[Acetylation of sulfanilamide substances in toxic lesions of the liver].

In experimental toxic hepatitis induced by injection of CCl4 into rats, the rat blood and urine content of acetylated sulfamonomethoxine diminishes, the acetylation of sulfamonomethoxine and norsulfazole in an isolated stomach of the rat reduces, and acetylation of sulfamonomethoxine is inhibited by rat liver and small intestine homogenates. This confirms that different types of pathology (infectious and non-infectious) provoke the same line of changes, namely the reduction of acetylation of sulfanilamide substances in the body. CCl1 decreases sulfamonomethoxine acetylation by a mixture of the mitochondria and microsomes of the rat liver, i. e. eliminates the synergistic effect characteristic for intact rats. The reduction of acetylation recorded at different levels of the organization of the living systems--bodily, organ and subcellular ones--is accounted for by the lowering of the acetylcoenzyme A content in the tissues. One of the reasons for reduction of acetylation during the CCl4-induced liver injury lies in the impairment in the liver cells of the interaction between the mitochondria and endoplasmic reticulum.