title: The effects of S-allylmercaptocaptopril, the synthetic product of allicin and captopril, on cardiovascular risk factors associated with the metabolic syndrome.
abstract: Pure allicin, prepared biosynthetically by reacting synthetic alliin with an immobilized alliinase enzyme, is known to possess cardioprotective effects. However, in its pure form, allicin is pharmacologically unstable. S-allylmercaptocaptopril (CPSSA) is a new stable synthetic compound produced by chemical reaction between allicin and the angiotensin converting enzyme inhibitor captopril. Using the fructose-induced metabolic syndrome rat model we studied the effects of short-term treatment with two doses of CPSSA on cardiovascular risk factors associated with the metabolic syndrome, in comparison to the effects of allicin and captopril separately. Allicin (8 mg/(kg day)) significantly reduced insulin, triglycerides, and homocysteine concentrations, and had a slight effect on SBP. Captopril (50mg/(kg day)) only improved blood pressure and homocysteine. Treatment with low dose of CPSSA (5mg/(kg day)) lowered SBP but did not improve any other measured parameter, while treatment with a higher dose (50mg/(kg day)) significantly decreased blood pressure, triglycerides, and homocysteine concentrations. We conclude that the combined molecule CPSSA integrates the anti-hypertensive, lipid-lowering, and homocysteine-reducing effects of both allicin and captopril, making it a potential cardiovascular protective agent.
authors.affiliation: Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel. mor.oron@sheba.health.gov.il
authors.forename: Mor
authors.initials: M
authors.lastname: Oron-Herman
authors.forename: Talma
authors.initials: T
authors.lastname: Rosenthal
authors.forename: David
authors.initials: D
authors.lastname: Mirelman
authors.forename: Talia
authors.initials: T
authors.lastname: Miron
authors.forename: Aharon
authors.initials: A
authors.lastname: Rabinkov
authors.forename: Meir
authors.initials: M
authors.lastname: Wilchek
authors.forename: Ben-Ami
authors.initials: BA
authors.lastname: Sela
mesh_terms: D000818:Animals; D000959:Antihypertensive Agents / Q000737:chemistry / Q000627:therapeutic use*; D001794:Blood Pressure / Q000187:drug effects; D002216:Captopril / Q000737:chemistry / Q000627:therapeutic use*; D003521:Cyclopropanes / Q000138:chemical synthesis / Q000627:therapeutic use*; D004195:Disease Models, Animal; D004220:Disulfides; D006710:Homocysteine / Q000097:blood / Q000187:drug effects; D006973:Hypertension / Q000097:blood / Q000209:etiology / Q000517:prevention & control*; D007004:Hypoglycemic Agents / Q000737:chemistry / Q000627:therapeutic use*; D007328:Insulin / Q000097:blood; D008297:Male; D024821:Metabolic Syndrome / Q000097:blood / Q000150:complications* / Q000188:drug therapy; D051381:Rats; D017207:Rats, Sprague-Dawley; D012307:Risk Factors; D013441:Sulfinic Acids / Q000737:chemistry / Q000627:therapeutic use*; D016896:Treatment Outcome; D014280:Triglycerides / Q000097:blood
chemical_list: D000959:Antihypertensive Agents; D003521:Cyclopropanes; D004220:Disulfides; D007004:Hypoglycemic Agents; D007328:Insulin; D013441:Sulfinic Acids; D014280:Triglycerides; D006710:Homocysteine; C048914:1-formylcyclopropane-2-carboxylic acid; C006452:allicin; D002216:Captopril