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镉在肾脏应激性过氧化反应中的作用。

The role of cadmium in the peroxidative response of kidney to stress.

作者信息

Oner G, Sentürk U K, Izgüt-Uysal N

机构信息

Akdeniz University, Faculty of Medicine, Department of Physiology, Kampüs, Antalya-Turkey.

出版信息

Biol Trace Elem Res. 1995 Apr;48(1):111-7. doi: 10.1007/BF02789083.

DOI:10.1007/BF02789083
PMID:7626368
Abstract

Since the kidney is a main target for cadmium, its accumulation in the kidney tissue by increasing peroxidative damage make the kidney functions vulnerable to stress. For this reason, the effect of cadmium-induced peroxidative damage to kidney responses to stress was investigated in this study. Two-month-old albino rats receiving 15 micrograms/mL containing Cd drinking water for 30 d were exposed to restraint and cold stress for 6 h, and their responses were compared with those of unstressed counterparts. Lipid peroxidation was found to be significantly higher in the cortical portion of kidney in cadmium-exposed rats than that of unexposed animals. The mean thiobarbutyric acid reactive substance (TBARS) level rose from 211.6 +/- 64.2 to 303.4 +/- 46.4 nmol/g protein (p < 0.01). Six hours of cold and restraint stress caused an elevation in the cortical TBARS level in control animals without affecting its level in cadmium-exposed rats. Despite unaltered cortical TBARS, its medullar levels increased significantly in cadmium-exposed rats because of stress. These results suggested that cadmium accumulation in the kidney increases the susceptibility of medulla against peroxidative damage. However, further functional studies are necessary to explain the role of cadmium in the stress-induced deterioration of medullar functions.

摘要

由于肾脏是镉的主要靶器官,镉在肾脏组织中的蓄积通过增加过氧化损伤,使肾脏功能易受应激影响。因此,本研究探讨了镉诱导的过氧化损伤对肾脏应激反应的影响。给2月龄白化大鼠饮用含15微克/毫升镉的饮用水30天,然后对其施加6小时的束缚和冷应激,并将它们的反应与未受应激的对照组大鼠进行比较。结果发现,镉暴露大鼠肾脏皮质部分的脂质过氧化水平显著高于未暴露动物。硫代巴比妥酸反应性物质(TBARS)的平均水平从211.6±64.2上升至303.4±46.4纳摩尔/克蛋白质(p<0.01)。6小时的冷应激和束缚应激使对照动物的皮质TBARS水平升高,但对镉暴露大鼠的该水平没有影响。尽管皮质TBARS水平未改变,但由于应激,镉暴露大鼠的髓质TBARS水平显著升高。这些结果表明,镉在肾脏中的蓄积增加了髓质对过氧化损伤的易感性。然而,需要进一步的功能研究来解释镉在应激诱导的髓质功能恶化中的作用。

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