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钙、锌和维生素E可改善镉诱导的白化Wistar大鼠肾氧化损伤。

Calcium, zinc and vitamin E ameliorate cadmium-induced renal oxidative damage in albino Wistar rats.

作者信息

Adi Pradeepkiran Jangampalli, Burra Siva Prasad, Vataparti Amardev Rajesh, Matcha Bhaskar

机构信息

Division of Animal Biotechnology, Department of Zoology, Sri Venkateswara University, Tirupati - 517502, Andhra Pradesh, India.

出版信息

Toxicol Rep. 2016 Jul 29;3:591-597. doi: 10.1016/j.toxrep.2016.07.005. eCollection 2016.

Abstract

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.

摘要

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。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7825/5616016/d07314c0a953/fx1.jpg

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