作者: Y. Shen , S. Sangiah
DOI: 10.1007/BF00212967
关键词: IC50 、 Endocrinology 、 Vitamin 、 Radical 、 Chemistry 、 Toxicity 、 Internal medicine 、 Na+/K+-ATPase 、 Biochemistry 、 Cadmium chloride 、 Vitamin E 、 Glutathione
摘要: Cadmium chloride (CdCl2)-induced biochemical changes were characterized in male, CD-1 mouse testes. CdCl2 inhibited the testes microsomal Na–, K–-ATPase activity vitro and vivo. The inhibitory range was 30–50 μm concentration for half maximal inhibition (IC50 value) 90 over 5 min preincubation. (2mg/kg/day, s.c.) 2 days significantly (near 90% inhibition). content of testicular GSH ratio reduced glutathione (GSH)/GSSG (oxidized glutathione) decreased CdCl2-treated groups. Using salicylate as a trapping agent high pressure liquid chromatography with electrochemical detection (LCED), we measured OH production 2,5-dihydroxybenzoic acid (2,5-DHBA) 2,3-dihydroxybenzoic (2,3-DHBA) indices hydroxyl free radical formation increased after exposure. Pretreatment vitamin E (20 mg/kg, s.i.d., i.m., 7d) protected CdCl2-induced increase generation From this study, it demonstrated that induced toxicity could possibly be mediated by significant reduction activity. Vitamin seems to prevent generation.