S-allylcysteine attenuates oxidative stress in endothelial cells

Authors
Citation
N. Ide et Bhs. Lau, S-allylcysteine attenuates oxidative stress in endothelial cells, DRUG DEV IN, 25(5), 1999, pp. 619-624
Citations number
28
Categorie Soggetti
Pharmacology & Toxicology
Journal title
DRUG DEVELOPMENT AND INDUSTRIAL PHARMACY
ISSN journal
03639045 → ACNP
Volume
25
Issue
5
Year of publication
1999
Pages
619 - 624
Database
ISI
SICI code
0363-9045(1999)25:5<619:SAOSIE>2.0.ZU;2-6
Abstract
Oxidation of low-density lipoprotein (LDL) has been recognized as playing a n important role in the initiation and progression cf atherosclerosis. We r ecently reported that S-allylcysteine (SAC), one of the major compounds in the aged garlic extract (AGE), inhibited LDL oxidation and minimized oxidiz ed LDL-induced cell injury. In this study, the antioxidant effects of SAC w ere further determined using several in vitro assay systems. Pulmonary arte ry 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 2 4 hr. Lactate dehydrogenase (LDH) release, as an index of membrane injury, and intracellular glutathione (GSH) levels were determined. Oxidized LDL ca used an increase of LDH release and depletion of GSH. Pretreatment with SAC prevented these changes. Peroxides were measured directly in 24-well plate s using a fluorometric assay. SAC dose-dependently inhibited oxidized LDL-i nduced release of peroxides in PAEC. in a cell-free system, SAC was shown t o scavenge hydrogen peroxide. Our data demonstrate that SAC can protect end othelial cells from oxidized LDL-induced injury by removing peroxides and p reventing the intracellular GSH depletion and suggest that this compound ma y be useful for the prevention of atherosclerosis.