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自然杀伤细胞和杀伤细胞介导的细胞毒性、脂质过氧化作用与谷胱甘肽

Cell-mediated cytotoxicity by natural killer and killer cells, lipid peroxidation and glutathione.

作者信息

Younes M, Craig G, Stacey N H

出版信息

Experientia. 1986 Dec 1;42(11-12):1257-9. doi: 10.1007/BF01946412.

Abstract

In the course of spontaneous cell-mediated cytotoxicity (SCMC) and antibody-dependent cell-mediated cytotoxicity (ADCC) with human peripheral lymphocytes as effector cells, no lipid peroxidation occurred as measured by the production of ethane and thiobarbituric acid-reactive material. Furthermore, impairment of major cellular defense systems of target cells (K562 cells for SCMC, Chang liver cells for ADCC), by decreasing their glutathione content, had no effect on either lipid peroxidation or the cytotoxic response. These findings indicate that peroxidative damage is not a mechanism of NK and K cell-mediated cytotoxicity.

摘要

在以人外周淋巴细胞作为效应细胞的自发细胞介导细胞毒性(SCMC)和抗体依赖性细胞介导细胞毒性(ADCC)过程中,通过乙烷产生和硫代巴比妥酸反应性物质测定,未发生脂质过氧化。此外,通过降低靶细胞(SCMC中的K562细胞,ADCC中的Chang肝细胞)的谷胱甘肽含量来损害其主要细胞防御系统,对脂质过氧化或细胞毒性反应均无影响。这些发现表明,过氧化损伤不是自然杀伤细胞和K细胞介导的细胞毒性机制。

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