![]() Bavachinin Induces Oxidative Damage in HepaRG Cells through p38/JNK MAPK Pathways. ![]() These deleterious effects could be partly explained by BP metabolism alterations. A prior steatosis therefore enhanced the toxicity of BP/ethanol co-exposure in vitro and in vivo such a co-exposure might favor the appearance of a steatohepatitis-like state, with the development of inflammation. A change of BP metabolism with a decrease in detoxification was detected in HepaRG cells under these conditions. ![]() Cytotoxicity and expression of inflammation markers upon co-exposure were increased in all steatotic models, compared to non steatotic counterparts. Toxicity and inflammation were analyzed in all models the impact of steatosis and ethanol towards BP metabolism was studied in HepaRGcells. ![]() Steatosis was induced prior to chronic treatments (14, 5 or 7 days for HepaRG, WIF-B9 or zebrafish, respectively). The impact of the co-exposure to the environmental carcinogen benzopyrene (BP) and the lifestyle-related hepatotoxicant ethanol, was thus tested on in vitro models of steatosis (human HepaRG cell line hybrid human/rat WIF-B9 cell line), and on an in vivo model (obese zebrafish larvae). ![]() However, no study has so far analyzed how these different factors might interplay regarding the progression of liver diseases. lipid accumulation) and steatohepatitis have been related to diverse etiologic factors, including alcohol, obesity, environmental pollutants. ![]()
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