Abstract
Exogenous GSH provided rat alveolar type II cells with significant protection against injury induced by paraquat. This protection was also observed in cells treated with acivicin to inhibit GSH degradation and buthionine sulfoximine to inhibit GSH synthesis. Exogenous GSH was transported into cells by a Na+-dependent system. Addition of inhibitors of this transport system, gamma-glutamyl-glutamate and probenecid, prevented the protection against injury afforded by GSH. Thus, the results indicate that alveolar type II cells can supplement endogenous synthesis of GSH with uptake of exogenous GSH to protect against paraquat-induced injury.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Biological Transport
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Buthionine Sulfoximine
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Dipeptides / pharmacology
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Glutathione / metabolism
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Glutathione / therapeutic use*
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Isoxazoles / pharmacology
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Kinetics
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Lung Diseases / chemically induced*
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Lung Diseases / metabolism
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Lung Diseases / prevention & control
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Male
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Methionine Sulfoximine / analogs & derivatives
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Methionine Sulfoximine / pharmacology
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Paraquat / toxicity*
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Probenecid / pharmacology
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Pulmonary Alveoli / drug effects
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Pulmonary Alveoli / metabolism*
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Rats
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Rats, Inbred Strains
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Sodium / pharmacology
Substances
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Dipeptides
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Isoxazoles
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gamma-glutamylglutamine
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Methionine Sulfoximine
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Buthionine Sulfoximine
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Sodium
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Glutathione
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acivicin
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Paraquat
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Probenecid