Table 4.

Potential TAFLD/TASH mechanisms.

Hepatocellular necrosis	Altered hepatic lipid metabolism
Lipotoxicity	Proinflammatory cytokines
Insulin resistance with altered   adipokines	Oxidative stress with decreased   antioxidant levels
Mitochondrial dysfunction	Metabolic endotoxemia
Endoplasmic reticulum stress	Proteasomal dysfunction
Altered transmethylation/   transulfuration	Decreased intestinal barrier function
Autophagy	Altered intestinal microflora
Nuclear receptor activation	Nutrient-toxicant interactions
Kupffer cell activation	Liver sinusoidal endothelial cell damage
Carbonyl stress	Priming and Sensitization
Epigenetic modifications	Hypoxia

Note: TAFLD = toxicant-associated fatty liver disease; TASH = toxicant-associated steatohepatitis.