大鼠补充谷胱甘肽过程中甘氨酸的肾脏转运

Torres A.M., Ochoa E.J., Guibert E., Rodriguez J.V., Elias M.M.
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引用次数: 4

摘要

在对照组和谷胱甘肽缺失大鼠中研究了甘氨酸的肾转运。用马来酸二乙酯(4.0 mmol/kg体重,体重)作为谷胱甘肽消耗剂,分别在注射马来酸二乙酯后6和10 h进行研究。用清除法和快速滤过法分别测定了大鼠离体肾制剂的肾转运。与肾小球滤过率相比,在不同底物小管负荷下测量的甘氨酸小管重吸收在处理过的肾脏中更高。马来酸二乙酯处理的动物肾脏组织中14C的积累也更高。刷状边缘膜囊泡的研究表明,与对照制剂相比,谷胱甘肽耗竭诱导了更高的钠依赖性甘氨酸摄取。这种适应与τ-谷氨酰转移酶活性或蛋白质浓度的增加无关。这些结果可以部分解释谷胱甘肽衰竭肾脏中谷胱甘肽细胞水平的补充,其方式是甘氨酸(谷胱甘肽前体)的更高运输能力,即使在谷胱甘肽水平恢复时也能维持这种转运能力。
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Renal Transport of Glycine during Glutathione Replenishment in Rats

Renal transport of glycine was studied in control and glutathione-depleted rats. Diethylmaleate (4.0 mmol/kg body wt, ip) was used as a glutathione depletor agent and the studies were carried out 6 and 10 h post-diethylmaleate injection. Renal transport was measured in isolated rat kidney preparations by means of clearance techniques and in brush border membrane vesicles by a rapid filtration method. Tubular reabsorption of glycine, when compared to glomerular filtration rate, measured at different substrate tubular loads, was higher in treated kidneys. Tissue 14C accumulation was also higher in kidneys from diethylmaleate-treated animals. Studies with brush border membrane vesicles indicated that glutathione depletion induced higher sodium-dependent glycine uptake in contrast with control preparations. This adaptation was not associated with an increment in either τ-glutamyltransferase activity or in protein concentrations. These results could explain in part the replenishment of GSH cellular levels in glutathione-depleted kidneys by means of higher transport capacity for glycine (a glutathione precursor) which was maintained even when GSH levels were restored.

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