Sun Lei, Shi De-Jing, Gao Xiang-Chun, Mi Shu-Yong, Yu Ying, Han Qing
Department of Ophthalmology, The Fourth Hospital of Harbin Medical University, Harbin, 150001, Heilongjiang, People's Republic of China.
Biol Trace Elem Res. 2014 May;158(2):219-23. doi: 10.1007/s12011-014-9925-7. Epub 2014 Mar 8.
The present study was designed to investigate the effect of vanadium in alloxan-induced diabetes and cataract in rats. Different doses of vanadium was administered once daily for 8 weeks to alloxan-induced diabetic rats. To know the mechanism of action of vanadium, lens malondialdehyde (MDA), protein carbonyl content, activity of superoxide dismutase (SOD), activities of aldose reductase (AR), and sorbitol levels were assayed, respectively. Supplementation of vanadium to alloxan-induced diabetic rats decreased the blood glucose levels due to hyperglycemia, inhibited the AR activity, and delayed cataract progression in a dose-dependent manner. The observed beneficial effects may be attributed to polyol pathway activation but not decreased oxidative stress. Overall, the results of this study demonstrate that vanadium could effectively reduce the alloxan-induced hyperglycemia and diabetic cataracts in rats.
本研究旨在探讨钒对大鼠四氧嘧啶诱导的糖尿病和白内障的影响。将不同剂量的钒每日一次给予四氧嘧啶诱导的糖尿病大鼠，持续8周。为了解钒的作用机制，分别检测了晶状体丙二醛（MDA）、蛋白质羰基含量、超氧化物歧化酶（SOD）活性、醛糖还原酶（AR）活性及山梨醇水平。给四氧嘧啶诱导的糖尿病大鼠补充钒可降低因高血糖导致的血糖水平，抑制AR活性，并以剂量依赖方式延缓白内障进展。观察到的有益作用可能归因于多元醇途径的激活而非氧化应激的降低。总体而言，本研究结果表明钒可有效降低大鼠四氧嘧啶诱导的高血糖和糖尿病性白内障。
