Plasma lipid peroxidation in sporadic Parkinson's disease.: Role of the L-dopa

被引:55
作者
Agil, A
Durán, R
Barrero, F
Morales, B
Araúzo, M
Alba, F
Miranda, MT
Prieto, I
Ramírez, M
Vives, F
机构
[1] Fac Med Granada, Dept Physiol, Granada 18012, Spain
[2] Fac Med Granada, Inst Neurosci Granada, Granada 18012, Spain
[3] Dept Pharmacol, Granada, Spain
[4] Hosp Clin San Cecilio, Motor Dis Unit, Granada, Spain
[5] Univ Granada, Fac Med, Dept Biostat, E-18012 Granada, Spain
[6] Univ Jaen, Unit Physiol, Jaen, Spain
关键词
Parkinson's disease; oxidative stress; L-dopa; catecholamines; lipid peroxidation;
D O I
10.1016/j.jns.2005.08.016
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Oxidative stress plays an important role in the pathogenesis of neurodegenerative diseases, such as Parkinson's disease (PD). There are several methods to measure oxidative stress, being lipid peroxidation (LPO) one of the most frequently used. Endogenous Plasma LPO was determined by a spectrofluorimetric method in fifty two patients with sporadic PD and in forty controls. To know the maximum capacity of lipids to peroxidate, LPO was also measured after co-incubation with Fe2+/H2O2 (exogenous LPO). All PD patients were taken L-dopa and the effect of this treatment on LPO levels was additionally studied. Urine catecholamines and their main metabolites were also analyzed, and their possible correlation to LPO statistically studied. Endogenous plasma LPO levels were 33% higher in PD group than in control group (P < 0.001). Exogenous plasma or oxidizability was also higher in PD patients compared to controls (20%, P < 0.05). The intake of L-dopa was negatively dose-related to endogenous and exogenous plasma LPO. In conclusion, plasma of PD patients has elevated levels of LPO and also is more prone to peroxidation than that in the control group. The results also suggest an antioxidant effect of L-dopa. (c) 2005 Elsevier B.V. All rights reserved.
引用
收藏
页码:31 / 36
页数:6
相关论文
共 33 条
[11]   PARKINSONISM - ONSET PROGRESSION AND MORTALITY [J].
HOEHN, MM ;
YAHR, MD .
NEUROLOGY, 1967, 17 (05) :427-&
[12]   Hydroxyl radical and superoxide dismutase in blood of patients with Parkinson's disease: relationship to clinical data [J].
Ihara, Y ;
Chuda, M ;
Kuroda, S ;
Hayabara, T .
JOURNAL OF THE NEUROLOGICAL SCIENCES, 1999, 170 (02) :90-95
[13]  
Ilic TV, 1999, FUNCT NEUROL, V14, P141
[14]   NEW INSIGHTS INTO THE CAUSE OF PARKINSONS-DISEASE [J].
JENNER, P ;
SCHAPIRA, AHV ;
MARSDEN, CD .
NEUROLOGY, 1992, 42 (12) :2241-2250
[15]  
JENNER P, 1992, ANN NEUROL S, V32, P82
[16]  
JENNER P, 1996, NEUROLOGY S3, V47, P161
[17]   Comparative effects of melatonin, L-deprenyl, Trolox and ascorbate in the suppression of hydroxyl radical formation during dopamine autoxidation in vitro [J].
Khaldy, H ;
Escames, G ;
León, J ;
Vives, F ;
Luna, JD ;
Acuña-Castroviejo, D .
JOURNAL OF PINEAL RESEARCH, 2000, 29 (02) :100-107
[18]   Peripheral markers of oxidative stress in Parkinson's disease. The role of L-DOPA [J].
Martignoni, E ;
Blandini, F ;
Godi, L ;
Desideri, S ;
Pacchetti, C ;
Mancini, F ;
Nappi, G .
FREE RADICAL BIOLOGY AND MEDICINE, 1999, 27 (3-4) :428-437
[19]   Lipid peroxidation in adult epileptic patients treated with valproic acid [J].
Martínez-Ballesteros, C ;
Pita-Calandre, E ;
Sánchez-González,Y ;
Rodríguez-López, CM ;
Agil, A .
REVISTA DE NEUROLOGIA, 2004, 38 (02) :101-106
[20]   EXPERIMENTAL PARKINSONS-DISEASE IN MONKEYS - EFFECT OF ERGOT ALKALOID DERIVATIVE ON LIPID-PEROXIDATION IN DIFFERENT BRAIN-AREAS [J].
MARZATICO, F ;
CAFE, C ;
TABORELLI, M ;
BENZI, G .
NEUROCHEMICAL RESEARCH, 1993, 18 (10) :1101-1106