Hernández-Muñoz R, Glender W, Díaz Muñoz M, Adolfo J, García-Sáinz J A, Chagoya de Sánchez V
Biochem Pharmacol. 1984 Aug 15;33(16):2599-604. doi: 10.1016/0006-2952(84)90631-2.
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.
给予腺苷可延缓四氯化碳诱导的脂肪肝和细胞坏死,且不影响肝毒素对蛋白质合成和肝脏三酰甘油释放的作用。腺苷产生了显著的抗脂解作用,同时伴随着[1-14C]棕榈酸掺入肝脏三酰甘油和游离脂肪酸的减少。此外,在早期观察到酮体血清水平降低。在治疗的4小时内,该核苷还避免了细胞内酶的释放,并防止了四氯化碳产生的脂质过氧化。腺苷的保护作用是短暂的,持续3-4小时,这可能是其代谢所需的时间。结果表明,该核苷的抗脂解作用、对肝脏脂肪酸代谢的抑制以及其产生的四氯化碳诱导的脂质过氧化减少与四氯化碳诱导的急性肝毒性延迟有关。