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.

This study was undertaken to evaluate the preventive role of S-allyl cysteine sulphoxide (SACS) in isoproterenol (ISO)-induced cardiotoxicity in male Wistar rats. Myocardial infarction was induced by subcutaneous injection of ISO (150 mg/kg) once a day for 2 days. SACS (40 and 80 mg/kg) was given as pretreatment orally daily for a period of 35 days using an intragastric tube. SACS pretreatment significantly lowered thiobarbituric acid reactive substances (TBARS) and increased the activities of mitochondrial superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx), glutathione S-transferase (GST), and the concentration of reduced glutathione (GSH) in myocardial infarcted rats. SACS pretreatment also increased significantly the levels of mitochondrial phospholipids and decreased the levels of mitochondrial cholesterol, free fatty acids (FFAs), triglycerides (TGs) and calcium, and the activity of xanthine oxidase (XOD) in heart. Further, the activities of isocitrate dehydrogenase (ICDH), succinate dehydrogenase (SDH), alpha-ketoglutarate dehydrogenase (alpha-KGDH), NADH-dehydrogenase, and cytochrome C-oxidase were significantly elevated in the mitochondrial fraction of the heart in the SACS-pretreated ISO-induced rats. Oral administration of SACS for a period of 35 days to the normal control rats did not show any significant effect. Histopathological studies of the myocardial tissue showed a protective role of SACS in the myocardial-infarcted rats. The effect at a dose of SACS 80 mg/kg was more effective than the dose 40 mg/kg. The results of the study conclude that SACS protect the mitochondria of the ISO-induced myocardial-infarcted rats.

The antihyperlipidemic, antilipoperoxidative and antioxidant effects of S-allyl cysteine sulphoxide (SACS) in myocardial infarcted rats were reported previously. The present study was undertaken to evaluate the preventive role of SACS on some biochemical parameters, glycoproteins and hematology in experimentally induced myocardial infarction in rats. Myocardial infarction was induced in rats by subcutaneous injection of isoproterenol (ISO) (150 mg kg(-1)) at an interval of 24 h for 2 days. ISO-treated rats showed a significant increase in the levels of serum iron, uric acid and blood glucose, Na(+) and Ca(2+) in the heart and a significant decrease in the levels of plasma iron binding capacity, serum total protein, albumin/globulin ratio, heart K(+) and heart glycogen. The levels/concentrations of glycoproteins in serum and the heart were increased in myocardial infarcted rats. Myocardial infarcted rats also showed a significant increase in red blood cells, hemoglobin, packed cell volume, white blood cells, neutrophils, platelet count and fibrinogen level and a significant decrease in erythrocyte sedimentation rate, eosinophils, lymphocytes, bleeding, clotting and prothrombin time. Oral pretreatment with SACS (40 and 80 mg kg(-1)) daily for a period of 35 days showed a positive effect on all the biochemical parameters studied in ISO-induced rats. Thus, the study showed the protective effect of SACS on ISO-induced cardiotoxicity in male Wistar rats.

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The cardioprotective property of ellagic acid in rats has been reported previously. The present study reveals the protective role of ellagic acid in biochemical parameters including serum iron, plasma iron binding capacity, uric acid, glycoprotein, and electrolytes along with hematological parameters. Rats were subcutaneously injected with isoproterenol (ISO) (100 mg/kg) for 2 days to induce myocardial infarction. ISO-induced rats showed a significant increase in their levels of serum iron, serum uric acid, and blood glucose, and a significant decrease in their levels of plasma iron binding capacity, serum total protein, albumin/globulin ratio, and heart glycogen, when compared with normal control rats. The altered hematological parameters were also observed in ISO-induced rats when compared with normal control rats. Pretreatment with ellagic acid at doses of 7.5 and 15 mg/kg produced significant beneficial effect by returning all the above-mentioned biochemical and hematological parameters to near normal levels.