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Catechins protect against acrylamide- and glycidamide-induced cellular toxicity via rescuing cellular apoptosis and DNA damage
Acrylamide (AA) occurs in both various environmental and dietary sources and has raised widespread concern as a probable carcinogen. Glycidamide (GA) is the main genotoxic metabolite through P450 2E1 (CYP2E1). In the present study, we investigated the protective effect of (−)-epigallocatechin gallat...
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Published in: | Food and chemical toxicology 2022-09, Vol.167, p.113253-113253, Article 113253 |
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Main Authors: | , , , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Acrylamide (AA) occurs in both various environmental and dietary sources and has raised widespread concern as a probable carcinogen. Glycidamide (GA) is the main genotoxic metabolite through P450 2E1 (CYP2E1). In the present study, we investigated the protective effect of (−)-epigallocatechin gallate (EGCG) and (−)-epicatechin (EC) against AA- and GA-induced hepatotoxicity in HepG2 cells. The results demonstrated that EC and EGCG inhibited AA- and GA-induced cytotoxicity and mitochondria-mediated cellular apoptosis. Moreover, exposure to AA (100 μg/mL) and GA (50 μg/mL) caused cell cycle arrest and DNA damage, while EC and EGCG ranging from 12.5 to 50 μg/mL rescued cell cycle arrest and inhibited DNA damage. Furthermore, EC and EGCG down-regulated pro-apoptotic protein Bax and Caspase 3 after a 24-h treatment in HepG2 cells exposed to AA (100 μg/mL) or GA (50 μg/mL). Also, the intervention with EC or EGCG up-regulated the expression of DNA repair related protein PARP and down-regulated the expression of Cleaved-PARP. Besides, EC exerted better protective effect than EGCG against AA- and GA-induced cytotoxicity in HepG2 cells. Altogether, EC and EGCG were effective in protecting AA- and GA-induced hepatotoxicity via rescuing cellular apoptosis and DNA damage, as well as promoting cell cycle progression in HepG2 cells.
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•The cellular toxicity of AA and GA is ascribed to cell apoptosis and DNA damage.•Both EC and EGCG protect against AA and GA induced toxicity in HepG2 cells.•Both EC and EGCG rescue mitochondrial-mediated cell apoptosis induced by AA and GA.•Both EC and EGCG contribute to DNA damage repair including Bax and PARP pathways.•The protective effect of EC against AA and GA is stronger than that of EGCG. |
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ISSN: | 0278-6915 1873-6351 |
DOI: | 10.1016/j.fct.2022.113253 |