S-allylcysteine attenuates oxidative stress in endothelial cells

Oxidation of low-density lipoprotein (LDL) has been recognized as playing an important role in the initiation and progression cf atherosclerosis. We recently reported that S-allylcysteine (SAC), one of the major compounds in the aged garlic extract (AGE), inhibited LDL oxidation and minimized oxidized LDL-induced cell injury. In this study, the antioxidant effects of SAC were further determined using several in vitro assay systems. Pulmonary artery endothelial cells (PAECs) were preincubated with SAC at 37 degrees C and 5% CO2 for 24 hr, washed, and then exposed to 0.1 mg/ml oxidized LDL for 24 hr. Lactate dehydrogenase (LDH) release, as an index of membrane injury, and intracellular glutathione (GSH) levels were determined. Oxidized LDL caused an increase of LDH release and depletion of GSH. Pretreatment with SAC prevented these changes. Peroxides were measured directly in 24-well plates using a fluorometric assay. SAC dose-dependently inhibited oxidized LDL-induced release of peroxides in PAEC. in a cell-free system, SAC was shown to scavenge hydrogen peroxide. Our data demonstrate that SAC can protect endothelial cells from oxidized LDL-induced injury by removing peroxides and preventing the intracellular GSH depletion and suggest that this compound may be useful for the prevention of atherosclerosis.