Effects of adenosine on liver cell damage induced by carbon tetrachloride.
Adenosine administration delayed the fatty liver and cell necrosis induced by carbon tetrachloride without affecting the action of the hepatotoxin on protein synthesis and liver triacylglycerol release. Adenosine produced a drastic antilipolytic effect accompanied by a decrease in the incorporation of [1-14C]palmitic acid into triacylglycerols and free fatty acids of the liver. Furthermore, a decrease in the serum levels of ketone bodies was observed at early times. The nucleoside also avoided the release of intracellular enzymes and prevented the lipid peroxidation produced by carbon tetrachloride during the 4 hr of treatment. The protective action of adenosine was transient, lasting 3-4 hr, probably the time required to be metabolized. The results suggest that the antilipolytic effect of the nucleoside, the inhibition of hepatic fatty acid metabolism, and the decrease in carbon tetrachloride-induced lipoperoxidation that it produced are involved in the delayed acute hepatotoxicity induced by carbon tetrachloride.
D000241:Adenosine / Q000494:pharmacology*; D000818:Animals; D002251:Carbon Tetrachloride / Q000633:toxicity*; D005230:Fatty Acids, Nonesterified / Q000378:metabolism; D005969:Glutamate Dehydrogenase / Q000032:analysis; D008054:Lipid Peroxides / Q000378:metabolism; D008099:Liver / Q000187:drug effects*; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains; D014280:Triglycerides / Q000378:metabolism
D005230:Fatty Acids, Nonesterified; D008054:Lipid Peroxides; D014280:Triglycerides; D002251:Carbon Tetrachloride; D005969:Glutamate Dehydrogenase; D000241:Adenosine