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首页> 外文期刊>Bulletin of experimental biology and medicine >Cysteine Prevents the Development of Experimental Diabetes Induced by Zinc-Binding Substances
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Cysteine Prevents the Development of Experimental Diabetes Induced by Zinc-Binding Substances

机译:半胱氨酸可防止锌结合物质诱导的实验糖尿病的发展

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In experimental rabbits, cysteine injected intravenously in a dose of 1000 mg/kg temporarily bound zinc in beta 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 beta 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 beta cells with possible fixation of Zn atom between sulfur atoms from SH groups of two cysteine molecules.
机译:在实验兔中,半胱氨酸以1000mg / kg的剂量静脉内注射β细胞的锌,并防止螯合锌络合物的形成响应于随后注射诱导细胞破坏的糖尿病锌结合物质。 将半胱氨酸注射到动物与β细胞中锌的急性反应相关,这证明了锌离子的阻断。 将半胱氨酸注射在二硫胺后几分钟和形成锌 - 二硫胺络合物,然后从复合物中移位并阻止大多数动物的糖尿病发育。 半胱氨酸的预防效果的最合理机制是在β细胞中形成2:1锌 - 半胱氨酸复合物,其在来自两个半胱氨酸分子的SH组的硫原子之间可能固定Zn原子。

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