Mercuric chloride-induced reactive oxygen species and its effect on antioxidant enzymes in different regions of rat brain

被引:70
作者
Hussain, S
Rodgers, DA
Duhart, HM
Ali, SF
机构
[1] FLORIDA A&M UNIV, COLL PHARM & PHARMACEUT SCI, TALLAHASSEE, FL 32307 USA
[2] UNIV ARKANSAS MED SCI HOSP, DEPT BIOCHEM & MOL BIOL, LITTLE ROCK, AR 72205 USA
[3] UNIV ARKANSAS MED SCI HOSP, DEPT NEUROL, LITTLE ROCK, AR 72205 USA
关键词
mercury; oxidative stress; reactive oxygen species; antioxidant enzymes; superoxide dismutase; glutathione peroxidase;
D O I
10.1080/03601239709373094
中图分类号
X [环境科学、安全科学];
学科分类号
08 ; 0830 ;
摘要
The present study was undertaken to determine if in vitro exposure to mercuric chloride produces reactive oxygen species (ROS) in the synaptosomes prepared from various regions of rat brain. The effects of in vivo exposure to mercury on antioxidant enzymes such as superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities in different regions of rat brain were also investigated. Adult male Sprague-Dawley (CD) rats were dosed with 0, 1, 2.0 or 4.0 mg HgCl2/kg body weight, for 7 days. One week after the last dose, animals were sacrificed by decapitation, their brains were removed and dissected and frozen in dry ice prior to measuring the activities of these enzymes. The results demonstrated that in vitro exposure to mercury produced a concentration-dependent increase of ROS in different regions of the rat brain. In vivo exposure to mercury produced a significant decrease of total SOD, Cu,Zn-SOD and Mn-SOD activities in the cerebellum of rats treated with different doses of mercury. SOD activity did not vary significantly in cerebral cortex and brain stem. GPx activity declined in a dose-dependent manner in the cerebellum with a significant reduction in animals receiving the 4 mg HgCl2/kg body weight. The activity of GPx increased in the brain stem while unchanged in the cerebral cortex. The results demonstrate that inorganic mercury decreased SOD activity significantly in the cerebellum while GPx activity was affected in both cerebellum and brain stem. Therefore, it can be concluded that oxidative stress may contribute to the development of neurodegenerative disorders caused by mercury intoxication.
引用
收藏
页码:395 / 409
页数:15
相关论文
共 30 条
[1]  
ALI SF, 1992, NEUROTOXICOLOGY, V13, P637
[2]   METHYLMERCURY POISONING IN IRAQ - INTERUNIVERSITY REPORT [J].
BAKIR, F ;
DAMLUJI, SF ;
AMINZAKI, L ;
MURTADHA, M ;
KHALIDI, A ;
ALRAWI, NY ;
TIKRITI, S ;
DHAHIR, HI ;
CLARKSON, TW ;
SMITH, JC ;
DOHERTY, RA .
SCIENCE, 1973, 181 (4096) :230-241
[3]  
CHUNG AS, 1982, BIOCHEM PHARMACOL, V31, P3093
[4]  
Cotman CW, 1989, BASIC NEUROCHEMISTRY, P382
[5]  
FLOHE L, 1984, METHOD ENZYMOL, V105, P114
[6]   SUPEROXIDE RADICAL - AN ENDOGENOUS TOXICANT [J].
FRIDOVICH, I .
ANNUAL REVIEW OF PHARMACOLOGY AND TOXICOLOGY, 1983, 23 :239-257
[7]  
Ganther H E, 1980, Ann N Y Acad Sci, V355, P212
[9]   MERCURIC-CHLORIDE EFFECTS ON RAT RENAL REDOX ENZYMES ACTIVITIES - SOD PROTECTION [J].
GIRARDI, G ;
ELIAS, MM .
FREE RADICAL BIOLOGY AND MEDICINE, 1995, 18 (01) :61-66
[10]  
Goyer R.A., 1991, CASARETT DOULLS TOXI, P629