Abstract
For unknown reasons, extensive centrilobular hepatic necrosis results from in vivo carbon disulfide administration to phenobarbital-pretreated rats, while only few hepatocytes are affected when carbon disulfide is administered to noninduced rats. Under certain experimental conditions, liver P-450 hemoproteins from phenobarbital-induced rats are, however, known to generate large amounts of reduced toxic forms of oxygen. The possibility of such an occurrence has been tested in the present investigation. (1) Carbon disulfide increases the ability of liver P-450 hemoprotein from phenobarbital-treated rats (and not from untreated rats) to consume oxygen, and (2) the increased oxygen taken up gives rise to an increased superoxide anion production when cyanide, aniline, or NADH is added to the incubation medium. It is suggested that both the increased superoxide anion production and the previously reported decrease in liver protective enzymes against reduced forms of oxygen, observed after CS 2 administration to phenobarbital pretreated rats only, might be responsible in part for liver necrosis.
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