immunotherapy via targeted intracerebroventricular delivery 2013 an international journal concerned with the effects of chemicals on living systems and immunotoxicology Amsterdam [u.a.] (DE-627)ELV011413085 volume:425 year:2019 day:1 month:09 pages:0 https://doi.org/10.1016/j.tox.2019.152246 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U GBV_ILN_22 GBV_ILN_40 GBV_ILN_105 52.56 Regenerative Energieformen alternative Energieformen VZ AR 425 2019 1 0901 0 |
| allfieldsGer |
10.1016/j.tox.2019.152246 doi GBV00000000000726.pica (DE-627)ELV047697911 (ELSEVIER)S0300-483X(19)30202-1 DE-627 ger DE-627 rakwb eng 610 VZ 530 VZ 52.56 bkl Liu, Aimei verfasserin aut DNA methylation and RASSF4 expression are involved in T-2 toxin-induced hepatotoxicity 2019transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier T-2 toxin is a secondary metabolite produced by Fusarium species and commonly contaminates food and animal feed. T-2 toxin can induce hepatotoxicity through apoptosis and oxidative stress; however, the underlying mechanism is not clear. Recent studies indicated that RASSF4, a member of the RASSF family, participates in cell apoptosis and some cancers due to its inactivation via DNA hypermethylation. However, its role in T-2 toxin-induced liver toxicity is poorly understood. Therefore, in this study, female Wistar rats were given a single dose of T-2 toxin at 2 mg/kg b.w. and were sacrificed at 1, 3 and 7 days post-exposure. A normal rat liver cell line (BRL) was exposed to different concentrations of T-2 toxin (10, 20, 40 nM) for 4, 8, 12 h, respectively. Histopathological analysis revealed with apoptosis in some liver cells and clear proliferation under T-2 toxin exposure. Expression analysis by immunohistochemical assays, quantitative real-time PCR (qPCR) and western blot demonstrated that T-2 toxin activated PI3K-Akt/Caspase/NF-κB signaling pathways. Additionally, DNA methylation assays revealed that the expression of RASSF4 was silenced by promoter hypermethylation after exposure to T-2 toxin for 1 and 3 days as compared to the control group. Moreover, joint treatment of 5-Aza-2′-deoxycytidine (DAC) (5 μM) and T-2 toxin (40 nM) increased expression of RASSF4 and PI3K-Akt/caspase/NF-κB signaling pathways-related genes, inducing cell apoptosis. These findings for the first time demonstrated that DNA methylation regulated the RASSF4 expression under T-2 toxin, along with the activation of its downstream pathways, resulting in apoptosis. T-2 toxin is a secondary metabolite produced by Fusarium species and commonly contaminates food and animal feed. T-2 toxin can induce hepatotoxicity through apoptosis and oxidative stress; however, the underlying mechanism is not clear. Recent studies indicated that RASSF4, a member of the RASSF family, participates in cell apoptosis and some cancers due to its inactivation via DNA hypermethylation. However, its role in T-2 toxin-induced liver toxicity is poorly understood. Therefore, in this study, female Wistar rats were given a single dose of T-2 toxin at 2 mg/kg b.w. and were sacrificed at 1, 3 and 7 days post-exposure. A normal rat liver cell line (BRL) was exposed to different concentrations of T-2 toxin (10, 20, 40 nM) for 4, 8, 12 h, respectively. Histopathological analysis revealed with apoptosis in some liver cells and clear proliferation under T-2 toxin exposure. Expression analysis by immunohistochemical assays, quantitative real-time PCR (qPCR) and western blot demonstrated that T-2 toxin activated PI3K-Akt/Caspase/NF-κB signaling pathways. Additionally, DNA methylation assays revealed that the expression of RASSF4 was silenced by promoter hypermethylation after exposure to T-2 toxin for 1 and 3 days as compared to the control group. Moreover, joint treatment of 5-Aza-2′-deoxycytidine (DAC) (5 μM) and T-2 toxin (40 nM) increased expression of RASSF4 and PI3K-Akt/caspase/NF-κB signaling pathways-related genes, inducing cell apoptosis. These