Higuchi Y
Department of Pharmacology, Kanazawa University School of Medicine, Kanazawa 920-8640, Japan.
Arch Biochem Biophys. 2001 Aug 1;392(1):65-70. doi: 10.1006/abbi.2001.2428.
It has been reported that glutamate decreased the intracellular glutathione (GSH) concentration and thereby induced cell death in C6 rat glioma cells. Polyunsaturated fatty acids such as arachidonic acid, gamma-linolenic acid, and linoleic acid enhanced lipid peroxidation promoting 8-hydroxy-2'-deoxyguanosine (8-OH-dG) formation under the glutamate-induced GSH-depletion. The enhancement of lipid peroxidation by polyunsaturated fatty acids was species-dependent. Some antioxidants capable of scavenging oxygen and lipid radicals and some iron or copper scavengers inhibited both the lipid peroxidation and the 8-OH-dG formation, consequently protecting against cell death induced by glutamate-induced GSH depletion. These results suggest that GSH depletion caused by glutamate induces lipid peroxidation and consequently 8-OH-dG formation and that polyunsaturated fatty acids enhance lipid peroxidation associated with mediated 8-OH-dG formation through a chain reaction.
据报道，谷氨酸会降低细胞内谷胱甘肽（GSH）浓度，从而诱导C6大鼠胶质瘤细胞死亡。多不饱和脂肪酸，如花生四烯酸、γ-亚麻酸和亚油酸，在谷氨酸诱导的GSH耗竭情况下会增强脂质过氧化，促进8-羟基-2'-脱氧鸟苷（8-OH-dG）的形成。多不饱和脂肪酸对脂质过氧化的增强作用具有物种依赖性。一些能够清除氧和脂质自由基的抗氧化剂以及一些铁或铜清除剂，既能抑制脂质过氧化，也能抑制8-OH-dG的形成，从而防止谷氨酸诱导的GSH耗竭所导致的细胞死亡。这些结果表明，谷氨酸导致的GSH耗竭会诱导脂质过氧化，进而导致8-OH-dG的形成，并且多不饱和脂肪酸通过连锁反应增强与介导的8-OH-dG形成相关的脂质过氧化。
