Preventive effect of S-allyl cysteine sulfoxide (alliin) on cardiac marker enzymes and lipids in isoproterenol-induced myocardial injury

The present study was designed to evaluate the preventive effect of S-allyl cysteine sulfoxide (SACS) in isoproterenol (ISO)-induced myocardial ischaemia in male Wistar rats. Rats were pretreated with SACS (40 and 80 mg kg ^-1 body-weight) for 5 weeks. After the treatment period, ISO (150 mg kg^-1 body-weight) was administered subcutaneously to rats at intervals of 24 h for 2 days. The activities of creatine kinase, creatine kinase-MB, lactate dehydrogenase, aspartate transaminase and alanine transferase were significantly increased in serum and significantly decreased in the hearts of ISO-treated rats. Pretreatment with SACS decreased the activities of these enzymes significantly in serum and significantly increased the activities in heart in ISO-treated rats. The levels of cholesterol, triglycerides and free fatty acids increased in serum and heart, while the levels of phospholipids increased in serum and decreased in heart in ISO-treated rats. SACS pretreatment showed a significant effect on the lipids studied. The activity of 3-hydroxy 3-methyl glutaryl coenzyme A (HMG CoA) reductase was significantly increased and the activity of lecithin cholesterol acyl transferase (LCAT) was significantly reduced in ISO-induced rats. Oral pretreatment with SACS significantly decreased the activity of HMG CoA reductase and significantly increased the activity of LCAT in ISO-induced rats. The levels of plasma thiobarbituric acid reactive substances and hydroperoxides were increased in ISO-treated rats. Pretreatment with SACS significantly decreased the levels of lipidperoxides in ISO-treated rats. The effect at a dose of 80 mg kg^-1 body-weight was more effective than at a dose of 40 mg kg^-1 body-weight and brought back all the biochemical parameters to near normal levels. Thus our study shows that SACS has a lipid-lowering effect in ISO-induced rats. Our study may have clinical relevance.