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Effects of methionine on selenium embryotoxicity in cultured rat embryos
Makoto Usami1, Hirobumi Tabata, Yasuo Ohno
1Division of Pharmacology, National Institute of Health Sciences, Tokyo, Japan. usami@nihs.go.jp
Effects of methionine, an essential amino acid, on the embryotoxicity of selenium (Se) were examined using the rat embryo culture. Rat embryos at day 9.5 of gestation were cultured for 48 h in the presence of sodium selenite at 10 and 20 microM or sodium selenate at 30 and 100 microM with or without the addition of 1 mM DL-methionine. Selenite at 20 microM or selenate at 100 microM alone increased the incidence of embryonic malformation and inhibited the embryonic growth. The addition of methionine increased the incidence of embryonic malformation at 10 microM of selenite but decreased the incidence of embryonic malformation at 100 microM of selenate. On the other hand, the addition of methionine partially restored the inhibited embryonic growth at 20 microM of selenite or at 100 microM of selenate. It was considered from these results that the methionine availability in the embryonic environment and the oxidation state of Se are critical in Se embryotoxicity.
Effects of methionine, an essential amino acid, on the embryotoxicity of selenium (Se) were examined using the rat embryo culture. Rat embryos at day 9.5 of gestation were cultured for 48 h in the presence of sodium selenite at 10 and 20 microM or sodium selenate at 30 and 100 microM with or without the addition of 1 mM DL-methionine. Selenite at 20 microM or selenate at 100 microM alone increased the incidence of embryonic malformation and inhibited the embryonic growth. The addition of methionine increased the incidence of embryonic malformation at 10 microM of selenite but decreased the incidence of embryonic malformation at 100 microM of selenate. On the other hand, the addition of methionine partially restored the inhibited embryonic growth at 20 microM of selenite or at 100 microM of selenate. It was considered from these results that the methionine availability in the embryonic environment and the oxidation state of Se are critical in Se embryotoxicity.