s-allylcysteine and Myocardial-Ischemia

To investigate the effect of S-allyl-L-cysteine (SAC) on isolated rat heart subject to ischemia/reperfusion(I/R) injury and the mechanisms.. The isolated perfused rat hearts on a Langendorff apparatus were subjected to global ischemia for 30 min and followed by 120 min of reperfusion. Hemodynamic index, the production of formazan and the level of lactate dehydrogenase (LDH) in the coronary effluent were determined. Superoxide dismutase (SOD) and reactive oxygen species (ROS) in myocardial homogenates were measured.. Compared with I/R group, the hemodynamics were greatly improved, the production of formazan was increased, and LDH level in effluent was reduced in SAC group. SAC improved the SOD activity and significantly decreased the level of ROS. In addition, threonine (Thr) attenuated the protective effect of SAC significantly.. SAC has protective effect against myocardial ischemia/reperfusion injury on rats. The possible mechanism is that SAC be transported into the cell through alanine-serine-cysteine-transporter 1 (ASCT-1) improves SOD activity and reduces the level of ROS.

Topics: Animals; Cysteine; In Vitro Techniques; Male; Myocardial Ischemia; Myocardial Reperfusion Injury; Protective Agents; Rats; Rats, Sprague-Dawley; Reactive Oxygen Species; Superoxide Dismutase

The current study was designed to evaluate the pharmacologic effects of three novel cysteine-containing compounds: S-propyl-l-cysteine (SPC), S-allyl-l-cysteine (SAC), and S-propargyl-l-cysteine (SPRC) on H(2)S production and antioxidant defenses in an acute myocardial infarction (MI) rat model. The enzymatic activities of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx), as well as glutathione redox status and malonaldehyde (MDA) content, also were determined. All three compounds were found to preserve SOD and GPx activities and also tissue GSH levels while reducing the formation of the lipid peroxidation product MDA in ventricular tissues. With immunfluorescence assays, we observed the expression of CSE and Mn-SOD. The morphologic changes of the cardiac cells are seen with both light and electron microscopy. The corresponding pathologic alterations were characterized mainly as loss of adherence between cardiac myocytes and swollen or ruptured mitochondria at the ultrastructural level. Propargylglycine, a selective inhibitor of CSE, abolished the protective effects of each compound used in the current model. Our study provides novel evidence that SPC, SAC, and SPRC have cardioprotective effects in MI by reducing the deleterious effects of oxidative stress by modulating the endogenous levels of H(2)S and preserving the activities of antioxidant defensive enzymes like SOD.

Topics: Air Pollutants; Animals; Antioxidants; Cardiotonic Agents; Catalase; Cysteine; Glutathione Peroxidase; Humans; Hydrogen Sulfide; Lipid Peroxidation; Male; Malondialdehyde; Myocardial Ischemia; Myocardium; Oxidation-Reduction; Oxidative Stress; Rats; Rats, Sprague-Dawley; RNA, Messenger; Superoxide Dismutase