Chen S M, Young T K
Department of Medical Research and Education, Nephrology Laboratory, Veterans General Hospital-Taipei, Taiwan.
J Formos Med Assoc. 1998 Nov;97(11):750-6.
We evaluated the effects of zinc deficiency on the activities of endogenous antioxidant enzymes and lipid peroxidation in rat glomerular cells (GCs). Male Sprague-Dawley rats (n = 48) were fed a zinc-deficient diet and deionized distilled water for 1 week to induce zinc deficiency. Half of the rats (zinc-deficient group) continued on this diet for 4 weeks, and the other half (zinc-replete group) were maintained on the same diet but with zinc-supplemented water (150 mg/Lzinc sulfate solution). Half of each group underwent five-sixths nephrectomy, while the other half underwent a sham operation. Another 12 normal rats (controls) were fed standard rat chow (containing 23.4% protein and 70 ppm zinc) and drank deionized distilled water. The zinc-deficient rats, including sham and five-sixths nephrectomized rats, showed severe growth retardation and poor appetite. Their mean plasma zinc concentrations were half that of normal control rats, but their plasma copper concentration was significantly higher than that of the control rats. Zinc supplementation corrected the abnormality of plasma zinc and copper concentrations and the loss of body weight in zinc-deficient rats. Zinc-deficient rats exhibited lower renal creatinine clearance and higher GC-malondialdehyde (GC-MDA) than zinc-replete rats. The remnant kidney of all five-sixths nephrectomized rats, including zinc-deficient and zinc-replete rats, showed a compensatory elevation in renal creatinine clearance and increased GC-MDA concentrations. Zinc concentrations in the renal cortex were decreased in zinc-deficient rats and the activities of GC-superoxide dismutase and GC-glutathione peroxidase were increased, while zinc-replete rats exhibited normal activities of GC-superoxide dismutase and GC-glutathione peroxidase. We suggest that zinc deficiency enhances the formation of reactive oxygen species but does not affect the activities of endogenous antioxidant enzymes in glomerular cells.
我们评估了锌缺乏对大鼠肾小球细胞(GCs)内源性抗氧化酶活性和脂质过氧化的影响。将雄性Sprague-Dawley大鼠(n = 48)喂以缺锌饮食和去离子蒸馏水1周以诱导锌缺乏。一半大鼠(缺锌组)继续这种饮食4周,另一半(补锌组)维持相同饮食但饮用补锌水(150 mg/L硫酸锌溶液)。每组的一半大鼠接受六分之五肾切除术,另一半接受假手术。另外12只正常大鼠(对照组)喂以标准大鼠饲料(含23.4%蛋白质和70 ppm锌)并饮用去离子蒸馏水。缺锌大鼠,包括假手术和六分之五肾切除的大鼠,表现出严重的生长迟缓且食欲不佳。它们的平均血浆锌浓度是正常对照大鼠的一半,但血浆铜浓度显著高于对照大鼠。补锌纠正了缺锌大鼠血浆锌和铜浓度的异常以及体重减轻。缺锌大鼠的肾肌酐清除率低于补锌大鼠,且GC-丙二醛(GC-MDA)水平更高。所有六分之五肾切除大鼠的残余肾,包括缺锌和补锌大鼠,肾肌酐清除率均有代偿性升高且GC-MDA浓度增加。缺锌大鼠肾皮质中的锌浓度降低,GC-超氧化物歧化酶和GC-谷胱甘肽过氧化物酶的活性增加,而补锌大鼠的GC-超氧化物歧化酶和GC-谷胱甘肽过氧化物酶活性正常。我们认为锌缺乏会增强活性氧的形成,但不影响肾小球细胞内源性抗氧化酶的活性。