Ultrastructural changes in rat hepatocytes following acute methyl mercury intoxication

Hg- and Cu-Induced Hepatocellular Changes in the Mummichog, Fundulus heteroclitus

“…Thus, the increase in hepatic lipid could be a mechanism to sequester this lipid-soluble form of the metal. Hepatic lipid was found to be increased in humans with Minamata disease (17) and was experimentally induced by treatment with methylmercury in rats (18) and in ducks (13). But, as discussed by Bhatnagar et al (13), lipid accumulation is a typical reaction to cytotoxicity, probably related to inhibition of protein synthesis (19,20).…”

Polychlorinated Biphenyls, Lead, and Mercury Are Associated with Liver Disease in American Adults: NHANES 2003–2004

“…However, acute and chronic toxicity studies conducted in rats and cats demonstrated that mercury exposure resulted in the depletion of body fat, the development of centrilobular hepatic steatosis, an increase in lipid peroxidation products, the proliferation of the endoplasmic reticulum, and floccular degeneration of the mitochondria with extrusion of diseased organelles into the sinusoidal space (Chang and Yamaguchi 1974; Desnoyers and Chang 1975a, 1975b; Klein et al 1972; Lin et al 1996). Many of these changes were irreversible after exposure to MeHg was discontinued.…”

Ellagic acid: Pharmacological activities and molecular mechanisms involved in liver protection

“…Exposure to mercurial compounds induces hepatotoxicity associated with oxidative stress [182][183][184][185], generating hepatocellular defects like hepatomegaly, centrilobular hepatic steatosis [186,187], decrease in the synthesis of hepatic coagulation factors [188][189][190][191][192] and diminution in the activity of metabolic enzymes [193]. EA reduces mercuric chloride damage, avoiding the generation of oxidative stress and diminishing the possibility of damage to liver cells [194,195].…”