Effects of glutathione depletion on selenite- and selenate-induced embryotoxicity in cultured rat embryos

✍ Scribed by Makoto Usami; Hirobumi Tabata; Yasuo Ohno

• Publisher: John Wiley and Sons
• Year: 1999
• Tongue: English
• Weight: 98 KB
• Volume: 19
• Category: Article
• ISSN: 0270-3211
• DOI: 10.1002/(sici)1520-6866(1999)19:4<257::aid-tcm2>3.0.co;2-3

✦ Synopsis

Effects of depletion of reduced glutathione (GSH) on selenium (Se) embryotoxicity in cultured rat embryos were examined. Rat embryos at day 9.5 of gestation were cultured for 48 h in the presence of Se as either sodium selenite at 10 and 20 µM or sodium selenate at 30 and 100 µM. Embryonic GSH was depleted by the addition of 0.1 mM of L-buthionine-[S,R]-sulfoximine (BSO) without embryotoxicity, i.e., significant growth retardation and malformation of the embryos. Selenite at 10 µM or selenate at 100 µM significantly increased the incidence of malformation of the embryos. The incidence of selenite-induced malformation of the embryos at 20 µM was significantly decreased with BSO. On the contrary, the incidence of selenate-induced malformation at 30 µM was significantly increased with BSO. It was noted that the major malformed regions of the embryos by the embryotoxic concentration of BSO alone were the same to those affected by selenite or selenate. It was considered from these results that embryonic GSH was involved in the embryotoxicity of selenite and selenate. The embryotoxicity of selenate may not be mediated through the reduction to selenite. It was suggested that the formation of selenodiglutathione and the oxidative stress were involved in the embryotoxicity of selenite and selenate, respectively.