Lipid peroxidation in isolated rat hepatocytes: relationship to toxicity of CCl4, ADP/Fe3+, and diethyl maleate.
Lipid peroxidation in isolated rat hepatocytes: relationship to toxicity of CCl4, ADP/Fe3+, and diethyl maleate.
复制标题
离体大鼠肝细胞中的脂质过氧化：与 CCl4、ADP/Fe3 和马来酸二乙酯毒性的关系。
DOI：
10.1016/0041-008x(78)90026-1
复制
发表时间：
1978
影响因子：
3.8
通讯作者：
B. Priestly
中科院分区：
文献类型：
--
作者：
N. Stacey;B. Priestly
采用胶原酶灌流技术分离大鼠肝细胞，研究脂质过氧化、谷胱甘肽（GSH）含量与CCl 4诱导的毒性之间的关系。研究了两种脂质过氧化的化学引发剂，铁离子与二磷酸腺苷（ADP Fe 3+）和马来酸二乙酯的络合物，用于比较。CCl 4引起细胞内K+的减少和丙氨酸氨基转移酶（ALT）释放到培养基中，但没有证据表明脂质过氧化，通过硫代巴比妥酸（TBA）反应材料和脂质提取物二烯共轭的吸光度测定。ADP Fe ~（3+）引起膜脂过氧化，而K ~+的损失较小。马来酸二乙酯引起的脂质过氧化和细胞损伤比ADP Fe 3+。这两种反应似乎都与GSH含量有关，马来酸二乙酯可降低GSH含量，但ADP Fe 3+不能降低GSH含量，而CCl 4仅在最高剂量下降低GSH含量。结果表明，脂质过氧化不是一个必要的步骤，四氯化碳诱导的离体肝细胞的毒性。
The relationship between lipid peroxidation, glutathione (GSH) content, and CCl4-induced toxicity was investigated in rat hepatocytes isolated by a collagenase-perfusion technique. Two chemical initiators of lipid peroxidation, ferric ions complexed with adenosine diphosphate (ADP Fe3+) and diethyl maleate, were studied for comparison. CCl4caused a reduction of intracellular K+and release of alanine aminotransferase (ALT) into the medium, but no evidence of lipid peroxidation, as measured by the absorbance of thiobarbituric acid (TBA)-reacting materials and lipid-extract diene conjugation. ADP Fe3+caused lipid peroxidation, but only a small loss of K+. Diethyl maleate caused a greater amount of lipid peroxidation and cell damage than did ADP Fe3+. Neither response appeared to be related to the GSH content, which was reduced by diethyl maleate, but not by ADP Fe3+, and by CCl4only at the highest dose. The results suggest that lipid peroxidation is not a requisite step in CCl4-induced toxicity in isolated hepatocytes.