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Role of free Radicals

Neurological Diseases

Oxidative stress in the brain is likely to occur as the brain uses up to 20% of the body's inspired oxygen, yet only accounts for 2% body weight. The brain also houses large concentrations of polyunsaturated fatty acids, which may undergo lipid per-oxidation in such an oxygen-rich environment. ROS have been implicated in the pathology of a number of neurological disorders.

Parkinson's Disease

Dopamine is metabolized in the cytosol and can result in the production of hydrogen peroxide. Increased dopamine turnover has been reported in the cytosol of patients suffering from Parkinson's disease, which leaves them predisposed to higher levels of hydrogen peroxide. Hydrogen peroxide can be converted to highly reactive hydroxyl radicals which are extremely toxic and can cause damage to dopaminergic neurons. Increased lipid per-oxidation, elevated iron levels, increased production of ROS and decreased levels of reduced glutathione have all been identified in the substantia nigra of patients suffering from Parkinson's disease.

Down's Syndrome (DS)

Altered antioxidant systems and increased oxidative stress have been implicated in the etiology of Down's Syndrome. Down’s Syndrome generally results from a trisomy of chromosome 21, which also encodes SOD. SOD activity is therefore 50% higher in all tissues in DS patients including the brain. This enzyme converts superoxide radicals to oxygen and hydrogen peroxide, which can then f highly reactive hydroxyl radicals. DS patients have increased levels of SOD, GPx and lipid per-oxidation.

Alzheimer's Disease

A. d. is associated with loss of neurons, neurofibrillary tangles, deposition of amorphous protein, among others. Increased oxidative stress has also been identified in the brain of these patients. Decreased levels of vitamin E, C and plasmaaluminium have also been associated with Alzheimer's disease. Increased thought to enhance iron induced lipid peroxidation.

References
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  2. Ohlemiller KK. Wright JS. Dugan LL. Early elevation of cochlear reactive oxygen species following noise exposure. Audiology & Neuro-Otology. 4(5):229-36, 1999.

  3. Socci DJ. Bjugstad KB. Jones HC. Pattisapu JV. Arendash GW. Evidence that oxidative stress is associated with the pathophysiology of inherited hydrocephalus in the H-Tx rat model.Experimental Neurology. 155(1):109-17, 1999

  4. Delanty N. Dichter MA. Oxidative injury in the nervous system. Acta Neurologica Scandinavica. 98(3):145-53, 1998.

  5. Calabrese V. Bella R. Testa D. Spadaro F. Scrofani A. Rizza V. Pennisi G. Increased cerebrospinal fluid and plasma levels of ultraweak chemiluminescence are associated with changes in the thiol pool and lipid-soluble fluorescence in multiple sclerosis: the pathogenic role of oxidative stress. Drugs Under Experimental & Clinical Research. 24(3):125-31, 1998.

  6. Reardon JT. Bessho T. Kung HC. Bolton PH. Sancar A. In vitro repair of oxidative DNA damage by human nucleotide excision repair system: possible explanation for neurodegeneration in xeroderma pigmentosum patients. Proceedings of the National Academy of Sciences of the United States of America. 94(17):9463-8, 1997.

  7. Bondy SC. The relation of oxidative stress and hyperexcitation to neurological disease. Proceedings of the Society for Experimental Biology & Medicine. 208(4):337-45, 1995.

  8. Halliwell B. Oxygen radicals as key mediators in neurological disease: fact or fiction?. Annals of Neurology. 32 Suppl:S10-5, 1992

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