S-allylcysteine inhibits free radical production, lipid peroxidation and neuronal damage in rat brain ischemia

被引:102
作者
Numagami, Y [1 ]
Ohnishi, ST [1 ]
机构
[1] Philadelphia Biomed Res Inst, King Of Prussia, PA 19406 USA
关键词
S-allylcysteine; brain ischemia; motor performance; memory impairment; free radicals; lipid peroxidation;
D O I
10.1093/jn/131.3.1100S
中图分类号
R15 [营养卫生、食品卫生]; TS201 [基础科学];
学科分类号
100403 ;
摘要
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.
引用
收藏
页码:1100S / 1105S
页数:6
相关论文
共 48 条
[1]   STRONG ATTENUATION OF ISCHEMIC AND POSTISCHEMIC BRAIN EDEMA IN RATS BY A NOVEL FREE-RADICAL SCAVENGER [J].
ABE, K ;
YUKI, S ;
KOGURE, K .
STROKE, 1988, 19 (04) :480-485
[2]   RETENTION OF A PASSIVE AVOIDANCE RESPONSE AS A FUNCTION OF INTENSITY AND DURATION OF ELECTRIC SHOCK [J].
ADER, R ;
MOLEMAN, P ;
WEIJNEN, JAW .
PSYCHONOMIC SCIENCE, 1972, 26 (03) :125-&
[3]   THE ANTIOXIDANT ACTION OF N-ACETYLCYSTEINE - ITS REACTION WITH HYDROGEN-PEROXIDE, HYDROXYL RADICAL, SUPEROXIDE, AND HYPOCHLOROUS ACID [J].
ARUOMA, OI ;
HALLIWELL, B ;
HOEY, BM ;
BUTLER, J .
FREE RADICAL BIOLOGY AND MEDICINE, 1989, 6 (06) :593-597
[4]  
Aust SD, 1985, CRC HDB METHODS OXYG, P203
[5]   INHIBITION OF LUNG-TISSUE OXIDATION DURING ISCHEMIA-REPERFUSION BY 2-MERCAPTOPROPIONYLGLYCINE [J].
AYENE, IS ;
ALMEHDI, AB ;
FISHER, AB .
ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS, 1993, 303 (02) :307-312
[6]  
BRAUGHLER JM, 1987, J BIOL CHEM, V262, P10438
[7]   PROTECTION AGAINST OXIDATIVE DAMAGE TO CNS BY ALPHA-PHENYL-TERT-BUTYL NITRONE (PBN) AND OTHER SPIN-TRAPPING AGENTS - A NOVEL SERIES OF NONLIPID FREE-RADICAL SCAVENGERS [J].
CARNEY, JM ;
FLOYD, RA .
JOURNAL OF MOLECULAR NEUROSCIENCE, 1991, 3 (01) :47-57
[8]   BRAIN INFARCTION IS NOT REDUCED IN SOD-1 TRANSGENIC MICE AFTER A PERMANENT FOCAL CEREBRAL-ISCHEMIA [J].
CHAN, PH ;
KAMII, H ;
YANG, GY ;
GAFNI, J ;
EPSTEIN, CJ ;
CARLSON, E ;
REOLA, L .
NEUROREPORT, 1993, 5 (03) :293-296
[9]   COLD-INDUCED BRAIN EDEMA AND INFARCTION ARE REDUCED IN TRANSGENIC MICE OVEREXPRESSING CUZN-SUPEROXIDE DISMUTASE [J].
CHAN, PH ;
YANG, GY ;
CHEN, SF ;
CARLSON, E ;
EPSTEIN, CJ .
ANNALS OF NEUROLOGY, 1991, 29 (05) :482-486
[10]   A MODEL OF FOCAL ISCHEMIC STROKE IN THE RAT - REPRODUCIBLE EXTENSIVE CORTICAL INFARCTION [J].
CHEN, ST ;
HSU, CY ;
HOGAN, EL ;
MARICQ, H ;
BALENTINE, JD .
STROKE, 1986, 17 (04) :738-743