[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.
D000081:Acetamides / Q000494:pharmacology*; D000818:Animals; D050356:Lipid Metabolism; D008099:Liver / Q000187:drug effects* / Q000378:metabolism; D008103:Liver Cirrhosis / Q000139:chemically induced*; D008297:Male; D010713:Phosphatidylcholines / Q000378:metabolism; D010743:Phospholipids / Q000096:biosynthesis; D051381:Rats; D011919:Rats, Inbred Strains; D013109:Sphingomyelins / Q000378:metabolism; D013853:Thioacetamide / Q000494:pharmacology* / Q000633:toxicity
D000081:Acetamides; D010713:Phosphatidylcholines; D010743:Phospholipids; D013109:Sphingomyelins; D013853:Thioacetamide
Alteraciones en el metabolismo lipídico que acompañan a la cirrosis inducida por tioacetamida.