Pérez-Gallardo Rocío V, Noriega-Cisneros Ruth, Esquivel-Gutiérrez Edgar, Calderón-Cortés Elizabeth, Cortés-Rojo Christian, Manzo-Avalos Salvador, Campos-García Jesús, Salgado-Garciglia Rafael, Montoya-Pérez Rocío, Boldogh Istvan, Saavedra-Molina Alfredo
Instituto de Investigaciones Químico-Biológicas, Universidad Michoacana de San Nicolás de Hidalgo, Edificio B-3. C.U., Morelia, Mich, 58030, Mexico.
J Bioenerg Biomembr. 2014 Dec;46(6):511-8. doi: 10.1007/s10863-014-9594-4. Epub 2014 Nov 26.
Diabetes mellitus (DM) is characterized by chronic hyperglycemia resulting from defects in the secretion and/or action of insulin. Diabetic nephropathy (DN) develops in diabetic patients and is characterized by a progressive deterioration of renal function. The mitochondrial electron transport chain (ETC) produces most of the reactive oxygen species (ROS) that are involved in diabetic nephropathy. Due to the high incidence of DM in the elderly, the aim of this study was to evaluate oxidative and nitrosative stress in kidney mitochondria from aged rats. We evaluated lipid peroxidation (LPO), nitric oxide (NO(•)) production, S-nitrosylation profiles, glutathione levels, and glutathione reductase and aconitase activities under streptozotocin (STZ)-induced experimental diabetes in kidney mitochondria from aged rats. The results showed an increase in LPO, NO(•) production, and S-nitrosylated proteins in rats with STZ-induced diabetes. A decrease in glutathione (GSH) levels and glutathione reductase (GR) and aconitase activities in the rats that received the STZ-induced diabetes treatment was also observed, when compared with the age-related controls. The data suggest that oxidative and nitrosative stresses promote mitochondrial oxidative dysfunction in the more advanced age rat kidney in STZ-induced diabetes.
糖尿病（DM）的特征是由于胰岛素分泌和/或作用缺陷导致的慢性高血糖。糖尿病肾病（DN）在糖尿病患者中发生，其特征是肾功能进行性恶化。线粒体电子传递链（ETC）产生了参与糖尿病肾病的大部分活性氧（ROS）。由于老年人中DM的发病率较高，本研究的目的是评估老年大鼠肾脏线粒体中的氧化应激和亚硝化应激。我们评估了链脲佐菌素（STZ）诱导的老年大鼠肾脏线粒体实验性糖尿病状态下的脂质过氧化（LPO）、一氧化氮（NO(•)）生成、S-亚硝基化谱、谷胱甘肽水平以及谷胱甘肽还原酶和乌头酸酶活性。结果显示，STZ诱导糖尿病的大鼠中LPO、NO(•)生成和S-亚硝基化蛋白增加。与年龄相关的对照组相比，接受STZ诱导糖尿病治疗的大鼠中谷胱甘肽（GSH）水平、谷胱甘肽还原酶（GR）和乌头酸酶活性也降低。数据表明，氧化应激和亚硝化应激在STZ诱导的糖尿病中促进了老年大鼠肾脏中更严重的线粒体氧化功能障碍。
