Protective role of dietary butylated hydroxyanisole against chemical-induced acute liver damage in mice.
Prior consumption of a diet containing the food antioxidant, butylated hydroxyanisole (BHA), by female mice prevented the development of or minimized the acute liver damage caused by monocrotaline, acetaminophen, or bromobenzene. In contrast, neither the incidence nor the severity of carbon tetrachloride-induced hepatotoxicity was affected by dietary BHA. Hepatotoxicity was judged by plasma alanine aminotransferase and aspartate aminotransferase levels, hepatic cytochrome P-450 content, and liver histology. The protective effect of BHA against acetaminophen-induced hepatotoxicity was not demonstrated in male mice. The observed protection by dietary BHA against acetaminophen- and bromobenzene-induced hepatotoxicity was associated with the increase of liver glutathione. It is concluded that the protective action of BHA is dependent upon the nature of the toxic agent.
D000818:Animals; D000840:Anisoles / Q000494:pharmacology*; D002083:Butylated Hydroxyanisole / Q000494:pharmacology*; D056486:Chemical and Drug Induced Liver Injury / Q000201:enzymology / Q000378:metabolism / Q000517:prevention & control*; D004032:Diet; D005260:Female; D005978:Glutathione / Q000378:metabolism; D008297:Male; D051379:Mice
D000840:Anisoles; D002083:Butylated Hydroxyanisole; D005978:Glutathione