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. 2023 Jul 14;12(7):1425. doi: 10.3390/antiox12071425

Table 2.

Studies included in our systematic review that focused on the effects of chronic ethanol exposure on cell models.

First Author, Year Models and Methods Summary of Effects
Guo et al., 2015 [39] HepG2 cells treated with 100 mM ethanol for 4 days. Ethanol and acetaldehyde increase IL-6 and IFN-γ levels and suppress autophagy in ADH1-expressing HepG2 cells. Lysosomal inhibitors mimic ethanol-induced p62 accumulation.
Wu et al., 2012 [40] HepG2 cells treated with 100 mM ethanol for 8 days. Inhibiting autophagy enhances ethanol hepatotoxicity, steatosis, and oxidative stress in CYP2E1-expressing HepG2 cells. These cells show increased fat accumulation and oxidative stress but decreased autophagy. The antioxidant N-acetylcysteine and CYP2E1 inhibition blunt these effects.
Wu et al., 2010 [41] HepG2 cells treated with 50, 100, and 150 mM ethanol for 4–5 days. CYP2E1-expressing HepG2 cells have exacerbated lipid and TG accumulation and increased p62 levels. HepG2 cells show increased autophagy. Inhibiting autophagy increases lipid accumulation and TG levels in HepG2 cells and, to a lesser extent, in CYP2E1-expressing HepG2 cells. Ethanol induces CYP2E1 activity and oxidative stress in CYP2E1-expressing HepG2 cells.

HepG2, human epidermoid carcinoma strain 2; IL-6, interleukin 6; IFN-γ, interferon-γ; ADH1, alcohol dehydrogenase 1; CYP2E1, cytochrome P450 2E1; TG, triglycerides.