{"title":"抗氧化剂对大鼠胚胎和培养的支持细胞的调节作用。","authors":"D Anderson, A J Francis","doi":"10.1007/978-1-4615-2984-2_18","DOIUrl":null,"url":null,"abstract":"<p><p>The male and female reproductive systems are targets for the toxicity of a wide range of compounds. There is a paucity of information regarding the modulating effects of antioxidants in such systems. Enzymically generated oxygen radicals have been shown to be toxic and/or mutagenic in a variety of in vitro test systems. It is known that vitamins C and E can modify responses in such systems. Malformations and growth reductions have been observed in whole rat embryo cultures in this laboratory after treatment with the oxygen radical generating system of xanthine/xanthine oxidase. Groups of 9.5-day-old rat embryos were treated with this system with or without vitamin C or E. Vitamin C at the doses given totally abolished neural suture defects while vitamin E only partially did so. Vitamins C and E administered alone had no effect on the embryos. Germ cell detachment has been shown to occur in mixed cultures of Sertoli and germ cells in response to some known in vivo testicular toxins. Such cultures were also treated with the oxygen radical generating system of xanthine/xanthine oxidase. There was an increase in germ cell detachment with this treatment which was reduced by vitamin C but not by vitamin E at the doses administered. These findings would suggest that vitamin supplementation could protect somatic cells of reproductive systems against toxins that act through oxygen radical mechanisms.</p>","PeriodicalId":8697,"journal":{"name":"Basic life sciences","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"1993-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/978-1-4615-2984-2_18","citationCount":"11","resultStr":"{\"title\":\"The modulating effects of antioxidants in rat embryos and Sertoli cells in culture.\",\"authors\":\"D Anderson, A J Francis\",\"doi\":\"10.1007/978-1-4615-2984-2_18\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>The male and female reproductive systems are targets for the toxicity of a wide range of compounds. There is a paucity of information regarding the modulating effects of antioxidants in such systems. Enzymically generated oxygen radicals have been shown to be toxic and/or mutagenic in a variety of in vitro test systems. It is known that vitamins C and E can modify responses in such systems. Malformations and growth reductions have been observed in whole rat embryo cultures in this laboratory after treatment with the oxygen radical generating system of xanthine/xanthine oxidase. Groups of 9.5-day-old rat embryos were treated with this system with or without vitamin C or E. Vitamin C at the doses given totally abolished neural suture defects while vitamin E only partially did so. Vitamins C and E administered alone had no effect on the embryos. Germ cell detachment has been shown to occur in mixed cultures of Sertoli and germ cells in response to some known in vivo testicular toxins. Such cultures were also treated with the oxygen radical generating system of xanthine/xanthine oxidase. There was an increase in germ cell detachment with this treatment which was reduced by vitamin C but not by vitamin E at the doses administered. These findings would suggest that vitamin supplementation could protect somatic cells of reproductive systems against toxins that act through oxygen radical mechanisms.</p>\",\"PeriodicalId\":8697,\"journal\":{\"name\":\"Basic life sciences\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":0.0000,\"publicationDate\":\"1993-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1007/978-1-4615-2984-2_18\",\"citationCount\":\"11\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Basic life sciences\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1007/978-1-4615-2984-2_18\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Basic life sciences","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1007/978-1-4615-2984-2_18","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
The modulating effects of antioxidants in rat embryos and Sertoli cells in culture.
The male and female reproductive systems are targets for the toxicity of a wide range of compounds. There is a paucity of information regarding the modulating effects of antioxidants in such systems. Enzymically generated oxygen radicals have been shown to be toxic and/or mutagenic in a variety of in vitro test systems. It is known that vitamins C and E can modify responses in such systems. Malformations and growth reductions have been observed in whole rat embryo cultures in this laboratory after treatment with the oxygen radical generating system of xanthine/xanthine oxidase. Groups of 9.5-day-old rat embryos were treated with this system with or without vitamin C or E. Vitamin C at the doses given totally abolished neural suture defects while vitamin E only partially did so. Vitamins C and E administered alone had no effect on the embryos. Germ cell detachment has been shown to occur in mixed cultures of Sertoli and germ cells in response to some known in vivo testicular toxins. Such cultures were also treated with the oxygen radical generating system of xanthine/xanthine oxidase. There was an increase in germ cell detachment with this treatment which was reduced by vitamin C but not by vitamin E at the doses administered. These findings would suggest that vitamin supplementation could protect somatic cells of reproductive systems against toxins that act through oxygen radical mechanisms.