title: Oxidant-antioxidant imbalance in the erythrocytes of sporadic amyotrophic lateral sclerosis patients correlates with the progression of disease.
abstract: Free radicals are implicated in numerous disease processes including motor neuron degeneration (MND). Antioxidant defense enzymes: superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSHPx), glutathione reductase (GR) and glucose-6-phosphate dehydrogenase (G-6-PDH) in the erythrocytes are capable of detoxifying reactive oxygen species produced endogenously or exogenously. In the present study, the extent of lipid peroxidation (LPO) and antioxidant defenses were evaluated in the erythrocytes of 20 sporadic amyotrophic lateral sclerosis (ALS) patients and 20 controls. We observed that lipid peroxidation in the erythrocytes of amyotrophic lateral sclerosis patients significantly increased with respect to controls (P<0.001). On the other hand, catalase activity was found to be significantly lower (P<0.001). The activities of glucose-6-phosphate dehydrogenase, glutathione reductase and glutathione levels were also found to be significantly reduced in ALS patients compared to healthy subjects (P<0.001, P<0.01 and P<0.01, respectively). It was further observed that lipid peroxidation started to increase and catalase, glutathione reductase, glucose-6-phosphate dehydrogenase enzyme activities and glutathione levels started to decrease as amyotrophic lateral sclerosis progressed from 6 to 24 months, suggesting a correlation between these parameters and duration of amyotrophic lateral sclerosis. This study confirms the involvement of oxidative stress during the progression of amyotrophic lateral sclerosis and the need to develop specific peripheral biomarkers.
authors.affiliation: Department of Neurology, Sanjay Gandhi Post Graduate Institute of Medical Sciences, Raebareli Road, Lucknow 226014, UP, India. gnageshbabu@yahoo.com <gnageshbabu@yahoo.com>
authors.forename: G Nagesh
authors.initials: GN
authors.lastname: Babu
authors.forename: Alok
authors.initials: A
authors.lastname: Kumar
authors.forename: Ramesh
authors.initials: R
authors.lastname: Chandra
authors.forename: S K
authors.initials: SK
authors.lastname: Puri
authors.forename: R L
authors.initials: RL
authors.lastname: Singh
authors.forename: Jayantee
authors.initials: J
authors.lastname: Kalita
authors.forename: U K
authors.initials: UK
authors.lastname: Misra
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000690:Amyotrophic Lateral Sclerosis / Q000097:blood* / Q000503:physiopathology; D000975:Antioxidants / Q000378:metabolism*; D015415:Biomarkers / Q000032:analysis / Q000378:metabolism; D002374:Catalase / Q000378:metabolism; D002490:Central Nervous System / Q000378:metabolism* / Q000503:physiopathology; D018450:Disease Progression; D004912:Erythrocytes / Q000378:metabolism*; D005260:Female; D005954:Glucosephosphate Dehydrogenase / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D005980:Glutathione Reductase / Q000378:metabolism; D006801:Humans; D015227:Lipid Peroxidation / Q000502:physiology; D008297:Male; D008875:Middle Aged; D016877:Oxidants / Q000378:metabolism*; D010084:Oxidation-Reduction; D018384:Oxidative Stress / Q000502:physiology*; D013482:Superoxide Dismutase / Q000378:metabolism; D000072105:Superoxide Dismutase-1; D013997:Time Factors
chemical_list: D000975:Antioxidants; D015415:Biomarkers; D016877:Oxidants; C000606290:SOD1 protein, human; D005954:Glucosephosphate Dehydrogenase; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D000072105:Superoxide Dismutase-1; D005980:Glutathione Reductase