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霉菌毒素孢霉菌素的毒性机制研究。I. 孢霉菌素产生超氧自由基的过程。

Studies on the mechanism of toxicity of the mycotoxin, sporidesmin. I. Generation of superoxide radical by sporidesmin.

作者信息

Munday R

出版信息

Chem Biol Interact. 1982 Sep;41(3):361-74. doi: 10.1016/0009-2797(82)90112-0.

DOI:10.1016/0009-2797(82)90112-0
PMID:6286158
Abstract

Sporidesmin (SDMS2), the mycotoxin responsible for 'facial eczema' in ruminants, contains a disulphide group which appears to be intimately involved in its toxic action. The reduced (dithiol) form of sporidesmin has been shown readily to undergo autoxidation in vitro in a reaction which generates superoxide radical (O2-). The autoxidation reaction, which takes place over a wide pH range, is strongly catalysed by trace amounts of copper, although the reaction was inhibited at high concentrations of this metal. Inhibition of the autooxidation of reduced sporidesmin (SDM(SH)2) was also observed in the presence of nickel, cobalt and manganese. Superoxide radical is also generated from SDMS2 itself in a cyclic reduction/autoxidation reaction with glutathione and other thiols; in view of the known toxicity of superoxide and its derivatives, it is suggested that oxygen-free-radicals may be involved in the initiation of the deleterious effects of the mycotoxin.

摘要

孢霉菌素(SDMS2)是导致反刍动物“面部湿疹”的霉菌毒素,它含有一个二硫键,该二硫键似乎与其毒性作用密切相关。已表明,孢霉菌素的还原(二硫醇)形式在体外很容易发生自氧化反应,该反应会产生超氧自由基(O2-)。自氧化反应在很宽的pH范围内进行,微量铜会强烈催化该反应,不过在高浓度的这种金属存在下反应会受到抑制。在镍、钴和锰存在的情况下,也观察到还原型孢霉菌素(SDM(SH)2)的自氧化受到抑制。超氧自由基也会在与谷胱甘肽和其他硫醇的循环还原/自氧化反应中由SDMS2自身产生;鉴于超氧及其衍生物已知的毒性,有人提出氧自由基可能参与了这种霉菌毒素有害作用的起始过程。

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