Torres A M, Ochoa J E, Elias M M
Facultad de Ciencias Bioquímicas y Farmaceuticas, Universidad Nacionalde Rosario, Instituto de Fisiología Experimental-Consejo Nacional de Investigaciones Científicas y Técnicas, (CONICET), Argentina.
Toxicology. 1991;70(2):163-72. doi: 10.1016/0300-483x(91)90043-z.
This study was designed to investigate the role of lipid peroxidation in the pathogenesis of renal dysfunction in glutathione (GSH)-depleted rats. Renal function parameters and acid-base status were analyzed in diethylmaleate (DEM)-treated rats previously injected with vitamin E (Vit.E). Vit.E was effective in inhibiting the elevation in renal lipid peroxidation found in GSH-depleted rats. Vit.E also ameliorated the renal response to the metabolic acidosis without modification in lactate production induced by DEM administration. The increase in sodium and water urine excretion and the diminution of the urine to plasma osmolalities ratio were not reversed in these animals. These results lead us to conclude that lipid peroxidation is associated with distal acidification impairment observed with GSH-depletion, but it is not related to the sodium reabsorption alteration in the ascending loop of Henle.
本研究旨在探讨脂质过氧化在谷胱甘肽（GSH）耗竭大鼠肾功能障碍发病机制中的作用。对先前注射维生素E（Vit.E）的马来酸二乙酯（DEM）处理大鼠的肾功能参数和酸碱状态进行了分析。Vit.E有效抑制了GSH耗竭大鼠肾脂质过氧化的升高。Vit.E还改善了对代谢性酸中毒的肾反应，而DEM给药诱导的乳酸产生没有改变。这些动物的钠和水尿排泄增加以及尿与血浆渗透压比值降低并未逆转。这些结果使我们得出结论，脂质过氧化与GSH耗竭时观察到的远端酸化损伤有关，但与髓袢升支钠重吸收改变无关。
