Efficacy of catalpol as protectant against oxidative stress and mitochondrial dysfunction on rotenone-induced toxicity in mice brain

被引:51
作者
Mao, Yu-Rong
Jiang, Lan
Duan, Yan-Long
An, Li-Jia
Jiang, Bo [1 ]
机构
[1] Dalian Univ Technol, Sch Environm & Biol Sci & Technol, Dalian 116024, Peoples R China
[2] Northeastern Univ, Sch Met & Mat, Shenyang 110004, Peoples R China
关键词
complex I; rotenone; catalpol; GSH; protection;
D O I
10.1016/j.etap.2006.11.012
中图分类号
X [环境科学、安全科学];
学科分类号
08 ; 0830 ;
摘要
Rotenone, a specific inhibitor of mitochondrial complex 1, reproduces many features of Parkinson's disease. The aim of the study was carried out to investigate how rotenone affected the mitochondrial function and antioxidant/oxidant parameters of mouse striatum, and secondly, to evaluate the ameliorating effects of catalpol against rotenone-induced damage. Our results showed that rotenone induced significant changes in mitochondrial function such as complex I activity and mitochondrial membrane potential decreased, and enhanced antioxidant status as glutathione depletion, enzymatic (glutathione peroxidase and superoxide dismutase) disorders, and increased lipid peroxidation. Catalpol increased complex 1, superoxide dismutase and glutathione peroxidase activities, reduced lipid peroxidation and loss of mitochondrial membrane potential in rotenone-treated mice. These in vivo data indicated that catalpol might have protection against deleterious mouse damage caused by rotenone. (c) 2006 Elsevier B.V. All rights reserved.
引用
收藏
页码:314 / 318
页数:5
相关论文
共 31 条
[1]   Risk factors of Parkinson's disease in Indian patients [J].
Behari, M ;
Srivastava, AK ;
Das, RR ;
Pandey, RM .
JOURNAL OF THE NEUROLOGICAL SCIENCES, 2001, 190 (1-2) :49-55
[2]   Chronic systemic pesticide exposure reproduces features of Parkinson's disease [J].
Betarbet, R ;
Sherer, TB ;
MacKenzie, G ;
Garcia-Osuna, M ;
Panov, AV ;
Greenamyre, JT .
NATURE NEUROSCIENCE, 2000, 3 (12) :1301-1306
[3]  
BRADFORD MM, 1976, ANAL BIOCHEM, V72, P248, DOI 10.1016/0003-2697(76)90527-3
[4]   The parkinsonian neurotoxin MPP+ opens the mitochondrial permeability transition pore and releases cytochrome c in isolated mitochondria via an oxidative mechanism [J].
Cassarino, DS ;
Parks, JK ;
Parker, WD ;
Bennett, JP .
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE, 1999, 1453 (01) :49-62
[5]   Genetic and environmental risk factors for Parkinson's disease in a Chinese population [J].
Chan, DKY ;
Woo, J ;
Ho, SC ;
Pang, CP ;
Law, LK ;
Ng, PW ;
Hung, WT ;
Kwok, T ;
Hui, E ;
Orr, K ;
Leung, MF ;
Kay, R .
JOURNAL OF NEUROLOGY NEUROSURGERY AND PSYCHIATRY, 1998, 65 (05) :781-784
[6]   Nicotine protects rat brain mitochondria against experimental injuries [J].
Cormier, A ;
Morin, C ;
Zini, R ;
Tillement, JP ;
Lagrue, G .
NEUROPHARMACOLOGY, 2003, 44 (05) :642-652
[7]   RHODAMINE-123 AS A PROBE OF TRANSMEMBRANE POTENTIAL IN ISOLATED RAT-LIVER MITOCHONDRIA - SPECTRAL AND METABOLIC PROPERTIES [J].
EMAUS, RK ;
GRUNWALD, R ;
LEMASTERS, JJ .
BIOCHIMICA ET BIOPHYSICA ACTA, 1986, 850 (03) :436-448
[8]   Modulation of oxidative events by multivalent manganese complexes in brain tissue [J].
HaMai, D ;
Campbell, A ;
Bondy, SC .
FREE RADICAL BIOLOGY AND MEDICINE, 2001, 31 (06) :763-768
[9]   Chronic systemic complex I inhibition induces a hypokinetic multisystem degeneration in rats [J].
Höglinger, GU ;
Féger, J ;
Prigent, A ;
Michel, PP ;
Parain, K ;
Champy, P ;
Ruberg, M ;
Oertel, WH ;
Hirsch, EC .
JOURNAL OF NEUROCHEMISTRY, 2003, 84 (03) :491-502
[10]   Role of the mitochondrial membrane permeability transition (MPT) in rotenone-induced apoptosis in liver cells [J].
Isenberg, JS ;
Klaunig, JE .
TOXICOLOGICAL SCIENCES, 2000, 53 (02) :340-351