INHIBITION OF ETHANOL AND CARBON TETRACHLORIDE INDUCED FATTY LIVER BY ANTIOXIDANTS
INHIBITION OF ETHANOL AND CARBON TETRACHLORIDE INDUCED FATTY LIVER BY ANTIOXIDANTS
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DOI：
10.1016/0014-4800(65)90030-4
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发表时间：
1965-01-01
影响因子：
3.6
通讯作者：
COSTALES, F
中科院分区：
文献类型：
--
作者：
DILUZIO, NR;COSTALES, F
预先施用α-生育酚乙酸酯显着抑制了大鼠中急性乙醇诱导的脂肪肝的发展。通过预先腹腔内施用抗氧化剂N,N-二苯基对苯二胺（DPPD）诱导乙醇诱导的脂肪肝的完全抑制。当与乙醇同时口服给药时，DPPD 减少但不能阻止乙醇诱导的肝脏甘油三酯积累。还注意到，用 DPPD 预处理的四氯化碳治疗大鼠的肝脏甘油三酯积累受到显着抑制。 CC14治疗组表现出脂肪变态、中心坏死、多形核细胞浸润和网状结构破坏。在接受 DPPD 治疗的 CCl4 治疗大鼠中，这些变化显着减少。由于抗氧化剂给药显着改变了乙醇和 CC14 诱导的脂肪肝，因此表明在某种程度上，这些药物引起的脂肪肝的发病机制涉及一个共同因素。建议使用抗氧化剂来预防或减轻肝损伤。
The development of the acute ethanol-induced fatty liver in the rat was significantly inhibited by the prior administration of [alpha]-tocopherol acetate. Complete inhibition of the ethanol-induced fatty liver was induced by the prior intraperitoneal administration of the antioxidant, N,N[image]-Diphenyl-p-phenylenediamine (DPPD). DPPD reduced, but did not prevent, the ethanol-induced hepatic-triglyceride accumulation when administered orally simultaneously with ethanol. Significant inhibition of hepatic-trigly-ceride accumulation in carbon tetrachloride-treated rats, pre -treated with DPPD, was also noted. The CC14-treated group manifested fatty metamorphosis, central necrosis, polymorphonuclear cell infiltration, and a disruption of the architecture of the reticulum. These changes were markedly reduced in CCl4-treated rats which had received DPPD. Since both the ethanol- and CC14-induced fatty livers were significantly modified by antioxidant administration, it is suggestive that, to some degree, a common factor is involved in the pathogenesis of fatty livers from these agents. The possible use of antioxidants in the prevention or modification of liver injury is sug-gested.