Oxidative stress in serum and peripheral blood leukocytes in patients with different disease courses of multiple sclerosis

被引:71
作者
Koch, M
Ramsaransing, GSM
Arutjunyan, AV
Stepanov, M
Teelken, A
Heersema, DJ
De Keyser, J
机构
[1] Univ Groningen, Med Ctr, Dept Neurol, NL-9713 GZ Groningen, Netherlands
[2] Russian Acad Med Sci, Lab Perinatal Biochem, DO Ott Res Inst Obstet & Gynecol, St Petersburg, Russia
关键词
multiple sclerosis; reactive oxygen species; antioxidant capacity; oxidative stress;
D O I
10.1007/s00415-005-0037-3
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Background The role of oxidative stress in patients with multiple sclerosis (MS) is poorly understood. Objective To investigate oxidative stress in serum and peripheral blood leukocytes in patients with different disease courses of MS. Methods Diene conjugate (DC) levels (a measure of lipid peroxidation), total antioxidative activity (AOA) and total anti-radical activity (ARA) were measured in serum and peripheral blood leukocytes from 30 patients with benign relapsing remitting MS (BMS), 27 with secondary progressive MS (SPMS), 29 with primary progressive MS (PPMS), and 30 healthy controls. All MS patients were in a clinically stable phase. Results Serum DC levels were elevated in patients with BMS (p < 0.05), SPMS (p < 0.01) and PPMS (p < 0.001). Serum total AOA and ARA were not different between MS patients and controls. Compared to controls, leukocyte DC levels were not different in each MS subgroup, but total ARA was elevated. There was a strong correlation, both in controls and MS patients, between leukocyte D C levels and leukocyte total ARA (p < 0.0001) and leukocyte total AOA (p < 0.0001). Conclusion Oxidative stress occurs in progressive as well as benign MS. The finding that cells withstand oxidative stress, due to upregulated cellular antioxidant defence mechanisms, suggests that reactive oxygen species (ROS) formation in MS is not necessarily deleterious.
引用
收藏
页码:483 / 487
页数:5
相关论文
共 31 条
[1]   Oxidative stress in neurodegeneration: cause or consequence? [J].
Andersen, JK .
NATURE MEDICINE, 2004, 10 (07) :S18-S25
[2]   Mitochondrial dysfunction plays a key role in progressive axonal loss in multiple sclerosis [J].
Andrews, HE ;
Nichols, PP ;
Bates, D ;
Turnbull, DM .
MEDICAL HYPOTHESES, 2005, 64 (04) :669-677
[3]   Effects of phentermine and phenformin on biomarkers of aging in rats [J].
Anisimova, VN ;
Ukraintseva, SV ;
Anikin, IV ;
Popovich, IG ;
Zabezhinski, MA ;
Bertsein, LM ;
Arutjunyan, AV ;
Ingram, DK ;
Lane, MA ;
Roth, GS .
GERONTOLOGY, 2005, 51 (01) :19-28
[4]   DO DEFECTS IN MITOCHONDRIAL ENERGY-METABOLISM UNDERLIE THE PATHOLOGY OF NEURODEGENERATIVE DISEASES [J].
BEAL, MF ;
HYMAN, BT ;
KOROSHETZ, W .
TRENDS IN NEUROSCIENCES, 1993, 16 (04) :125-131
[5]  
Browne SE, 1999, BRAIN PATHOL, V9, P147
[6]  
Burmistrov S O, 1997, Klin Lab Diagn, P14
[7]   Mitochondrial involvement in brain function and dysfunction: Relevance to aging, neurodegenerative disorders and longevity [J].
Calabrese, V ;
Scapagnini, G ;
Stella, AMG ;
Bates, TE ;
Clark, JB .
NEUROCHEMICAL RESEARCH, 2001, 26 (06) :739-764
[8]   Production of reactive oxygen species by mitochondria - Central role of complex III [J].
Chen, Q ;
Vazquez, EJ ;
Moghaddas, S ;
Hoppel, CL ;
Lesnefsky, EJ .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2003, 278 (38) :36027-36031
[9]   Induction of cytoprotective genes through Nrf2/antioxidant response element pathway: A new therapeutic approach for the treatment of inflammatory diseases [J].
Chen, XL ;
Kunsch, C .
CURRENT PHARMACEUTICAL DESIGN, 2004, 10 (08) :879-891
[10]   INFRARED SPECTROSCOPIC CHARACTERIZATION OF MULTIPLE-SCLEROSIS PLAQUES IN THE HUMAN CENTRAL-NERVOUS-SYSTEM [J].
CHOO, LP ;
JACKSON, M ;
HALLIDAY, WC ;
MANTSCH, HH .
BIOCHIMICA ET BIOPHYSICA ACTA, 1993, 1182 (03) :333-337