Increased NADH oxidase activity in the retina of the BBZ/WOR diabetic rat
Increased NADH oxidase activity in the retina of the BBZ/WOR diabetic rat
复制标题
DOI：
10.1016/s0891-5849(97)00202-5
复制
发表时间：
1998-01-01
影响因子：
7.4
通讯作者：
Lutty, GA
中科院分区：
文献类型：
--
作者：
Ellis, EA;Grant, MB;Lutty, GA
该形态学研究证实了内皮细胞在BBZ/Wor大鼠视网膜病变早期产生活性氧的作用，BBZ/Wor大鼠是一种肥胖、非胰岛素依赖型糖尿病模型。高血压诱导的假性缺氧导致胞质NADH/NAD+失衡。在视网膜的富氧环境中，NADH氧化酶产生超氧化物自由基，其歧化为过氧化氢。铈NADH氧化酶活性细胞化学定位技术的过氧化氢的本地化显示了一个统计学显着增加过氧化物本地化在糖尿病大鼠的视网膜中央相比，年龄匹配，非糖尿病对照。内源性血清白蛋白的渗漏表明内皮细胞功能障碍，与NADH氧化酶活性定位区域一致。在糖尿病大鼠中，过氧化氢定位区域的纤连蛋白水平增加。这种在体内的形态学研究是第一次证明氧化损伤和内皮细胞功能障碍的视网膜自发的，非胰岛素依赖型糖尿病模型。(C)1997年爱思唯尔科学公司
This morphological study demonstrates a role for endothelial cells in generating reactive oxygen species in early stages of retinopathy in the BBZ/Wor rat, an obese, noninsulin dependent model of diabetes. Hyperglycemia induced pseudohypoxia results in an imbalance in cytosolic NADH/NAD+. In the oxygen-rich environment of the retina, NADH oxidase generates superoxide radical which is dismutated to hydrogen peroxide. Localization of hydrogen peroxide by the cerium NADH oxidase enzyme activity cytochemical localization technique shows a statistically significant increase of peroxide localization in the central retina of diabetic rats as compared to age-matched, nondiabetic controls. Endothelial cell dysfunction, indicated by leakage of endogenous serum albumin, coincided with areas of NADH oxidase activity localization. In diabetic rats there are increased levels of fibronectin in areas of hydrogen peroxide localization. This in vivo, morphological study is the first demonstration of oxidative injury and endothelial cell dysfunction in the retina of a spontaneous, noninsulin dependent model of diabetes. (C) 1997 Elsevier Science Inc.