findings for the first time demonstrated that DNA methylation regulated the RASSF4 expression under T-2 toxin, along with the activation of its downstream pathways, resulting in apoptosis. APS Elsevier DMSO Elsevier DTT Elsevier Bcl-x Elsevier JNK Elsevier MTT Elsevier Caspase-3 Elsevier RIPA Elsevier BSA Elsevier NF-κB Elsevier p38 Elsevier PI3K Elsevier ANOVA Elsevier OD Elsevier RASSF4 Elsevier FBS Elsevier Akt1 Elsevier qPCR Elsevier BSP Elsevier QUMA Elsevier PBS Elsevier BCA Elsevier SDS Elsevier DAB Elsevier DAC Elsevier MST1 Elsevier LD<ce:inf loc="post">50</ce:inf> Elsevier T-2 toxin Elsevier PAGE Elsevier MSP Elsevier P53 Elsevier p-Akt Elsevier STAT Elsevier JAK Elsevier PMSF Elsevier Caspase-9 Elsevier Bax Elsevier MDM2 Elsevier Fas Elsevier BRL Elsevier HE Elsevier C-jun Elsevier Xu, Xiaoqing oth Hou, Ren oth Badawy, Sara oth Tao, Yanfei oth Chen, Dongmei oth Ihsan, Awais oth Wang, Xu oth Wu, Qinghua oth Yuan, Zonghui oth Enthalten in Elsevier Science Too late or too little? Potential for Alzheimer's disease passive immunotherapy via targeted intracerebroventricular delivery 2013 an international journal concerned with the effects of chemicals on living systems and immunotoxicology Amsterdam [u.a.] (DE-627)ELV011413085 volume:425 year:2019 day:1 month:09 pages:0 https://doi.org/10.1016/j.tox.2019.152246 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U GBV_ILN_22 GBV_ILN_40 GBV_ILN_105 52.56 Regenerative Energieformen alternative Energieformen VZ AR 425 2019 1 0901 0 |
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Therefore, in this study, female Wistar rats were given a single dose of T-2 toxin at 2 mg/kg b.w. and were sacrificed at 1, 3 and 7 days post-exposure. A normal rat liver cell line (BRL) was exposed to different concentrations of T-2 toxin (10, 20, 40 nM) for 4, 8, 12 h, respectively. Histopathological analysis revealed with apoptosis in some liver cells and clear proliferation under T-2 toxin exposure. Expression analysis by immunohistochemical assays, quantitative real-time PCR (qPCR) and western blot demonstrated that T-2 toxin activated PI3K-Akt/Caspase/NF-κB signaling pathways. Additionally, DNA methylation assays revealed that the expression of RASSF4 was silenced by promoter hypermethylation after exposure to T-2 toxin for 1 and 3 days as compared to the control group. Moreover, joint treatment of 5-Aza-2′-deoxycytidine (DAC) (5 μM) and T-2 toxin (40 nM) increased expression of RASSF4 and PI3K-Akt/caspase/NF-κB signaling pathways-related genes, inducing cell apoptosis. These findings for the first time demonstrated that DNA methylation regulated the RASSF4 expression under T-2 toxin, along with the activation of its downstream pathways, resulting in apoptosis. T-2 toxin is a secondary metabolite produced by Fusarium species and commonly contaminates food and animal feed. T-2 toxin can induce hepatotoxicity through apoptosis and oxidative stress; however, the underlying mechanism is not clear. Recent studies indicated that RASSF4, a member of the RASSF family, participates in cell apoptosis and some cancers due to its inactivation via DNA hypermethylation. However, its role in T-2 toxin-induced liver toxicity is poorly understood. Therefore, in this study, female Wistar rats were given a single dose of T-2 toxin at 2 mg/kg b.w. and were sacrificed at 1, 3 and 7 days post-exposure. A normal rat liver cell line (BRL) was exposed to different concentrations of T-2 toxin (10, 20, 40 nM) for 4, 8, 12 h, respectively. Histopathological analysis revealed with apoptosis in some liver cells and clear proliferation under T-2 toxin exposure. Expression analysis by immunohistochemical assays, quantitative real-time PCR (qPCR) and western blot demonstrated that T-2 toxin activated PI3K-Akt/Caspase/NF-κB signaling pathways. Additionally, DNA methylation assays revealed that the expression of RASSF4 was silenced by promoter hypermethylation after exposure to