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

被引:33
作者
Adi, Pradeepkiran Jangampalli [1 ]
Burra, Siva Prasad [1 ]
Vataparti, Amardev Rajesh [1 ]
Matcha, Bhaskar [1 ]
机构
[1] Sri Venkateswara Univ, Dept Zool, Div Anim Biotechnol, Tirupati 517502, Andhra Pradesh, India
关键词
Cadmium (Cd); Oxidative stress; Lipid peroxidation; Nephrotoxicity; PAGE analysis;
D O I
10.1016/j.toxrep.2016.07.005
中图分类号
R99 [毒物学(毒理学)];
学科分类号
100405 ;
摘要
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. (C) 2016 Published by Elsevier Ireland Ltd.
引用
收藏
页码:591 / 597
页数:7
相关论文
共 48 条
[21]   DIFFERENTIAL COMBINED EFFECT OF CADMIUM AND NICKEL ON HEPATIC AND RENAL GLUTATHIONE S-TRANSFERASES OF THE GUINEA-PIG [J].
ISCAN, M ;
COBAN, T ;
EKE, BC .
ENVIRONMENTAL HEALTH PERSPECTIVES, 1994, 102 :69-72
[22]   Mechanism of cadmium-induced cytotoxicity in rat hepatocytes: Cadmium-induced active oxygen-related permeability changes of the plasma membrane [J].
Koizumi, T ;
Shirakura, H ;
Kumagai, H ;
Tatsumoto, H ;
Suzuki, KT .
TOXICOLOGY, 1996, 114 (02) :125-134
[23]  
KOSTIC MM, 1993, EUR J HAEMATOL, V51, P86
[24]   Effects of antioxidant enzymes in the molecular control of reactive oxygen species toxicology [J].
Matés, JM .
TOXICOLOGY, 2000, 153 (1-3) :83-104
[25]  
Matovic V, 2015, FOOD CHEM TOXICOL, V78, P130, DOI [10.1016/j.fct.2015.02.011, 10.1016/jict.2015.02.011]
[26]   SELENIUM-DEPENDENT GLUTATHIONE-PEROXIDASE INHIBITORS INCREASE TOXICITY OF PROOXIDANT COMPOUNDS IN CHICKS [J].
MERCURIO, SD ;
COMBS, GF .
JOURNAL OF NUTRITION, 1986, 116 (09) :1726-1734
[27]   VITAMIN-E [J].
MEYDANI, M .
LANCET, 1995, 345 (8943) :170-175
[28]  
MISRA HP, 1972, J BIOL CHEM, V247, P3170
[29]   Evidence that the reactions of cadmium in the presence of metallothionein can produce hydroxyl radicals [J].
O'Brien, P ;
Salacinski, HJ .
ARCHIVES OF TOXICOLOGY, 1998, 72 (11) :690-700
[30]  
OGNJANOVIC B, 1995, PHYSIOL RES, V44, P293