{"title":"N-acetylcysteine stimulates hepatic glycogen deposition in the rat.","authors":"A M Itinose, M L Doi-Sakuno, A Bracht","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>The action of N-acetylcysteine on hepatic glycogen deposition was investigated. Emphasis was also given to the protective action of this compound against hepatic glycogen depletion by paracetamol. Rats fasted for 24 hours were injected intraperitoneally with (1) vehicle, (2) paracetamol (500 mg/kg), (3) N-acetylcysteine (1200 mg/kg) and (4) paracetamol plus N-acetylcysteine. The rats were refed immediately after the drug injections. Paracetamol inhibited glycogen deposition in the 12 hours following injection. The plasma levels of paracetamol were in the range that inhibits energy metabolism in isolated mitochondria and in the isolated perfused liver. N-Acetylcysteine increased the rate of glycogen deposition either in the presence or in the absence of paracetamol. The latter effect may be responsible, partly at least, for the protective action of N-acetylcysteine against glycogen depletion caused by toxic doses of paracetamol.</p>","PeriodicalId":21140,"journal":{"name":"Research communications in chemical pathology and pharmacology","volume":"83 1","pages":"87-92"},"PeriodicalIF":0.0000,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Research communications in chemical pathology and pharmacology","FirstCategoryId":"1085","ListUrlMain":"","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
The action of N-acetylcysteine on hepatic glycogen deposition was investigated. Emphasis was also given to the protective action of this compound against hepatic glycogen depletion by paracetamol. Rats fasted for 24 hours were injected intraperitoneally with (1) vehicle, (2) paracetamol (500 mg/kg), (3) N-acetylcysteine (1200 mg/kg) and (4) paracetamol plus N-acetylcysteine. The rats were refed immediately after the drug injections. Paracetamol inhibited glycogen deposition in the 12 hours following injection. The plasma levels of paracetamol were in the range that inhibits energy metabolism in isolated mitochondria and in the isolated perfused liver. N-Acetylcysteine increased the rate of glycogen deposition either in the presence or in the absence of paracetamol. The latter effect may be responsible, partly at least, for the protective action of N-acetylcysteine against glycogen depletion caused by toxic doses of paracetamol.