{"title":"The effect of phenytoin on the corticoidogenesis in the mitochondria and the endoplasmic reticulum of bovine adrenal cortex.","authors":"M Funakoshi","doi":"10.2330/joralbiosci1965.31.95","DOIUrl":null,"url":null,"abstract":"<p><p>In the mitochondria and endoplasmic reticulum of bovine adrenal cortex, the influence of phenytoin on corticoidogenesis was studied using 0.1 microCi 4-14C-cholesterol, 0.01 microCi 4-14C-17 alpha-hydroxyprogesterone, deoxycorticosterone and NADPH-generating system. The cholesterol side-chain cleaving activity in the mitochondria was facilitated by 0.1 microM phenytoin, but was inhibited by higher concentrations. Steroid 11 beta-hydroxylase activity was inhibited by phenytoin. The steroid 21-hydroxylase activity in the endoplasmic reticulum, on the contrary, was mildly stimulated by 1 and 10 microM phenytoin. Phenytoin formed a modified type I spectrum in the adrenocortical mitochondria-malate complex.</p>","PeriodicalId":21847,"journal":{"name":"Shika Kiso Igakkai zasshi = Japanese journal of oral biology","volume":"31 1","pages":"95-101"},"PeriodicalIF":0.0000,"publicationDate":"1989-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2330/joralbiosci1965.31.95","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Shika Kiso Igakkai zasshi = Japanese journal of oral biology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.2330/joralbiosci1965.31.95","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
In the mitochondria and endoplasmic reticulum of bovine adrenal cortex, the influence of phenytoin on corticoidogenesis was studied using 0.1 microCi 4-14C-cholesterol, 0.01 microCi 4-14C-17 alpha-hydroxyprogesterone, deoxycorticosterone and NADPH-generating system. The cholesterol side-chain cleaving activity in the mitochondria was facilitated by 0.1 microM phenytoin, but was inhibited by higher concentrations. Steroid 11 beta-hydroxylase activity was inhibited by phenytoin. The steroid 21-hydroxylase activity in the endoplasmic reticulum, on the contrary, was mildly stimulated by 1 and 10 microM phenytoin. Phenytoin formed a modified type I spectrum in the adrenocortical mitochondria-malate complex.