Lipid peroxidation products as a mediator of toxicity and adaptive response-The regulatory role of selenoprotein and vitamin E
Lipid peroxidation products as a mediator of toxicity and adaptive response-The regulatory role of selenoprotein and vitamin E
复制标题
脂质过氧化产物作为毒性和适应性反应介质——硒蛋白和维生素E的调节作用
DOI：
10.1016/j.abb.2021.108840
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发表时间：
2021
影响因子：
3.9
通讯作者：
Saito Yoshiro
中科院分区：
文献类型：
--
作者：
Suzuki T*;Hori Y*;Sawazaki T;Shimizu Y;Nemoto Y;Taniguchi A;Ozawa S;Sohma Y;Kanai M;Tomita T;Saito Yoshiro
脂质过氧化及其产物已被广泛研究，它们的生物学重要性，特别是在生理和病理生理条件下，已受到相当大的关注。脂质通过三种不同的机制氧化，即，酶促氧化、非酶促自由基介导的氧化和非酶促非自由基介导的氧化，它们分别产生特定的产物。脂质氢过氧化物是形成的主要初级产物，并通过抗氧化酶如硒蛋白还原为相应的氢氧化物，和/或经历二次氧化，产生具有亲电性质的各种产物，如4-羟基-2-壬烯醛。脂质过氧化导致脂质的精细结构和天然功能丧失，并可产生细胞毒性和/或新的生物活性。这篇综述广泛讨论了脂质过氧化及其产物的机制，其效用作为氧化应激的生物标志物，脂质过氧化产物的生物学效应，包括其作为适应性反应的介质的作用，以及抗氧化系统的作用，特别是硒蛋白和维生素E，在防止脂质过氧化和铁凋亡。
Lipid peroxidation and its products have been investigated extensively and their biological importance, particularly in relation to physiological and pathophysiological conditions, has received considerable attention. Lipids are oxidized by three distinct mechanisms, i.e., enzymatic oxidation, nonenzymatic, free radical-mediated oxidation, and nonenzymatic, nonradical-mediated oxidation, which respectively yield specific products. Lipid hydroperoxides are the major primary products formed and are reduced to the corresponding hydroxides by antioxidative enzymes such as selenoproteins, and/or undergo secondary oxidation, generating various products with electrophilic properties, such as 4-hydroxy-2-nonenal. Lipid peroxidation induces a loss of fine structure and natural function of lipids, and can produce cytotoxicity and/or novel biological activity. This review broadly discusses the mechanisms of lipid peroxidation and its products, its utility as a biomarker for oxidative stress, the biological effects of lipid peroxidation products, including their action as a mediator of the adaptive response, and the role of the antioxidant system, particularly selenoproteins and vitamin E, in preventing lipid peroxidation and ferroptosis.