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Corticosteroids increase superoxide anion production by rat liver microsomes
The Journal of Clinical Investigation
|October 1, 1975
Summary
Cortisol therapy increases superoxide anion production in rat liver microsomes, potentially contributing to corticosteroid side effects. Superoxide dismutase significantly reduced these free radicals.
Area of Science:
- Biochemistry
- Endocrinology
- Pharmacology
Background:
- Corticosteroids are widely used for their anti-inflammatory and immunosuppressive effects.
- However, prolonged or high-dose use can lead to adverse effects.
- The role of reactive oxygen species, such as superoxide anion, in corticosteroid toxicity is not fully understood.
Purpose of the Study:
- To investigate the effect of cortisol on superoxide anion production in rat liver microsomes.
- To determine the relationship between cortisol dosage and superoxide anion generation.
- To assess the potential involvement of NADPH-cytochrome c reductase in this process.
Main Methods:
- Superoxide anion production was measured in liver microsomes from intact, adrenalectomized, and cortisol-treated adrenalectomized rats.
- NADPH-cytochrome c reductase activity was assessed.
- The effect of superoxide dismutase on superoxide anion levels was evaluated.
Main Results:
- Cortisol administration dose-dependently increased superoxide anion production.
- A similar trend was observed in the activity of NADPH-cytochrome c reductase.
- Superoxide dismutase significantly inhibited the measured superoxide anion production.
Conclusions:
- Cortisol therapy enhances superoxide anion production in rat liver microsomes.
- This increased free radical formation may contribute to the adverse effects of high-dose corticosteroids.
- NADPH-cytochrome c reductase activity is potentially linked to cortisol-induced oxidative stress.
