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壳聚糖对四氯化碳诱导的大鼠慢性肝损伤的抗氧化作用。

Antioxidative effect of chitosan on chronic carbon tetrachloride induced hepatic injury in rats.

作者信息

Jeon Tae Il, Hwang Seong Gu, Park Nam Gyu, Jung Yu Ri, Shin Soo Im, Choi Sung Don, Park Dong Ki

机构信息

Department of Applied Biology and Chemistry, Konkuk University, 1 Hwayang-dong, Kwanghin-gu, Seoul 143-701, South Korea.

出版信息

Toxicology. 2003 May 1;187(1):67-73. doi: 10.1016/s0300-483x(03)00003-9.

Abstract

Carbon tetrachloride (CCl(4)) is a toxic material known to induce lipid peroxidation and liver damage. To determine if chitosan has antioxidative effects on CCl(4)-induced liver injury, we administered 1 ml/kg of CCl(4) resolved in a 50% corn oil solution to rats every week by intraperitoneal injection. Chitosan (200 mg/kg body weight per day, MW 380,000 Da) was administered to the CCl(4) + chitosan treated rats by oral gavage during the experimental period. Chitosan significantly decreased liver thiobarbituric acid reactive substances (TBARS) and increased antioxidant enzyme activities (catalase and superoxide dismutase (SOD)). Fatty acid composition was not remarkably changed by chitosan; only arachidonic acid (20:4n-6) levels were significantly altered by CCl(4). Chitosan administration in the present experiment did not restore the decreased delta5-desaturase activity. In addition, chitosan supplementation did not prevent the CCl(4) induced degradation of CYP2E1. In conclusion, our results suggest that chitosan has antioxidative but not detoxifying effects on chronic CCl(4) induced hepatic injury in rats.

摘要

四氯化碳(CCl₄)是一种已知可诱导脂质过氧化和肝损伤的有毒物质。为了确定壳聚糖对四氯化碳诱导的肝损伤是否具有抗氧化作用,我们每周通过腹腔注射给大鼠施用1 ml/kg溶解于50%玉米油溶液中的四氯化碳。在实验期间,通过灌胃给四氯化碳加壳聚糖处理的大鼠施用壳聚糖(每天200 mg/kg体重,分子量380,000 Da)。壳聚糖显著降低了肝脏硫代巴比妥酸反应性物质(TBARS)并提高了抗氧化酶活性(过氧化氢酶和超氧化物歧化酶(SOD))。壳聚糖对脂肪酸组成没有显著改变;只有花生四烯酸(20:4n-6)水平因四氯化碳而显著改变。在本实验中施用壳聚糖并未恢复降低的δ5-去饱和酶活性。此外,补充壳聚糖并不能防止四氯化碳诱导的CYP2E1降解。总之,我们的结果表明壳聚糖对大鼠慢性四氯化碳诱导的肝损伤具有抗氧化作用,但没有解毒作用。

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