To investigate the effects of angiotensin-converting enzyme (ACE) inhibitors on the cellular function and structure in a variety of organs during the aging process, one hundred CF1 mice were divided into four groups of 25 animals each. Groups A, B, and C received enalapril in drinking water from weaning until the age of 24 mo. Doses administered were (in mg/l): group A, 20; group B, 10; group C, 5. Group D is the control. Animals were killed, and morphometric studies were performed in heart, kidney, liver, and spleen. As a result, there was a decrease of renal and myocardial sclerosis and an increase in the number of mitochondria in heart and liver cells, which is associated with a significant increase in survival of animals receiving ACE inhibitors. These findings lead us to think that natural aging mechanisms have been altered in those animals.

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We have characterized the effect of angiotensin converting enzyme (ACE) inhibitors on the activity of CuZn-snperoxide dismntase (CuZn-SOD), Mn-snperoxide dismutase (Mn-SOD), catalase, and selenium-dependent glutathione peroxidase (Se-GPx). CF1 mice (4-month-old females) were administered water containing enalapril (20 rag/l) or captopril (50 rag/I), during 4 to 11 weeks. After 11 weeks, enalapril treatment caused an increase in the activity of CuZn-SOD, Mn-SOD and Se-GPx, from 19 -+ 4 to 46 +-7, 2.1 -+ 0.2 to 3.8 --0.2 units/mg protein and 27--3 to 54--3 milliunits/mg protein, respectively. After 11 weeks, captopril treatment increased the activities (P < 0.05) of CuZn-SOD, MnSOD and Se-GPx to 35 -+ 4, 2.9 --0.2 nnitslmg protein, and 38 + 2 millianits/mg protein, respectively. Catalase activity was not affected by the treatments. These results suggest that ACE inhibitors may protect cell components from oxidative damage by increasing the enzymatic antioxidant defenses.