These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


PUBMED FOR HANDHELDS

Search MEDLINE/PubMed


  • Title: Sequential changes in hepatic and renal glutathione and development of renal karyomegaly in 1-cyano-3,4-epithiobutane toxicity in rats.
    Author: VanSteenhouse JL, Fettman MJ, Gould DH.
    Journal: Food Chem Toxicol; 1989 Nov; 27(11):731-9. PubMed ID: 2613119.
    Abstract:
    The effect of 1-cyano-3,4-epithiobutane (CEB) on glutathione (GSH) metabolism was investigated in rat liver, kidney and pancreas. Male Fischer 344 rats were gavaged with a single dose (125 mg/kg body weight or 50 mg/kg body weight) of CEB. Tissue samples were taken for histological examination, determination of GSH and oxidized glutathione (GSSG) concentrations and gamma-glutamyl transpeptidase (GGT) and glutathione S-transferase (GST) activities. Urine samples were analysed for non-protein thiol (NP-RSH) content. The high dose of CEB induced hepatic GSH depletion followed by increased GSH. The low dose of CEB induced elevated hepatic GSH by 12 hr without depletion. Renal GSH was increased with both doses without an observed depletion phase. Renal tubule epithelial cell death was observed only with the high dose of CEB, but both doses caused renal proximal tubule karyomegaly. Pancreatic GSH content was unaffected. No alterations of GSSG were observed. GST activity was unaffected in any tissue. Renal GGT activity was decreased at 12 hr with both doses and at 24 and 48 hr with the high dose. Urinary NP-RSH excretion was increased with both doses. Depletion of hepatic GSH concurrent with increased urinary NP-RSH excretion suggests that conjugation with GSH is a significant pathway in CEB metabolism.
    [Abstract] [Full Text] [Related] [New Search]