自由基诱导的大脑皮层切片中磷脂降解和细胞水肿

Phospholipid degradation and cellular edema induced by free radicals in brain cortical slices.

作者信息

Chan P H, Yurko M, Fishman R A

出版信息

J Neurochem. 1982 Feb;38(2):525-31. doi: 10.1111/j.1471-4159.1982.tb08659.x.

DOI:10.1111/j.1471-4159.1982.tb08659.x

Abstract

Cellular edema and increased lactate production were induced in rat brain cortical slices by xanthine oxidase and xanthine, in the presence of ferric dialdehyde, was increased 174%. Among the various subcellular fractions of brain cortex, xanthine oxidase-stimulated lipid peroxidation was highest in myelin, mitochondria, and synaptosomes, followed by microsomes and nuclei. Antioxidants, catalase, chlorpromazine, and butylated hydroxytoluene inhibited lipid peroxidation in both homogenates and synaptosomes, indicating H2O2 and radicals were involved. Further, several free fatty acids, especially oleic acid (18:1), arachidonic acid (20:4), and docosahexaenoic acid (22:6) were released from the phospholipid pool concomitant with the degradation of membrane phospholipids in xanthine oxidase-treated synaptosomes. These data suggest that lipases are activated by free radicals and lipid peroxides in the pathogenesis of cellular swelling.

摘要

黄嘌呤氧化酶和黄嘌呤可诱导大鼠脑皮质切片出现细胞水肿并增加乳酸生成，在存在戊二醛的情况下，（戊二醛含量）增加了174%。在大脑皮质的各种亚细胞组分中，黄嘌呤氧化酶刺激的脂质过氧化在髓磷脂、线粒体和突触体中最高，其次是微粒体和细胞核。抗氧化剂、过氧化氢酶、氯丙嗪和丁基化羟基甲苯在匀浆和突触体中均抑制脂质过氧化，表明过氧化氢和自由基参与其中。此外，在黄嘌呤氧化酶处理的突触体中，伴随着膜磷脂的降解，几种游离脂肪酸，特别是油酸（18:1）、花生四烯酸（20:4）和二十二碳六烯酸（22:6）从磷脂池中释放出来。这些数据表明，在细胞肿胀的发病机制中，脂肪酶被自由基和脂质过氧化物激活。