Na+, K+-ATPase, glutathione, and hydroxyl free radicals in cadmium chloride-induced testicular toxicity in mice

Abstract

Cadmium chloride (CdCl2)-induced biochemical changes were characterized in male, CD-1 mouse testes. CdCl2 inhibited the testes microsomal Na+,K(+)-ATPase activity in vitro and in vivo. The inhibitory range was 30-50 microns and the concentration for half maximal inhibition (IC50 value) was 90 microns over 5 min preincubation. CdCl2 (2mg/kg/day, s.c.) for 2 days significantly inhibited testes Na+,K(+)-ATPase (near 90% inhibition). The content of testicular GSH and the ratio of reduced glutathione (GSH)/GSSG (oxidized glutathione) decreased in CdCl2-treated groups. Using salicylate as a trapping agent and high pressure liquid chromatography with electrochemical detection (LCED), we measured the OH production in vivo. 2,5-dihydroxybenzoic acid (2,5-DHBA) and 2,3-dihydroxybenzoic acid (2,3-DHBA) as indices of hydroxyl free radical formation significantly increased after 5 days CdCl2 exposure. Pretreatment with vitamin E (20 mg/kg, s.i.d., i.m., 7d) protected CdCl2-induced increase in OH. generation in testes. From this study, it was demonstrated that CdCl2 induced testicular toxicity could possibly be mediated by a significant increase in hydroxyl free radical formation and a reduction in GSH content and Na+,K(+)-ATPase activity. Vitamin E seems to prevent the CdCl2 induced increase in hydroxyl free radical generation.

Vitamin E protects against oxidative damage caused by cadmium in the blood of rats

“…The present results have clearly demonstrated the ability of Cd to induce oxidative stress in rat plasma and RBC as evidenced by increased lipid peroxidation after 20 days of Cd treatment. This finding is in agreement with several reports demonstrating that Cd induces oxidative stress in tissues by increasing lipid peroxidation and by altering the antioxidant status in several tissues (4)(5)(6)25).…”

Integrated NMR-Based Metabonomic Investigation of Early Metabolic Effects of Ethylene Glycol Monomethyl Ether (Egme) on Male Reproductive Organs in Rats

“…The significant reduction in GSH level in mouse or rat testes has been previously documented (Shen and Sangiah, 1995;Turk et al, 2007). In the present study, testicular GSH also decreased after the administration of EGME.…”

Protective role of zinc against the toxicity induced by exposure to cadmium during gestation and lactation on testis development

“…Similar results were obtained by Pillai et al [5] after gestational and lactational exposure to Cd. Reduction in testicular weight has been, partly, attributed to the necrotic and degenerative Cd-induced changes [41,42]. Lower serum testosterone levels noted in Cd-exposed animals might be due to the direct effect of Cd on Leydig cells [43][44][45] or to an indirect effect by altering gonadotrophin from pituitary, because Cd have been shown to accumulate in the hypothalamus and the pituitary [46].…”