Protective Effect of Troxerutin on Nickel-Induced Testicular Toxicity in Wistar Rats

J Environ Pathol Toxicol Oncol. 2016;35(2):133-46. doi: 10.1615/JEnvironPatholToxicolOncol.2016015384.


Nickel (Ni)-induced oxidative damage is a serious problem that leads to reproductive system failure through testicular damage. The present investigation was carried out to determine the effect of troxerutin (Txn) on testicular toxicity induced by Ni in experimental rat testes. The oral administration of Txn (100 mg/kg body weight [bw]) showed a significant (p < 0.01) increase in superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione-S-transferase (GST), glutathione reductase (GR), glucose-6-phosphate dehydrogenase (G6PD), reduced glutathione, ascorbate, total sulphydryl groups, and testis-organ weight. Subsequently, the administration of Txn also significantly reduced the accumulation of Ni, lipid peroxidation products, and protein carbonyl levels in Txn-treated animals. Testicular protection in the experimental animals by Txn is further substantiated by a remarkable reduction of Ni, which was revealed through testicular tissue histopathology. These studies suggest that Txn could prevent oxidative damage and testicular toxicity induced by Ni in experimental animals.

MeSH terms

  • Animals
  • Antioxidants / metabolism*
  • Antioxidants / therapeutic use
  • Cell Membrane / drug effects
  • Cell Membrane / enzymology
  • Chemical and Drug Induced Liver Injury / drug therapy
  • Chemical and Drug Induced Liver Injury / prevention & control*
  • Hydroxyethylrutoside / analogs & derivatives*
  • Hydroxyethylrutoside / pharmacology
  • Hydroxyethylrutoside / therapeutic use
  • Male
  • Nickel / toxicity*
  • Oxidative Stress / drug effects*
  • Random Allocation
  • Rats
  • Rats, Wistar
  • Testis / drug effects*
  • Testis / enzymology


  • Antioxidants
  • Hydroxyethylrutoside
  • nickel sulfate
  • Nickel
  • troxerutin