Bannai S, Sato H, Ishii T, Taketani S
Department of Biochemistry, Tsukuba University Medical School, Ibaraki, Japan.
Biochim Biophys Acta. 1991 Apr 17;1092(2):175-9. doi: 10.1016/0167-4889(91)90153-o.
Glutathione content of mouse peritoneal macrophages markedly increased when they were exposed to insulting agents like sodium arsenite, cadmium chloride, and glucose/glucose oxidase which generates hydrogen peroxide. This increase was attributed to the induction of the cystine transport activity by these agents. The transport activity for other amino acids was not induced, but rather diminished by these agents. Heat shock treatment did not induce the cystine transport activity, nor did it augment glutathione. Since glutathione protects cells against the cytotoxic effects of these agents, the induction of the cystine transport activity constitutes a protective mechanism related to the stress caused by the agents. The protein component(s) for cystine transport may fall into the category of the stress protein.
当小鼠腹腔巨噬细胞暴露于诸如亚砷酸钠、氯化镉以及能产生过氧化氢的葡萄糖/葡萄糖氧化酶等损伤性因子时，其谷胱甘肽含量显著增加。这种增加归因于这些因子诱导了胱氨酸转运活性。这些因子并未诱导其他氨基酸的转运活性，反而使其降低。热休克处理既未诱导胱氨酸转运活性，也未增加谷胱甘肽含量。由于谷胱甘肽可保护细胞免受这些因子的细胞毒性作用，胱氨酸转运活性的诱导构成了一种与这些因子所引起的应激相关的保护机制。胱氨酸转运的蛋白质成分可能属于应激蛋白范畴。
