Adi Pradeepkiran Jangampalli, Burra Siva Prasad, Vataparti Amardev Rajesh, Matcha Bhaskar
Division of Animal Biotechnology, Department of Zoology, Sri Venkateswara University, Tirupati - 517502, Andhra Pradesh, India.
Toxicol Rep. 2016 Jul 29;3:591-597. doi: 10.1016/j.toxrep.2016.07.005. eCollection 2016.
This study was aimed to examine the protective effects of supplementation with calcium + zinc (Ca + Zn) or vitamin E (Vit-E) on Cd-induced renal oxidative damage. Young albino Wistar rats (180 ± 10 g) (n = 6) control rats, Cd, Cd + Ca + Zn, and Cd + Vit-E experimental groups and the experimental period was 30 days. Rats were exposed to Cd (20 mg/kg body weight) alone treated as Cd treated group and the absence or presence of Ca + Zn (2 mg/kg each) or Vit-E (20 mg/kg body weight) supplementation treated as two separate groups. The activities of the stress marker enzymes superoxide dismutase (SOD), catalase (CAT), glutathione reductase (GR), glutathione peroxidase (GPx), glutathione-S-transferase (GST) and lipid peroxidase (LPx) were determined in renal mitochondrial fractions of experimental rats. We observed quantitative changes in SOD isoenzymatic patterns by non-denaturing PAGE analysis, and quantified band densities. These results showed that Cd exposure leads to decreases in SOD, CAT, GR, and GPx activities and a concomitant increase in LPx and GST activities. Ca + Zn and Vit-E administration with Cd significantly reversed Cd-induced perturbations in oxidative stress marker enzymes. However, Vit-E showed more inhibitory activity against Cd than did Ca + Zn, and it protected against Cd-induced nephrotoxicity.
本研究旨在探讨补充钙 + 锌(Ca + Zn)或维生素E(Vit-E)对镉诱导的肾脏氧化损伤的保护作用。选用年轻的白化Wistar大鼠(180 ± 10 g)(n = 6),分为对照组、镉处理组、镉 + 钙 + 锌处理组和镉 + 维生素E处理组,实验期为30天。单独给予大鼠镉(20 mg/kg体重)作为镉处理组,分别给予或不给予钙 + 锌(各2 mg/kg)或维生素E(20 mg/kg体重)作为两个单独的组。测定实验大鼠肾脏线粒体部分应激标记酶超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽还原酶(GR)、谷胱甘肽过氧化物酶(GPx)、谷胱甘肽-S-转移酶(GST)和脂质过氧化物酶(LPx)的活性。通过非变性PAGE分析观察SOD同工酶模式的定量变化,并对条带密度进行定量。这些结果表明,镉暴露导致SOD、CAT、GR和GPx活性降低,同时LPx和GST活性增加。与镉同时给予钙 + 锌和维生素E可显著逆转镉诱导的氧化应激标记酶的紊乱。然而,维生素E对镉的抑制活性比钙 + 锌更强,它能保护大鼠免受镉诱导的肾毒性。