[Changes in lipid metabolism which accompany thioacetamide-induced cirrhosis].

Intraperitoneally-administered thioacetamide to rats produces the incorporation of 3H2O into the liver lipids during eight days, diminishing thereafter together with a decrease in 32P incorporation to phosphatidyl choline. Contrarily, the sphingomyelin incorporated 32P increases by the effect of the toxic action of the drug, while the 3H binding decreases. The cirrhosis-inducing agent possibly produces a shunt of the common CDP-choline precursor to the biosynthesis of sphingomyelin with detriment to the synthesis of phosphatidyl choline. The role of the unsaturation of fatty acids by thioacetamide is considered.