Abstract
The free thiol group of captopril is important in the action and metabolism of this drug. It has been postulated that the thiol group may allow captopril to act in a manner similar to glutathione and protect against oxidative injury. This study investigated the ability of captopril, enalaprilat, and N-acetylcysteine to prevent tertbutyl hydroperoxide induced oxidative injury in rat renal homogenates. Lipid peroxidation was significantly increased in homogenates from captopril-treated animals (p < 0.05), and following glutathione depletion this was further enhanced (p < 0.001). Renal glutathione content was significantly reduced by captopril treatment (p < 0.01). These results suggest that captopril does not act as an alternate source of reducing equivalents to glutathione and does not protect against renal oxidative injury in this model.
Published Version
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