Abstract
Administration of .gamma.-glutamylcystine or of .gamma.-glutamylcysteine disulfide to mice leads to significantly increased levels of glutathione in the kidney as compared to controls given glutamate plus cysteine (or cystinylbisglycine). Studies with .gamma.-glutamylcystine selectively labeled with 35S in either the internal or external S atom indicate preferential utilization of the .gamma.-glutamylcysteine moiety of this compound for glutathione synthesis. Mice depleted of glutathione by treatment with buthionine sulfoximine do not significantly use the disulfides .gamma.-glutamylcystine or .gamma.-glutamylcysteine disulfide but do use .gamma.-glutamylcysteine for glutathione synthesis. These findings suggest a pathway in which .gamma.-glutamylcystine, formed by transpeptidation between glutathione and cystine, is transported and reduced by transhydrogenation with glutathione to cysteine and .gamma.-glutamylcysteine; the latter is used directly for glutathione synthesis. The findings show transport of .gamma.-glutamyl amino acids, indicate an alternative pathway of glutathione synthesis, and demonstrate a means of increasing kidney glutathione levels.

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