Prophylaxis of poisoning by carbon tetrachloride.

Abstract

CHRISTIE and Judah1 studied the biochemical basis of the hepatotoxicity of carbon tetrachloride and found that the earliest measurable changes, which precede histological evidence of necrosis, involved disorganization of mitochondrial tricarboxylic acid cycle activity. Enzyme systems first affected were those which required pyridine nucleotides for electron transfer and inactivation of these enzymes could be largely reversed by the addition of the appropriate coenzyme. Pre-incubation of liver mitochondria from normal rats with carbon tetrachloride produced a similar pattern of inhibition1. It was shown that carbon tetrachloride increased mitochondrial permeability to the entry of diphosphopyridine nucleo-tide, and it appeared that carbon tetrachloride attacked mitochondria directly to promote the loss of respiratory cofactors, thus inactivating pyridine nucleotide-dependent enzyme systems.