T-2 toxin for 1 and 3 days as compared to the control group. Moreover, joint treatment of 5-Aza-2′-deoxycytidine (DAC) (5 μM) and T-2 toxin (40 nM) increased expression of RASSF4 and PI3K-Akt/caspase/NF-κB signaling pathways-related genes, inducing cell apoptosis. These findings for the first time demonstrated that DNA methylation regulated the RASSF4 expression under T-2 toxin, along with the activation of its downstream pathways, resulting in apoptosis. APS Elsevier DMSO Elsevier DTT Elsevier Bcl-x Elsevier JNK Elsevier MTT Elsevier Caspase-3 Elsevier RIPA Elsevier BSA Elsevier NF-κB Elsevier p38 Elsevier PI3K Elsevier ANOVA Elsevier OD Elsevier RASSF4 Elsevier FBS Elsevier Akt1 Elsevier qPCR Elsevier BSP Elsevier QUMA Elsevier PBS Elsevier BCA Elsevier SDS Elsevier DAB Elsevier DAC Elsevier MST1 Elsevier LD<ce:inf loc="post">50</ce:inf> Elsevier T-2 toxin Elsevier PAGE Elsevier MSP Elsevier P53 Elsevier p-Akt Elsevier STAT Elsevier JAK Elsevier PMSF Elsevier Caspase-9 Elsevier Bax Elsevier MDM2 Elsevier Fas Elsevier BRL Elsevier HE Elsevier C-jun Elsevier Xu, Xiaoqing oth Hou, Ren oth Badawy, Sara oth Tao, Yanfei oth Chen, Dongmei oth Ihsan, Awais oth Wang, Xu oth Wu, Qinghua oth Yuan, Zonghui oth Enthalten in Elsevier Science Too late or too little? Potential for Alzheimer's disease passive immunotherapy via targeted intracerebroventricular delivery 2013 an international journal concerned with the effects of chemicals on living systems and immunotoxicology Amsterdam [u.a.] (DE-627)ELV011413085 volume:425 year:2019 day:1 month:09 pages:0 https://doi.org/10.1016/j.tox.2019.152246 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U GBV_ILN_22 GBV_ILN_40 GBV_ILN_105 52.56 Regenerative Energieformen alternative Energieformen VZ AR 425 2019 1 0901 0 |
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Too late or too little? Potential for Alzheimer's disease passive immunotherapy via targeted intracerebroventricular delivery |
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dna methylation and rassf4 expression are involved in t-2 toxin-induced hepatotoxicity |
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DNA methylation and RASSF4 expression are involved in T-2 toxin-induced hepatotoxicity |
| abstract |
T-2 toxin is a secondary metabolite produced by Fusarium species and commonly contaminates food and animal feed. T-2 toxin can induce hepatotoxicity through apoptosis and oxidative stress; however, the underlying mechanism is not clear. Recent studies indicated that RASSF4, a member of the RASSF family, participates in cell apoptosis and some cancers due to its inactivation via DNA hypermethylation. However, its role in T-2 toxin-induced liver toxicity is poorly understood. Therefore, in this study, female Wistar rats were given a single dose of T-2 toxin at 2 mg/kg b.w. and were sacrificed at 1, 3 and 7 days post-exposure. A normal rat liver cell line (BRL) was exposed to different concentrations of T-2 toxin (10, 20, 40 nM) for 4, 8, 12 h, respectively. Histopathological analysis revealed with apoptosis in some liver cells and clear proliferation under T-2 toxin exposure. Expression analysis by immunohistochemical assays, quantitative real-time PCR (qPCR) and western blot demonstrated that T-2 toxin activated PI3K-Akt/Caspase/NF-κB signaling pathways. Additionally, DNA methylation assays revealed that the expression of RASSF4 was silenced by promoter hypermethylation after exposure to T-2 toxin for 1 and 3 days as compared to the control group. Moreover, joint treatment of 5-Aza-2′-deoxycytidine (DAC) (5 μM) and T-2 toxin (40 nM) increased expression of RASSF4 and PI3K-Akt/caspase/NF-κB signaling pathways-related genes, inducing cell apoptosis. These findings for the first time demonstrated that DNA methylation regulated the RASSF4 expression under T-2 toxin, along with the activation of its downstream pathways, resulting in apoptosis. |
| abstractGer |
