The Scavenging of Oxygen Free Radicals by Angiotensin Converting Enzyme Inhibitors: The Importance of the Sulfhydryl Group in the Chemical Structure of the Compounds

Mira, M. L.; Silva, M. M.; Manso, C

doi:10.1111/j.1749-6632.1994.tb36771.x

Cited by 15 publications

(8 citation statements)

References 2 publications

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“…23 NAL is also able, both in vitro 24 and in vivo, 25 the same range as the one obtained by others (290 ) in a cell-free system using CL assays. 29 By contrast, to decrease the elastase levels in bronchial secretions. This property is of particular interest in patients with IC 50 values reported in the literature for ACC using CL produced by Formyl-Methionyl-Leucyl-Phenylcystic fibrosis and chronic bronchitis, where protease activity is greater than that of anti-protease.…”

Section: Resultsmentioning

confidence: 92%

Effect of the Mucoactive Drug Nacystelyn on the Respiratory Burst of Human Blood Polymorphonuclear Neutrophils

Nagy

Vanderbist²,

Parij

et al. 1997

Pulmonary Pharmacology & Therapeutics

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Section: Resultsmentioning

confidence: 92%

Effect of the Mucoactive Drug Nacystelyn on the Respiratory Burst of Human Blood Polymorphonuclear Neutrophils

Nagy

Vanderbist²,

Parij

et al. 1997

Pulmonary Pharmacology & Therapeutics

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“…29,42 It is demonstrated that the sulfhydryl compound GSH (glutathione) inhibits adriamycin-induced cardiotoxicity in rat. 43 Although some studies have suggested that the sulfhydryl portion of the ACE inhibitors is required for the optimal free radical scavenging effect, 12,41,42 other studies 10,44,45 have found that ACE inhibitors both with and without the sulfhydryl moiety act as effective free radical scavengers. In the present study captopril contains a sulfhydryl group, whereas enalapril does not; both drugs produced a similar protection against adriamycin-induced cardiac and liver toxicity.…”

Section: Discussionmentioning

confidence: 98%

Potential protective role of angiotensin‐converting enzyme inhibitors captopril and enalapril against adriamycin‐induced acute cardiac and hepatic toxicity in rats

El-Aziz

Othman

Amer

et al. 2001

J of Applied Toxicology

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Captopril and enalapril-angiotensin-converting enzyme (ACE) inhibitors-were evaluated for their antioxidative protective action against adriamycin-induced cardiac and hepatic toxicity. Rats were treated with either captopril (10 mg kg(-1)) or enalapril (2 mg kg(-1)) intragastrically (i.g.) daily for 7 days before single intraperitoneal (i.p.) injection with adriamycin (15 mg kg(-1)). The animals were killed 30 h after adriamycin administration. Adriamycin produced significant elevation in thiobarbituric acid reactive substances (TBARS), which is an indicator of lipid peroxidation, and significantly inhibited the activity of superoxide dismutase (SOD) in heart and liver tissues, with a significant rise in the serum levels of glutamic pyruvic transaminase (GPT), glutamic oxaloacetic transaminase (GOT), creatine kinase isoenzyme (CK-MB) and lactic dehydrogenase (LDH), indicating acute cardiac toxicity. A single injection of adriamycin did not affect the cardiac or hepatic glutathione (GSH) content or cardiac catalase (CAT) activity, but hepatic CAT activity was elevated. Pretreatment with ACE inhibitors significantly reduced the TBARS concentration in both heart and liver and ameliorated the inhibition of cardiac and hepatic SOD activity. In addition, the ACE inhibitors significantly improved the serum levels of GOT, GPT, CK-MB and LDH in adriamycin-treated rats. Thus, these results suggest that captopril and enalapril possess antioxidative potential that may protect the heart against adriamycin-induced acute oxidative toxicity. This protective effect might be mediated, at least in part, by the limitation of culprit free radicals and the amelioration of oxidative stress.

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“…Captopril is the prototype of the sulfhydryl-containing ACE inhibitors; others are fentiapril, pivalopril, zofenopril, and alacepril. In vitro studies suggest that the presence of the sulfhydryl group may confer properties other than ACE inhibition to these drugs, such as free-radical scavenging and effects on prostaglandins 22,23 ; however, the clinical relevance of these effects remains to be demonstrated. Fosinopril is the only FDA-approved ACE inhibitor that contains a phosphinyl group as its reactive moiety.…”

Section: Pharmacologymentioning

confidence: 99%

Angiotensin-Converting Enzyme Inhibitors

1998

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Abstract-ACE inhibitors have achieved widespread usage in the treatment of cardiovascular and renal disease. ACE inhibitors alter the balance between the vasoconstrictive, salt-retentive, and hypertrophic properties of angiotensin II (Ang II) and the vasodilatory and natriuretic properties of bradykinin and alter the metabolism of a number of other vasoactive substances. ACE inhibitors differ in the chemical structure of their active moieties, in potency, in bioavailability, in plasma half-life, in route of elimination, in their distribution and affinity for tissue-bound ACE, and in whether they are administered as prodrugs. Thus, the side effects of ACE inhibitors can be divided into those that are class specific and those that relate to specific agents. ACE inhibitors decrease systemic vascular resistance without increasing heart rate and promote natriuresis. They have proved effective in the treatment of hypertension, they decrease mortality in congestive heart failure and left ventricular dysfunction after myocardial infarction, and they delay the progression of diabetic nephropathy. Ongoing studies will elucidate the effect of ACE inhibitors on cardiovascular mortality in essential hypertension, the role of ACE inhibitors in patients without ventricular dysfunction after myocardial infarction, and the role of ACE inhibitors compared with newly available angiotensin AT 1 receptor antagonists. MechanismACE, or kininase II, is a bivalent dipeptidyl carboxyl metallopeptidase present as a membrane-bound form in endothelial cells, in epithelial or neuroepithelial cells, and in the brain and as a soluble form in blood and numerous body fluids. 1 ACE, or kininase II, cleaves the C-terminal dipeptide from Ang I and bradykinin and a number of other small peptides that lack a penultimate proline residue. Thus, ACE is strategically poised to regulate the balance between the RAS and the kallikrein-kinin system.The RAS plays a pivotal role in blood pressure regulation (Fig 1). Reduced sodium delivery at the macula densa, decreased renal perfusion pressure, and sympathetic activation all stimulate secretion of renin by the juxtaglomerular cell, the classic source of renin in the circulating RAS.

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The Scavenging of Oxygen Free Radicals by Angiotensin Converting Enzyme Inhibitors: The Importance of the Sulfhydryl Group in the Chemical Structure of the Compounds

Cited by 15 publications

References 2 publications

Effect of the Mucoactive Drug Nacystelyn on the Respiratory Burst of Human Blood Polymorphonuclear Neutrophils

Effect of the Mucoactive Drug Nacystelyn on the Respiratory Burst of Human Blood Polymorphonuclear Neutrophils

Potential protective role of angiotensin‐converting enzyme inhibitors captopril and enalapril against adriamycin‐induced acute cardiac and hepatic toxicity in rats

Angiotensin-Converting Enzyme Inhibitors

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