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谷胱甘肽氧化还原对调节锌从金属硫蛋白向锌缺乏的山梨醇脱氢酶的转移。

The glutathione redox couple modulates zinc transfer from metallothionein to zinc-depleted sorbitol dehydrogenase.

作者信息

Jiang L J, Maret W, Vallee B L

机构信息

Center for Biochemical and Biophysical Sciences and Medicine, Harvard Medical School, Seeley G. Mudd Building, 250 Longwood Avenue, Boston, MA 02115, USA.

出版信息

Proc Natl Acad Sci U S A. 1998 Mar 31;95(7):3483-8. doi: 10.1073/pnas.95.7.3483.

Abstract

The release and transfer of zinc from metallothionein (MT) to zinc-depleted sorbitol dehydrogenase (EC 1.1.1.14) in vitro has been used to explore the role of MT in cellular zinc distribution. A 1:1 molar ratio of MT to sorbitol dehydrogenase is required for full reactivation, indicating that only one of the seven zinc atoms of MT is transferred in this process. Reduced glutathione (GSH) and glutathione disulfide (GSSG) are critical modulators of both the rate of zinc transfer and the ultimate number of zinc atoms transferred. GSSG increases the rate of zinc transfer 3-fold, and its concentration is the major determinant for efficient zinc transfer. GSH has a dual function. In the absence of GSSG, it inhibits zinc transfer from MT, indicating that MT is in a latent state under the relatively high cellular concentrations of GSH. In addition, it primes MT for the reaction with GSSG by enhancing the rate of zinc transfer 10-fold and by increasing the number of zinc atoms transferred to four. 65Zn-labeling experiments confirm the release of one zinc from MT in the absence of glutathione and the more effective release of zinc in the presence of GSH and GSSG. In vivo, MT may keep the cellular concentrations of free zinc very low and, acting as a temporary cellular reservoir, release zinc in a process that is dynamically controlled by its interactions with both GSH and GSSG. These results suggest that a change of the redox state of the cell could serve as a driving force and signal for zinc distribution from MT.

摘要

体外将金属硫蛋白(MT)中的锌释放并转移至锌缺乏的山梨醇脱氢酶(EC 1.1.1.14)已被用于探究MT在细胞锌分布中的作用。MT与山梨醇脱氢酶的摩尔比为1:1时才能实现完全重新激活,这表明在此过程中MT的七个锌原子中只有一个被转移。还原型谷胱甘肽(GSH)和氧化型谷胱甘肽(GSSG)是锌转移速率和最终转移锌原子数量的关键调节因子。GSSG可使锌转移速率提高3倍,其浓度是有效锌转移的主要决定因素。GSH具有双重功能。在没有GSSG的情况下,它会抑制MT的锌转移,这表明在细胞内相对较高的GSH浓度下MT处于潜伏状态。此外,它通过将锌转移速率提高10倍并将转移的锌原子数量增加到四个,使MT为与GSSG的反应做好准备。65Zn标记实验证实了在没有谷胱甘肽的情况下MT释放一个锌,以及在有GSH和GSSG的情况下更有效地释放锌。在体内,MT可能会使细胞内游离锌的浓度保持在非常低的水平,并作为细胞的临时储存库,在一个由其与GSH和GSSG的相互作用动态控制的过程中释放锌。这些结果表明,细胞氧化还原状态的变化可以作为锌从MT分布的驱动力和信号。

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