T-2 toxin is a secondary metabolite produced by Fusarium species and commonly contaminates food and animal feed. T-2 toxin can induce hepatotoxicity through apoptosis and oxidative stress; however, the underlying mechanism is not clear. Recent studies indicated that RASSF4, a member of the RASSF family, participates in cell apoptosis and some cancers due to its inactivation via DNA hypermethylation. However, its role in T-2 toxin-induced liver toxicity is poorly understood. Therefore, in this study, female Wistar rats were given a single dose of T-2 toxin at 2 mg/kg b.w. and were sacrificed at 1, 3 and 7 days post-exposure. A normal rat liver cell line (BRL) was exposed to different concentrations of T-2 toxin (10, 20, 40 nM) for 4, 8, 12 h, respectively. Histopathological analysis revealed with apoptosis in some liver cells and clear proliferation under T-2 toxin exposure. Expression analysis by immunohistochemical assays, quantitative real-time PCR (qPCR) and western blot demonstrated that T-2 toxin activated PI3K-Akt/Caspase/NF-κB signaling pathways. Additionally, DNA methylation assays revealed that the expression of RASSF4 was silenced by promoter hypermethylation after exposure to T-2 toxin for 1 and 3 days as compared to the control group. Moreover, joint treatment of 5-Aza-2′-deoxycytidine (DAC) (5 μM) and T-2 toxin (40 nM) increased expression of RASSF4 and PI3K-Akt/caspase/NF-κB signaling pathways-related genes, inducing cell apoptosis. These findings for the first time demonstrated that DNA methylation regulated the RASSF4 expression under T-2 toxin, along with the activation of its downstream pathways, resulting in apoptosis. |
| abstract_unstemmed |
T-2 toxin is a secondary metabolite produced by Fusarium species and commonly contaminates food and animal feed. T-2 toxin can induce hepatotoxicity through apoptosis and oxidative stress; however, the underlying mechanism is not clear. Recent studies indicated that RASSF4, a member of the RASSF family, participates in cell apoptosis and some cancers due to its inactivation via DNA hypermethylation. However, its role in T-2 toxin-induced liver toxicity is poorly understood. Therefore, in this study, female Wistar rats were given a single dose of T-2 toxin at 2 mg/kg b.w. and were sacrificed at 1, 3 and 7 days post-exposure. A normal rat liver cell line (BRL) was exposed to different concentrations of T-2 toxin (10, 20, 40 nM) for 4, 8, 12 h, respectively. Histopathological analysis revealed with apoptosis in some liver cells and clear proliferation under T-2 toxin exposure. Expression analysis by immunohistochemical assays, quantitative real-time PCR (qPCR) and western blot demonstrated that T-2 toxin activated PI3K-Akt/Caspase/NF-κB signaling pathways. Additionally, DNA methylation assays revealed that the expression of RASSF4 was silenced by promoter hypermethylation after exposure to T-2 toxin for 1 and 3 days as compared to the control group. Moreover, joint treatment of 5-Aza-2′-deoxycytidine (DAC) (5 μM) and T-2 toxin (40 nM) increased expression of RASSF4 and PI3K-Akt/caspase/NF-κB signaling pathways-related genes, inducing cell apoptosis. These findings for the first time demonstrated that DNA methylation regulated the RASSF4 expression under T-2 toxin, along with the activation of its downstream pathways, resulting in apoptosis. |
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DNA methylation and RASSF4 expression are involved in T-2 toxin-induced hepatotoxicity |
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https://doi.org/10.1016/j.tox.2019.152246 |
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Xu, Xiaoqing Hou, Ren Badawy, Sara Tao, Yanfei Chen, Dongmei Ihsan, Awais Wang, Xu Wu, Qinghua Yuan, Zonghui |
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Xu, Xiaoqing Hou, Ren Badawy, Sara Tao, Yanfei Chen, Dongmei Ihsan, Awais Wang, Xu Wu, Qinghua Yuan, Zonghui |
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