Pub Date : 1989-02-01DOI: 10.2330/joralbiosci1965.31.89
Y Kato, K Nishishita, H Sakai, M Tatsumi, K Yamamoto
The present study was performed to see the structure-activity relationships on the aspirin-induced hypocalcemia. Several kinds of salicylic acid (SA) analogues administered orally with a stomach tube. In general, the drugs were suspended in the 2% CMC solution. At the scheduled times after the treatment, 60 microliters of the blood was collected to determine the level of calcium. Aspirin, sodium salt of o-hydroxybenzoic acid (Na-salicylate), sodium salt of m- and p-hydroxybenzoic acid (HBA), 2,5-dihydroxybenzoic acid (DHBA), PAS sodium dihydrate (PAS-Na), salicylamide (SAM) and 2% CMC control were used. Hypocalcemia was induced by aspirin and Na-salicylate but not by m- and p-HBA-Na. In addition, DHBA and PAS caused hypocalcemia when they were administered intravenously but not orally. These results suggest that the carboxyl group must be adjacent to the hydroxyl group on the benzene ring to induce this type of hypocalcemia and that the SA structure would be able to induce hypocalcemia, even in the presence of the additional third substituent on the same ring. On the comparison between aspirin-DL lysine (water soluble aspirin) and SA-DL lysine, SA-DL lysine, which is not an inhibitor of PG synthetase, was more effective on the hypocalcemic action than ASP-DL lysine. The phenomenon was observed at the stage especially immediately after intravenous injection, when the acetyl group may be more responsible to acetylate the PG synthetase in the aspirin-DL lysine group. The present results seems to be consistent with the previous hypothesis that PGs are not involved in the process of aspirin-induced hypocalcemia in the rat.
{"title":"Hypocalcemic action of the several types of salicylic acid analogues.","authors":"Y Kato, K Nishishita, H Sakai, M Tatsumi, K Yamamoto","doi":"10.2330/joralbiosci1965.31.89","DOIUrl":"https://doi.org/10.2330/joralbiosci1965.31.89","url":null,"abstract":"<p><p>The present study was performed to see the structure-activity relationships on the aspirin-induced hypocalcemia. Several kinds of salicylic acid (SA) analogues administered orally with a stomach tube. In general, the drugs were suspended in the 2% CMC solution. At the scheduled times after the treatment, 60 microliters of the blood was collected to determine the level of calcium. Aspirin, sodium salt of o-hydroxybenzoic acid (Na-salicylate), sodium salt of m- and p-hydroxybenzoic acid (HBA), 2,5-dihydroxybenzoic acid (DHBA), PAS sodium dihydrate (PAS-Na), salicylamide (SAM) and 2% CMC control were used. Hypocalcemia was induced by aspirin and Na-salicylate but not by m- and p-HBA-Na. In addition, DHBA and PAS caused hypocalcemia when they were administered intravenously but not orally. These results suggest that the carboxyl group must be adjacent to the hydroxyl group on the benzene ring to induce this type of hypocalcemia and that the SA structure would be able to induce hypocalcemia, even in the presence of the additional third substituent on the same ring. On the comparison between aspirin-DL lysine (water soluble aspirin) and SA-DL lysine, SA-DL lysine, which is not an inhibitor of PG synthetase, was more effective on the hypocalcemic action than ASP-DL lysine. The phenomenon was observed at the stage especially immediately after intravenous injection, when the acetyl group may be more responsible to acetylate the PG synthetase in the aspirin-DL lysine group. The present results seems to be consistent with the previous hypothesis that PGs are not involved in the process of aspirin-induced hypocalcemia in the rat.</p>","PeriodicalId":21847,"journal":{"name":"Shika Kiso Igakkai zasshi = Japanese journal of oral biology","volume":"31 1","pages":"89-94"},"PeriodicalIF":0.0,"publicationDate":"1989-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2330/joralbiosci1965.31.89","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13664918","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1989-02-01DOI: 10.2330/joralbiosci1965.31.95
M Funakoshi
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.
{"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":"https://doi.org/10.2330/joralbiosci1965.31.95","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":0.0,"publicationDate":"1989-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2330/joralbiosci1965.31.95","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13664919","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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