Carbon tetrachloride depresses hepatic phospholipid synthesis in rats.
40 h after an acute dose of CCl4 (11.3 mmol/kg), the incorporation of [1-3H]ethanolamine into rat hepatic microsomal phospholipids was inhibited to 70% of control. Incorporation into phospholipids of the inner and outer mitochondrial membranes was 30-35% of control. Rates of incorporation were equal to or above normal rates in all membranes 65 h after dosage. The activity of methyltransferase in microsomal fractions isolated from rats 10 to 66 h after dosage was depressed. These data suggest that the alteration of mitochondrial phospholipids that parallels mitochondrial dysfunction after acute CCl4 dosage could be attributed to a CCl4-induced inhibition of the microsomal phospholipid biosynthetic pathways.
D000818:Animals; D002252:Carbon Tetrachloride Poisoning / Q000378:metabolism*; D019856:Ethanolamine; D004983:Ethanolamines / Q000378:metabolism; D008099:Liver / Q000187:drug effects* / Q000378:metabolism; D008297:Male; D008780:Methyltransferases / Q000378:metabolism; D010085:Oxidative Phosphorylation / Q000187:drug effects; D050941:Phosphatidyl-N-Methylethanolamine N-Methyltransferase; D010713:Phosphatidylcholines / Q000378:metabolism; D010714:Phosphatidylethanolamines / Q000378:metabolism; D010743:Phospholipids / Q000096:biosynthesis*; D051381:Rats; D011919:Rats, Inbred Strains
D004983:Ethanolamines; D010713:Phosphatidylcholines; D010714:Phosphatidylethanolamines; D010743:Phospholipids; D019856:Ethanolamine; D008780:Methyltransferases; D050941:Phosphatidyl-N-Methylethanolamine N-Methyltransferase