Elevation of the level of lipid peroxidation associated with hepatic injury in LEC mutant rat.
Elevation of the level of lipid peroxidation associated with hepatic injury in LEC mutant rat.
复制标题
LEC突变大鼠中与肝损伤相关的脂质过氧化水平升高。
DOI：
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发表时间：
1992
期刊：
影响因子：
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通讯作者：
K. Matsumoto
中科院分区：
文献类型：
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作者：
T. Yamada;K. Sogawa;Y. Suzuki;K. Izumi;T. Agui;K. Matsumoto
Long-Evans Cinnamon（LEC）突变大鼠在4-5月龄时自发地发生慢性坏死性肝损伤，表现出过量的肝铜蓄积。在回交后代中，肝损伤与过量的肝铜积累完全相关，支持先前的假设，即铜的细胞毒性导致LEC大鼠肝损伤。4月龄有症状LEC大鼠的脂质过氧化水平显著高于同龄无症状LEC大鼠和正常大鼠。这些结果表明，过量积累的铜引起肝损伤，通过启动脂质过氧化反应。
Long-Evans Cinnamon (LEC) mutant rat, which spontaneously develops a chronically necrotizing hepatic injury at 4-5 months of age, exhibits an excess hepatic copper accumulation. The hepatic injury was completely correlated to the excess hepatic copper accumulation in backcross progenies, supporting the previous hypothesis that the copper cytotoxicity causes the hepatic injury in LEC rat liver. The levels of the lipid peroxidation in symptomatic LEC rats at 4 months of age were significantly higher than those of age-matched asymptomatic LEC and normal rats. These results suggest that excessively accumulated copper provokes hepatic injury through initiating the lipid peroxidation.