Diabetologic Research Group, E. A. Buketov Karaganda State University, Karaganda, Kazakhstan.
E. A. Buketov Karaganda State University, Karaganda, Kazakhstan.
Bull Exp Biol Med. 2020 Mar;168(5):621-626. doi: 10.1007/s10517-020-04765-1. Epub 2020 Apr 4.
In experimental rabbits, cysteine injected intravenously in a dose of 1000 mg/kg temporarily bound zinc in β cells and prevented the formation of chelate zinc complexes in response to subsequent injection of diabetogenic zinc-binding substances that induce cell destruction. Injection of cysteine to animals was associated with a sharply negative reaction to zinc in β cells, which attests to blockade of zinc ions. Injection of cysteine few minutes after dithizone and formation of zinc-dithizone complex was followed by displacement of dithizone from the complex and prevented the development of diabetes in most animals. The most plausible mechanism of preventive effect of cysteine is the formation of 2:1 zinc-cysteine complex in β cells with possible fixation of Zn atom between sulfur atoms from SH groups of two cysteine molecules.
在实验兔中，静脉注射 1000mg/kg 的半胱氨酸可暂时结合β细胞中的锌，并防止随后注射致糖尿病的锌结合物质形成螯合锌复合物，从而诱导细胞破坏。向动物注射半胱氨酸会导致β细胞对锌产生强烈的负反应，这证明了锌离子的阻断。半胱氨酸在二硫腙注射几分钟后注射，并形成锌-二硫腙复合物，随后从复合物中置换二硫腙，并防止大多数动物发生糖尿病。半胱氨酸预防作用的最合理机制是在β细胞中形成 2:1 的锌-半胱氨酸复合物，可能将 Zn 原子固定在两个半胱氨酸分子的 SH 基团的硫原子之间。
