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Thiols, thiol depletion, and thermosensitivity.

J B Mitchell, A Russo

    Radiation Research
    |September 1, 1983
    PubMed
    Summary

    Elevated temperatures increase cellular glutathione (GSH), a key antioxidant. Depleting GSH sensitizes cells to heat, while its presence aids thermal tolerance, influencing heat shock protein production.

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    Area of Science:

    • Cellular Biology
    • Biochemistry
    • Oxidative Stress

    Background:

    • Hyperthermia's effects on cells involve complex mechanisms.
    • Cellular redox state, particularly glutathione (GSH), is crucial for cellular responses.
    • GSH is vital for maintaining redox balance and detoxifying harmful peroxides.

    Purpose of the Study:

    • To investigate the role of cellular oxidative-reductive state, specifically glutathione (GSH), in hyperthermia-induced sensitization and tolerance.
    • To understand how altering GSH concentrations affects cellular response to heat stress.

    Main Methods:

    • Measuring cellular GSH concentrations under various heat stress conditions (continuous 42.5°C, acute 43°C or 45.5°C).
    • Altering GSH levels using diethylmaleate (DEM) and buthionine sulfoximine (BSO) to induce depletion.
    • Administering ethanol to study its effect on GSH and thermal tolerance.
    • Investigating the impact of exogenous thiols (cysteine, N-acetylcysteine) on heat response.
    • Assessing heat shock protein (HSP) synthesis in relation to GSH levels and thermotolerance.

    Main Results:

    • Elevated temperatures (42.5°C, 43°C, 45.5°C) rapidly increased cellular GSH to 120-200% of control values.
    • The severity of heat exposure correlated with the speed of maximal GSH attainment.
    • Ethanol and heat increased intracellular GSH, inducing thermal tolerance.
    • GSH depletion via DEM or BSO resulted in thermal sensitization.
    • Once thermotolerance was established, GSH depletion had minimal impact.
    • Buthionine sulfoximine treatment reduced HSP synthesis and thermotolerance.
    • Exogenous cysteine enhanced oxygen consumption and caused thermosensitization, unlike N-acetylcysteine.

    Conclusions:

    • Cellular glutathione (GSH) plays a significant role in both hyperthermia-induced sensitization and tolerance.
    • GSH levels increase in response to heat stress, contributing to cellular protection.
    • Modulating GSH concentrations offers a potential strategy for influencing cellular responses to thermal stress.
    • Exogenous thiols may induce cell damage via peroxide mechanisms, with GSH involved in initial thermotolerance induction.

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