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单侧肾切除大鼠亚慢性暴露于镉后糖尿病性肾小球病变的加重

Potentiation of diabetic glomerulopathy in uninephrectomized rats subchronically exposed to cadmium.

作者信息

Bernard A, Schadeck C, Cardenas A, Buchet J P, Lauwerys R

机构信息

Unit of Industrial Toxicology and Occupational Medicine, Catholic University of Louvain, Brussels, Belgium.

出版信息

Toxicol Lett. 1991 Sep;58(1):51-7. doi: 10.1016/0378-4274(91)90190-h.

Abstract

The renal effects of diabetes mellitus and cadmium (Cd), separately or in combination, were investigated in unilaterally nephrectomized female Sprague-Dawley rats. Diabetes was induced by injection of streptozotocin and Cd was administered in drinking water at a concentration of 100 p.p.m. for 2.5 months. Cd did not affect the reduction in glomerular filtration rate or the rise in beta 2-microglobulinuria caused by diabetes. By contrast, the effect of diabetes on the urinary excretion of albumin, transferrin or IgG was greatly enhanced by concomitant exposure to Cd. This interaction occurred at Cd levels in the renal cortex which are very similar to those found in the general population of industrialized countries. These observations, in agreement with the results of a recent epidemiological study, suggest that Cd polluting the environment might potentiate the development of diabetic nephropathy.

摘要

在单侧肾切除的雌性斯普拉格-道利大鼠中,分别或联合研究了糖尿病和镉(Cd)对肾脏的影响。通过注射链脲佐菌素诱导糖尿病,并以100 ppm的浓度在饮用水中给予Cd,持续2.5个月。Cd不影响糖尿病引起的肾小球滤过率降低或β2-微球蛋白尿增加。相比之下,同时接触Cd会大大增强糖尿病对白蛋白、转铁蛋白或IgG尿排泄的影响。这种相互作用发生在肾皮质中的Cd水平,这与工业化国家普通人群中的水平非常相似。这些观察结果与最近一项流行病学研究的结果一致,表明污染环境的Cd可能会促进糖尿病肾病的发展。

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