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Am J Physiol Regul Integr Comp Physiol 278: R572-R577, 2000;
0363-6119/00 $5.00
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Vol. 278, Issue 3, R572-R577, March 2000

Enalapril and captopril enhance glutathione-dependent antioxidant defenses in mouse tissues

Elena M. V. de Cavanagh1, Felipe Inserra2, León Ferder2, and César G. Fraga1

1 Physical Chemistry-Programa de Radicales Libres, School of Pharmacy and Biochemistry, University of Buenos Aires, 1113 Buenos Aires; and 2 Institute of Cardiovascular Research, 1122 Buenos Aires, Argentina

The effect of enalapril and captopril on total glutathione content (GSSG + GSH) and selenium-dependent glutathione peroxidase (Se-GPx) and glutathione reductase (GSSG-Rd) activities was investigated in mouse tissues. CF-1 mice (4-mo-old females) received water containing enalapril (20 mg/l) or captopril (50 mg/l) for 11 wk. Enalapril increased GSSG + GSH content (P < 0.05) in erythrocytes (147%), brain (112%), and lung (67%), and captopril increased GSSG + GSH content in erythrocytes (190%) and brain (132%). Enalapril enhanced Se-GPx activity in kidney cortex (42%) and kidney medulla (23%) and captopril in kidney cortex (30%). GSSG-Rd activity was enhanced by enalapril in erythrocytes (21%), brain (21%), liver (18%), and kidney cortex (53%) and by captopril in erythrocytes (25%), brain (19%), and liver (34%). In vitro erythrocyte oxidant stress was evaluated by thiobarbituric acid-reactive substances (TBARS) production (control 365 ± 11, enalapril 221 ± 26, captopril 206 ± 17 nmol TBARS · g Hb-1 · h-1; both P < 0.05 vs. control) and phenylhydrazine-induced methemoglobin (MetHb) formation (control 66.5 ± 3.5, enalapril 52.9 ± 0.4, captopril: 56.4 ± 2.9 µmol MetHb/g Hb; both P < 0.05 vs. control). Both angiotensin-converting enzyme inhibitor treatments were associated with increased nitric oxide production, as assessed by plasma NO-3 + NO-2 level determination (control 9.22 ± 0.64, enalapril 13.7 ± 1.9, captopril 17.3 ± 3.0 µmol NO-3 + NO-2/l plasma; both P < 0.05 vs. control). These findings support our previous reports on the enalapril- and captopril-induced enhancement of endogenous antioxidant defenses and include new data on glutathione-dependent defenses, thus furthering current knowledge on the association of ACE inhibition and antioxidants.

oxygen radicals; antioxidants; angiotensin-converting enzyme inhibitors; hypertension; aging


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