Captopril Attenuates Diazinon-Induced Oxidative Stress: A Subchronic Study in Rats (original) (raw)
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Captopril: a free radical scavenger
British Journal of Clinical Pharmacology, 1989
The use of captopril in heart failure and hypertension is becoming increasingly accepted. Captopril has a sulphydryl group in its molecular structure. We wondered if this might confer free radical scavenging activity on the drug and have investigated this in an in vitro system. Results show that captopril is a free radical scavenger and we suggest that this action might be relevant in its use in heart failure and other vascular diseases.
The effect of captopril on inflammation-induced liver injury in male rats
Toxin Reviews, 2018
Activation of macrophages-induced by lipopolysaccharide (LPS) is accompanied by the production of reactive oxygen species and inflammatory cytokines to induce hepatic injury. Renin-angiotensin system may play a role in liver damage. In the current study, the effect of captopril on the injury of inflammation-induced liver was investigated. The rats were divided into (1) Control, (2) LPS, and (3-5) LPS as well as 10, 50, or 100 mg/kg captopril for 2 weeks. Captopril decreased NO metabolites, IL-6, and MDA, while it increased CAT, SOD, and total thiol in the liver. Captopril also attenuated AST, ALT, and ALK-P, whereas it increased albumin and total protein in serum. As an ACE inhibitor, captopril improved liver function and attenuated inflammation and oxidative stress induced by LPS injection.
1991
Captopril, an inhibitor of angiotensin-converting enzyme, has been suggested to have additional cardioprotective action because of its ability to act as an antioxidant. The rates of reaction of captopril with several biologically-relevant reactive oxygen species were determined. Captopril reacts slowly, if at all, with superoxide (rate constant < 108 M -1 s -1) or hydrogen peroxide (rate constant < 1 M-~ s-l). It does not inhibit peroxidation of lipids stimulated by iron ions and ascorbate or by the myoglobin]H202 system. Indeed, mixtures of ferric ion and captopril can stimulate lipid peroxidation. Captopril reacts rapidly with hydroxyl radical (rate constant > 109 M -1 s -1) but might be unlikely to compete with most biological molecules for "OH because of the low concentration of captopril that can be achieved in vivo during therapeutic use. Captopril did not significantly inhibit iron ion-dependent generation of hydroxyl radicals from hydrogen peroxide. By contrast, captopril is a powerful scavenger of hypochlorous acid: it was able to protect %-antiproteinase (%AP) against inactivation by this species and to prevent formation of chloramines from taurine. We suggest that the antioxidant action of captopril in vivo is likely to be limited, and may be restricted to protection against damage by hypochlorous acid derived from the action of neutrophil myeloperoxidase.