Key result
Alacepril inhibited 50% of oxygen radical production by murine lung alveolar macrophages at ~0.3 mM, whereas lisinopril required a higher concentration (1-5 mM) to achieve the same effect.
Why the study?
Do ACE inhibitors (alacepril and lisinopril) reduce oxygen radical production in murine lung alveolar macrophages?
Do ACE inhibitors (alacepril and lisinopril) reduce oxygen radical production in murine lung alveolar macrophages?
Absolute Event Rate: 50% vs 50%
An ACE inhibitor with an SH-group (alacepril) is a more potent antioxidant in murine lung macrophages than one without (lisinopril), suggesting potential benefits for reducing oxidant stress.
Alacepril's greater potency versus lisinopril in murine macrophages is hypothesis-generating; leaves open clinical relevance for human oxidant stress.
We examined the effect of angiotensin-converting enzyme (ACE) inhibitors on oxygen radical production before and generation after phorbol-myristate acetate (PMA) stimulation of lung alveolar macrophages. Lung free cells, predominantly pulmonary alveolar macrophages, were obtained from Fischer 344 rats and guinea pigs using bronchoalveolar lavage. The oxygen radicals produced by pulmonary alveolar macrophages with or without stimulation of PMA were measured by lucigenin-dependent chemiluminescence method using a photon counter, Lumat 9501 (Berthold, Germany). Alacepril, an ACE inhibitor with SH-group, inhibited the oxygen radical production and generation by lung alveolar macrophages harvested from both rats and guinea pigs in a dose-dependent fashion. Approximately 0.3 mM of alacepril inhibited 50% of oxygen radical production of lung alveolar macrophages in both rats and guinea pigs, whereas a higher concentration (1-5 mM) of lisinopril, an ACE inhibitor without SH-group, was necessary to inhibit 50% of oxygen radical production of lung alveolar macrophages in the animals. These results suggest that an ACE inhibitor with SH-group acts as an antioxidant in murine lungs and the treatment with the ACE inhibitor may reduce oxidant stress in hypertensive patients with asthma.
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Suzuki et al. (1999) studied this question. Alacepril vs. Lisinopril (1-5 mM) was evaluated on Inhibition of oxygen radical production. Alacepril inhibited 50% of oxygen radical production by murine lung alveolar macrophages at ~0.3 mM, whereas lisinopril required a higher concentration (1-5 mM) to achieve the same effect.
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