ISSN:
1432-0703
Source:
Springer Online Journal Archives 1860-2000
Topics:
Energy, Environment Protection, Nuclear Power Engineering
,
Medicine
Notes:
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 μm and the concentration for half maximal inhibition (IC50 value) was 90 μm 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.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/BF00212967
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