Rodríguez J V, Torres A M, Elías M M
Can J Physiol Pharmacol. 1987 Jan;65(1):84-6. doi: 10.1139/y87-016.
In this study we examined the response of the renal and hepatic glutathione (GSH) pool in rats to drastic GSH depletion treatments. For this purpose, we used a protein-free diet, starvation, and the injection of varying doses of diethyl maleate as depleting agents. We analysed GSH levels in both kidney and liver tissue homogenates after rats were fed a protein-free diet for 2 or 7 days or starved for 1, 2, or 3 days, as well as after diethyl maleate administration in a single maximal dose or in varying doses. The results indicated that the liver GSH pool was always more labile than the kidney GSH pool. Moreover, kidney GSH levels were almost unchanged after 7 days on a protein-free diet or after 2 days of starvation, while liver showed significant changes in GSH levels. When we analysed the repletion rate, kidney had higher kinetic parameters (k = 0.148 h-1) than liver (0.097 h-1). We conclude that efficient mechanisms of maintaining GSH levels exist in the kidney and these may serve to avoid GSH diminution and hence preserve renal function during states of GSH depletion.
在本研究中，我们检测了大鼠肾和肝中谷胱甘肽（GSH）库对剧烈GSH耗竭处理的反应。为此，我们采用无蛋白饮食、饥饿以及注射不同剂量的马来酸二乙酯作为耗竭剂。在大鼠接受无蛋白饮食2天或7天、饥饿1天、2天或3天之后，以及在给予单次最大剂量或不同剂量的马来酸二乙酯之后，我们分析了肾和肝组织匀浆中的GSH水平。结果表明，肝脏GSH库总是比肾脏GSH库更不稳定。此外，无蛋白饮食7天后或饥饿2天后，肾脏GSH水平几乎没有变化，而肝脏的GSH水平则出现了显著变化。当我们分析补充率时，肾脏的动力学参数（k = 0.148 h-1）高于肝脏（0.097 h-1）。我们得出结论，肾脏中存在维持GSH水平的有效机制，这些机制可能有助于避免GSH减少，从而在GSH耗竭状态下保护肾功能。
