EFFECTS OF ADENOSINE ON LIVER-CELL DAMAGE INDUCED BY CARBON-TETRACHLORIDE
EFFECTS OF ADENOSINE ON LIVER-CELL DAMAGE INDUCED BY CARBON-TETRACHLORIDE
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DOI：
10.1016/0006-2952(84)90631-2
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发表时间：
1984-01-01
影响因子：
5.8
通讯作者：
DESANCHEZ, VC
中科院分区：
文献类型：
--
作者：
HERNANDEZMUNOZ, R;GLENDER, W;DESANCHEZ, VC
腺苷给药延迟[大鼠]脂肪肝和细胞坏死诱导的四氯化碳不影响行动的肝毒素蛋白质合成和肝脏三酰甘油释放。腺苷产生了剧烈的抗脂肪分解作用，伴随着[1- 14 C]棕榈酸掺入三酰甘油和游离脂肪酸的肝脏减少。早期观察到血清酮体水平降低。核苷还避免了细胞内酶的释放，并防止在4小时的处理过程中由四氯化碳产生的脂质过氧化作用。腺苷的保护作用是短暂的，持续3-4小时，可能是代谢所需的时间。核苷的抗脂肪分解作用、抑制肝脂肪酸代谢和减少CCl 4诱导的脂质过氧化作用与CCl 4诱导的迟发性急性肝毒性有关。
Adenosine administration delayed the [rat] fatty liver and cell necrosis induced by CCl4 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. 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 CCl4 during the 4 h of treatment. The protective action of adenosine was transient, lasting 3-4 h, probably the time required to be metabolized. The antilipolytic effect of the nucleoside, the inhibition of hepatic fatty acid metabolism, and the decrease in CCl4-induced lipoperoxidation that it produced are involved in the delayed acute hepatotoxicity induced by CCl4.