Kadkhodaee M, Khastar H, Arab H A, Ghaznavi R, Zahmatkesh M, Mahdavi-Mazdeh M
Department of Physiology, Faculty of Medicine, Tehran Medical Sciences University, Tehran, Iran.
Transplant Proc. 2007 May;39(4):864-5. doi: 10.1016/j.transproceed.2007.02.038.
The clinical use of gentamicin (G) is limited due to its known nephrotoxic actions. Generation of reactive oxygen species has been proposed as a causative factor of cell death in G-induced acute renal failure (ARF). Previous studies using superoxide dismutase (SOD) mimetics have indirectly suggested a role for the superoxide ion in G-induced ARF. In this study, we directly measured the enzyme activities using in situ isolated kidneys seeking to investigate the effects of antioxidant therapy on preservation of endogenous antioxidant levels in ARF.
Thirty-five male Sprague-Dawley rats were randomly assigned to 5 groups: control, Tyrode-perfused; G, gentamicin (200 mg/L) added to the perfusate; G + vitamin E (Vit E; 100 mg/100 g BW, IM); G + vitamin C (Vit C) added to the drinking water for 3 days (200 mg/L) and to the perfusate (100 mg/L); G + Vit E + Vit C. SOD activities were determined in renal tissues based on NAPDH oxidation at 340 nm by spectrophotometry.
SOD activity was significantly reduced in the G group compared with the controls (P<.05). Administration of Vit E alone or in combination with Vit C significantly preserved enzyme activity levels compared with the G group (P<.05).
Antioxidant vitamins have a role in preservation of renal endogenous antioxidant activities, namely SOD, in G-induced nephrotoxicity.
庆大霉素(G)因其已知的肾毒性作用,临床应用受到限制。活性氧的产生被认为是G诱导的急性肾衰竭(ARF)中细胞死亡的一个致病因素。先前使用超氧化物歧化酶(SOD)模拟物的研究间接表明超氧阴离子在G诱导的ARF中起作用。在本研究中,我们使用原位分离的肾脏直接测量酶活性,旨在研究抗氧化治疗对ARF中内源性抗氧化水平的保护作用。
35只雄性Sprague-Dawley大鼠随机分为5组:对照组,用台氏液灌注;G组,在灌注液中加入庆大霉素(200 mg/L);G + 维生素E(Vit E;100 mg/100 g体重,肌肉注射)组;G + 维生素C(Vit C)组,在饮水中添加3天(200 mg/L)并在灌注液中添加(100 mg/L);G + Vit E + Vit C组。通过分光光度法基于340 nm处NAPDH的氧化来测定肾组织中的SOD活性。
与对照组相比,G组的SOD活性显著降低(P<.05)。与G组相比,单独给予Vit E或与Vit C联合给予可显著保留酶活性水平(P<.05)。
抗氧化维生素在保护G诱导的肾毒性中肾脏内源性抗氧化活性(即SOD)方面发挥作用。