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Indian Journal of Clinical Biochemistry logoLink to Indian Journal of Clinical Biochemistry
. 2009 May 8;24(1):98–101. doi: 10.1007/s12291-009-0017-y

Oxidative stress in Parkinson’s disease

Shashikant Nikam 2,3,, Padmaja Nikam 2, S K Ahaley 2, Ajit V Sontakke 1
PMCID: PMC3453463  PMID: 23105815

Abstract

Oxidative stress contributes to the cascade, leading to dopamine cell degeneration in Parkinson’s disease. However, oxidative stress is intimately linked to other components of the degenerative process, such as mitochondrial dysfunction, excitotoxicity, nitric oxide toxicity and inflammation. It is therefore difficult to determine whether oxidative stress leads to or is a consequence of, these events. Oxidative stress was assessed by estimating lipid peroxidation product in the form of thiobarbituric acid reactive substances, nitric oxide in the form of nitrite & nitrate. Enzymatic antioxidants in the form of superoxide dismutase, glutathione peroxidase, catalase, ceruloplasmin and non enzymatic antioxidant vitamins e.g. vitamin E and C in either serum or plasma or erythrocyte in 40 patients of Parkinson’s disease in the age group 40–80 years. Trace elements e.g. copper, zinc and selenium were also estimated. Plasma thiobarbituric acid reactive substances and nitric oxide levels were Significantly high but superoxide dismutase, glutathione peroxidase, catalase, ceruloplasmin, vitamin-E, vitamin-C, copper, zinc and selenium levels were significantly low in Parkinson’s disease when compared with control subjects. Present study showed that elevated oxidative stress may be playing a role in dopaminergic neuronal loss in substentia nigra pars compacta and involved in pathogenesis of the Parkinson’s disease.

Key Words: Oxidative stress, Antioxidants, Pathogenesis, Parkinson’s disease

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References

  • 1.Martin J.B. Moleculor basis of the neurodegenerative disorder. New Eng J Med. 1999;340(25):1970–1980. doi: 10.1056/NEJM199906243402507. [DOI] [PubMed] [Google Scholar]
  • 2.Pioro E.P. Antioxidant therapy in ALS. Amyotrophic Lateral Scleorsis. 2000;1:5–15. doi: 10.1080/14660820050515656. [DOI] [PubMed] [Google Scholar]
  • 3.Kowall W., Ferante R.J., Martin J.B. Patterns of cells in Huntington’s disease. Trends Neurosci. 1987;10:42–49. doi: 10.1016/0166-2236(87)90124-X. [DOI] [Google Scholar]
  • 4.Mmosley R.L., Benner E.J. Irena. Neuroinflammation, oxidative stress and the pathogenesis of Parkinson’s disease. Clin Neurochem Res. 2006;6(5):261–281. doi: 10.1016/j.cnr.2006.09.006. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 5.Jellinger K. Pathology of Parkinson’s disease, changes other than the nigrostritalpathway. Ann Neural. 1992;14:153–97. doi: 10.1007/BF03159935. [DOI] [PubMed] [Google Scholar]
  • 6.Forne LS. Pathology of Parkinson’s disease and importance of substentia nigra and Lewy bodies. Aetiology of Parkinson’s disease. Ed. Sterm. G. Baltimore Johns Hopkins Press: 1990; p 185–238.
  • 7.Kurtz JF. An overview of epidemiology of Parkinsonism. Progress inParkinson’s disease research. Eds. Hefti F. Weiner W.J. Mount Kisw Futura Publishing Company. 1992; p-119–p-169.
  • 8.Munch G. Oxidative stress and advanced glycation end products. Alzheimer’s Disease Review. 1996;1:71–74. [Google Scholar]
  • 9.Benecke R., Strumper P., Weiss H. Electron transport complex CI & IV of platelets are abnormal in Parkinson’s disease. Brain. 1993;116:1451–1463. doi: 10.1093/brain/116.6.1451. [DOI] [PubMed] [Google Scholar]
  • 10.Buege J.A., Aust A.D. Microsomal lipid peroxidation. In: Estbrook R.W., Pullman M.E., editors. methods Enzymeol. New York: Acad Press; 1987. pp. 302–310. [Google Scholar]
  • 11.Cortas W. Determination of nitrate in serum and urine by kinetic cadmium reduction method. Clin Chem. 1990;38(8pt.1):1440–1443. [PubMed] [Google Scholar]
  • 12.Randox Ltd. Determination of superoxide dismutase & Glutathione peroxide. Tech Bull on free radical 1994; 12–14.
  • 13.Aebi H. Catalase. In: Bergmeryer H.U., editor. methods, in enzymatic analysis. New York: Acadamic press; 1983. pp. 276–286. [Google Scholar]
  • 14.Karl H., Smith B.S.W., Wright H. Colorimetric method for serum Ceruloplasmin. Clin Chem. 1974;50:359–366. doi: 10.1016/0009-8981(74)90154-5. [DOI] [Google Scholar]
  • 15.Baker F., Vitamin E. In clinical vitaminology methods & interpretation. New York: Interscience publishers; 1968. pp. 169–176. [Google Scholar]
  • 16.Natelson S. In techniques of clinical chemistry. 3rd Edition. Illinios USA: Charles C Thomas; 1971. Ascorbic acid; pp. 162–165. [Google Scholar]
  • 17.Fahn S. Parkinson’s disease and other basal ganglion disorders. IN: Disease of nervous system. Clin Neurol. Eds.: Asbury AK et. al. W.B. Saunders company. 1992; 1144–1158.
  • 18.Ratan RR, Baraban JM. Apoptotic death in an invitro model of neuronal oxidative stress. Clin Ext Pharmacol Physical 1995; 309–310. [DOI] [PubMed]
  • 19.Mecocci The oxidative damage mitochondrial DNA shows age dependent increase in human brain. Ann Neural. 1993;34:159–163. doi: 10.1002/ana.410340416. [DOI] [PubMed] [Google Scholar]
  • 20.Floryed R.A. Antioxidants, oxidative stress and degenerative neurological disorders. Proc Soc Exper Biol Med. 1999;222(3):236–245. doi: 10.1046/j.1525-1373.1999.d01-140.x. [DOI] [PubMed] [Google Scholar]
  • 21.Behl C., Davis J., Cole G.M. Vitamin E protects nerves cells from amyloid beta protein toxicity. Biochem Biophy Res Commun. 1992;186:944–950. doi: 10.1016/0006-291X(92)90837-B. [DOI] [PubMed] [Google Scholar]
  • 22.Brown R. Mol Neurol. Scientific Americam: New York; 1998. ALS and the inherited motor neurons disease; p. 38. [Google Scholar]
  • 23.Burke R.E. Apoptosis in degenerative disease of the basal ganglia. Neurosciertist. 1998;4:301–311. [Google Scholar]
  • 24.Bhumik D., Medin J., Colmenms G. Mutational analysis of active site residue of human adenosine deaminase. J Biol Chem. 1993;8268:5461–5470. [PubMed] [Google Scholar]

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