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.

中文翻译：

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半胱氨酸预防由锌结合物质引起的实验性糖尿病的发展

在实验兔中，半胱氨酸以 1000 mg/kg 的剂量静脉注射，暂时结合 β 细胞中的锌，并阻止螯合锌复合物的形成，以应对随后注射诱导细胞破坏的致糖尿病锌结合物质。向动物注射半胱氨酸与 β 细胞中锌的急剧负反应有关，这证明锌离子被阻断。在双硫腙和锌-双硫腙复合物形成几分钟后注射半胱氨酸，随后双硫腙从复合物中置换出来，防止了大多数动物发生糖尿病。半胱氨酸预防作用最合理的机制是在 β 细胞中形成 2:1 的锌-半胱氨酸复合物，锌原子可能固定在两个半胱氨酸分子的 SH 基团的硫原子之间。