s-allylcysteine and Ischemic-Attack--Transient

The efficacy of S-allylcysteine (SAC) as a free radical scavenger was studied using rat brain ischemia models. In a middle cerebral artery occlusion model, preischemic administration of SAC had the following effects: it improved motor performance and memory impairment and reduced water content and the infarct size. In a transient global ischemia model, the time course of free radical (alkoxyl radical) formation as studied by electron paramagnetic resonance (EPR) spectroscopy and alpha-phenyl-N-tert-butylnitrone (PBN) was biphasic; the first peak occurred at 5 min and the second at 20 min after reperfusion. Although SAC did not attenuate the first peak, it did affect the second peak, which is related to lipid peroxidation. The lipid peroxidation as estimated by thiobarbituric acid reactive substances (TBARS) increased significantly at 20 min after reperfusion. SAC decreased TBARS to the levels found without ischemia. These results suggest that SAC could have beneficial effects in brain ischemia and that the major protective mechanism may be the inhibition of free radical-mediated lipid peroxidation.

Topics: Animals; Antioxidants; Cysteine; Disease Models, Animal; Dose-Response Relationship, Drug; Electron Spin Resonance Spectroscopy; Free Radicals; Ischemic Attack, Transient; Lipid Peroxidation; Male; Memory Disorders; Neurons; Rats; Rats, Sprague-Dawley; Reperfusion Injury; Thiobarbituric Acid Reactive Substances; Time Factors; Water

Effects of an aged garlic extract and its thioallyl components on rat brain ischemia were examined using a middle cerebral artery occlusion model and a transient global ischemia model. In focal ischemia, an aged garlic extract, S-allyl cysteine (SAC), Allyl sulfide (AS) or Allyl disulfide (ADS) was administered 30 min prior to ischemic insult. Three days after ischemic insult, water contents of both ischemic and contralateral hemispheres were measured to assess the degree of ischemic damage. The water content of the ischemic control (no drug treatment) group was 81.50 +/- 0.07% (mean +/- SEM). It was significantly reduced with the administration of 300 mg/kg of SAC; the water content was 80.66 +/- 0.11% (P < 0.001). The histological observation using 2,3,5-triphenyltetrazolium chloride staining demonstrated that the administration of SAC reduced infarct volume. Neither AS nor ADS was effective. In global ischemia, the production of reactive oxygen species (ROS) was measured ex vivo using a spin-trapping agent, alpha-phenyl-N-tert-butylnitrone, and electron paramagnetic resonance spectroscopy. The production of ROS had two peaks; first at 5 min and second at 20 min after reperfusion. Both SAC and 7-nitro indazole, a nitric oxide synthase inhibitor, did not attenuate the amount of ROS produced at the first peak, but did the amount of the second peak. A possible involvement of peroxinitrite, which may be formed from superoxide and nitric oxide and is known to be highly toxic in ischemia/reperfusion injury of the brain, was suggested.

Topics: Allyl Compounds; Animals; Antioxidants; Body Water; Brain; Brain Diseases; Cysteine; Electron Spin Resonance Spectroscopy; Free Radicals; Garlic; Ischemic Attack, Transient; Male; Plants, Medicinal; Rats; Rats, Sprague-Dawley; Sulfides; Time Factors