Effects of vanadate on male rat reproductive tract histology, oxidative stress markers and androgenic enzyme activities

Taurine reverses sodium fluoride-mediated increase in inflammation, caspase-3 activity, and oxidative damage along the brain–pituitary–gonadal axis in male rats

“…However, the reduction in the testosterone level is correlated with the testicular spermatogenic dysfunction. Epididymal sperm count is considered as one of the most sensitive tests for evaluating spermatogenesis because it provides the outcome D r a f t of all the stages of meiosis, spermiogenesis, and transition in the epididymis (Chandra et al 2007). The decrease in the sperm count and progressive motility with increased sperm abnormality observed in fluoride-treated rats in this study are attributable to induction of oxidative stress and reduced bioavailability of testosterone in the treated rats.…”

Antioxidant Systems and Oxidative Stress in the Testes

“…119 Similarly, vanadate is a testicular toxicant that induces lipid peroxidation in the testes along with significant suppression of testicular SOD and catalase and the disruption of 3β-and 17β-hydroxysteroid dehydrogenase activities. 120 In addition to the above, Table 1 154 In addition to this list of xenobiotic chemicals that can induce oxidative stress in the testes, physical factors such as static magnetic fields 155 and electromagnetic radiation in its various forms from heat 12,156 to X-ray 157 irradiation, can also trigger a state of oxidative stress in Intriguingly, the suppression of antioxidant activity in response to exogenous steroid treatment largely affects the Leydig cells that contain most of the catalase and GPx activities. Testicular SOD activities that are largely confined to the seminiferous tubules did not change dramatically under these circumstances.…”

Antioxidant enzyme activity and lipid peroxidation in the blood of rats co-treated with vanadium (V+5) and chromium (Cr+3)

“…Since it is a transitional metal having redox properties, it may enter redox processes and produce free radicals (Byczkowski and Kulkarni 1998), in this way inducing lipid peroxidation (LPO) in both in vitro (Donaldson and LaBella 1983; and in vivo conditions (Elfant and Keen 1987;Sheriff 1991; Russanov et al 1994) and disturbing, thereby, the pro-antioxidative balance in the organism. V may also decrease the activities of some antioxidative enzymes in erythrocytes (RBCs; Soussi et al 2006), in the liver (Oster et al 1993;Saxena et al 1993;Russanov et al 1994), kidneys (Russanov et al 1994), and testes (Chandra et al 2007) of rats. It may diminish the concentrations of GSH and/or L-ascorbic acid in blood and/or internal organs (especially in liver and/or kidneys) of these animals (Chakraborty et al 1977;Elfant and Keen 1987;Saxena et al 1993;Zaporowska 1994;Zaporowska et al 1997) and act as a mitogen, tumor promoter and co-carcinogen.…”