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氧化应激、线粒体呼吸与血糖控制:雄性Wistar大鼠长期补充Cr3+或As3+的线索

Oxidative stress, mitochondrial respiration, and glycemic control: clues from chronic supplementation with Cr3+ or As3+ to male Wistar rats.

作者信息

Cobo J M, Castiñeira M

机构信息

Facultad de Farmacia, Universidad de Alcalá de Henares, Spain.

出版信息

Nutrition. 1997 Nov-Dec;13(11-12):965-70. doi: 10.1016/s0899-9007(97)00338-9.

DOI:10.1016/s0899-9007(97)00338-9
PMID:9433712
Abstract

Multiple experiments in male Wistar rats were designed to clarify the role of mitochondrial dysfunction in the mechanisms of oxidative stress-related diseases and toxicity-induced pathologies. In this particular report, 21 male Wistar rats were supplemented ad libitum with either As3+ or Cr3+ salts in drinking water to assess insulin secretion patterns in vivo and in vitro, mitochondrial dysfunction, oxidative stress, liver damage, basal insulin, and glucose tolerance curves, among other parameters. Results were compared with a control group without any metal supplementation. The CrCl3 supplements were more invasive of metabolism and had a stronger effect on mitochondrial dysfunction than As3+, despite that both seem to use similar mechanisms of toxicity; viz.: binding to thiol or -SS- group in enzymes and proteins, and releasing oxidant species during their redox-cycling and metabolic activation processes, e.g., by cytochrome P450 in liver. Results support our aim to prove the influence of oxidative stress-induced mitochondrial dysfunction on glycemic control.

摘要

设计了多项针对雄性Wistar大鼠的实验,以阐明线粒体功能障碍在氧化应激相关疾病和毒性诱导病理机制中的作用。在这份特定报告中,21只雄性Wistar大鼠被随意补充饮用水中的As3+或Cr3+盐,以评估体内和体外的胰岛素分泌模式、线粒体功能障碍、氧化应激、肝损伤、基础胰岛素和葡萄糖耐量曲线等参数。结果与未补充任何金属的对照组进行了比较。尽管两者似乎使用相似的毒性机制,即:与酶和蛋白质中的硫醇或-SS-基团结合,并在其氧化还原循环和代谢激活过程中释放氧化物质,例如通过肝脏中的细胞色素P450,但CrCl3补充剂对代谢的侵入性更强,对线粒体功能障碍的影响也比As3+更强。结果支持了我们证明氧化应激诱导的线粒体功能障碍对血糖控制影响的目标。

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