Role of free radical and antioxidant imbalance in pathogenesis of Parkinson's disease

Oxidative stress contributes to the cascade, leading to dopamine cell degeneration in Parkinson's disease (PD). 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 [LPO] product in the form of thiobarbituric acid reactive substances [TBARS], and nitric oxide. Enzymatic antioxidants like superoxide dismutase [SOD], glutathione peroxidase [GSHpx], catalase, ceruloplasmin and non enzymatic antioxidant vitamins e.g. vitamin E,C in either serum or plasma or erythrocyte in 22 patients of Parkinson's disease [PD] in the age group 45-75 years. Trace elements e.g. copper, zinc and selenium were also estimated. Plasma TBARS and nitric oxide levels were Significantly high but activity of SOD, GSHpx, catalase, and levels of ceruloplasmin, vitamin-E, vitamin-C, copper, zinc and selenium were significantly low in Parkinson's disease when compared with control groups. Present study showed that imbalance between free radicals and antioxidants may be playing a role in dopaminergic neuronal loss in substentia nigra pars compacta and involved in pathogenesis of the Parkinson's disease.