{"title":"胆汁酸对苋菜胆汁排泄及肝脏线粒体呼吸的影响。","authors":"Z Gregus, F Varga, E Fischer","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>The effects of lithocholic acid (LCA), chenodeoxycholic acid (CDCA), deoxycholic acid (DOCA), cholic acid (CA) and dehydrocholic acid (DHCA) on the biliary excretion of amaranth (AM) in rats and on the respiration of isolated liver mitochondria were investigated. Bile acids diminished the biliary excretion of AM, and in vitro they enhanced the state 4 mitochondrial respiration and inhibited DNP- and ADP-stimulated oxygen consumption. The ID50 values (mumol/kg i.v.) and I50 concentrations (X 10(-5) M) of the bile acids for inhibiting AM excretion and ADP-stimulated mitochondrial respiration, respectively, were as follows: for LCA 16 and 3.3, for CDCA 160 and 24, for DOCA 230 and 31, for CA 680 and 105, and for DHCA 700 and 260. LCA, CDCA and DOCA inhibited the biliary excretion of AM uncompetitively. It is concluded that the toxic effect of LCA, CDCA and DOCA on mitochondria might play a role in their inhibitory action on the biliary transport of AM.</p>","PeriodicalId":7049,"journal":{"name":"Acta physiologica Academiae Scientiarum Hungaricae","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"1982-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Effect of bile acids on the biliary excretion of amaranth and the respiration of liver mitochondria.\",\"authors\":\"Z Gregus, F Varga, E Fischer\",\"doi\":\"\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>The effects of lithocholic acid (LCA), chenodeoxycholic acid (CDCA), deoxycholic acid (DOCA), cholic acid (CA) and dehydrocholic acid (DHCA) on the biliary excretion of amaranth (AM) in rats and on the respiration of isolated liver mitochondria were investigated. Bile acids diminished the biliary excretion of AM, and in vitro they enhanced the state 4 mitochondrial respiration and inhibited DNP- and ADP-stimulated oxygen consumption. The ID50 values (mumol/kg i.v.) and I50 concentrations (X 10(-5) M) of the bile acids for inhibiting AM excretion and ADP-stimulated mitochondrial respiration, respectively, were as follows: for LCA 16 and 3.3, for CDCA 160 and 24, for DOCA 230 and 31, for CA 680 and 105, and for DHCA 700 and 260. LCA, CDCA and DOCA inhibited the biliary excretion of AM uncompetitively. It is concluded that the toxic effect of LCA, CDCA and DOCA on mitochondria might play a role in their inhibitory action on the biliary transport of AM.</p>\",\"PeriodicalId\":7049,\"journal\":{\"name\":\"Acta physiologica Academiae Scientiarum Hungaricae\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":0.0000,\"publicationDate\":\"1982-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Acta physiologica Academiae Scientiarum Hungaricae\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Acta physiologica Academiae Scientiarum Hungaricae","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Effect of bile acids on the biliary excretion of amaranth and the respiration of liver mitochondria.
The effects of lithocholic acid (LCA), chenodeoxycholic acid (CDCA), deoxycholic acid (DOCA), cholic acid (CA) and dehydrocholic acid (DHCA) on the biliary excretion of amaranth (AM) in rats and on the respiration of isolated liver mitochondria were investigated. Bile acids diminished the biliary excretion of AM, and in vitro they enhanced the state 4 mitochondrial respiration and inhibited DNP- and ADP-stimulated oxygen consumption. The ID50 values (mumol/kg i.v.) and I50 concentrations (X 10(-5) M) of the bile acids for inhibiting AM excretion and ADP-stimulated mitochondrial respiration, respectively, were as follows: for LCA 16 and 3.3, for CDCA 160 and 24, for DOCA 230 and 31, for CA 680 and 105, and for DHCA 700 and 260. LCA, CDCA and DOCA inhibited the biliary excretion of AM uncompetitively. It is concluded that the toxic effect of LCA, CDCA and DOCA on mitochondria might play a role in their inhibitory action on the biliary transport of AM.