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Captopril and enalaprilat decrease antioxidant defences in human endothelial cells and are unable to protect against apoptosis
Author(s) -
Mailloux Agnès,
Deslandes Benjamin,
Vaubourdolle Michel,
Baudin Bruno
Publication year - 2003
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1016/s1065-6995(03)00162-8
Subject(s) - enalaprilat , captopril , pharmacology , glutathione peroxidase , endothelial dysfunction , superoxide dismutase , malondialdehyde , oxidative stress , chemistry , apoptosis , ace inhibitor , angiotensin converting enzyme , endocrinology , biology , biochemistry , blood pressure
Angiotensin‐converting enzyme (ACE) inhibitors were shown to improve endothelial dysfunction in various human diseases and some of these inhibitors have been proposed as enhancers of antioxidant defences. We measured glutathione peroxidase (GPX), superoxide dismutase (SOD) and malondialdehyde (MDA) in human endothelial cells treated with captopril or enalaprilat, two ACE inhibitors, and we showed that both inhibitors decreased GPX and SOD activities but not MDA, the end‐product of lipoperoxidation. Captopril and enalaprilat were also unable to protect against etoposide‐induced apoptosis in endothelial cells, indicating that they cannot be considered as protective drugs for the endothelium, in particular in clinical situations involving oxidative stress or apoptosis. Moreover, when used at high concentration captopril, but not enalaprilat, was toxic for endothelial cells with both necrotic and apoptotic effects.