Official websites use. Share sensitive information only on official, secure websites. Address for correspondence: Dr. Periyasamy Ravisankar, Department of Anatomy, S. This is an open access journal, and articles are distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4. Epidemiological studies have failed to identify specific environmental, dietary or lifestyle factors for PD.
However oxidative stress in the substantia nigra SN and Corpus striatum is the most broadly accepted hypothesis for the etiopathology of PD. Many experiments state the notion that augmentation of neurotrophic factors and glial cell-derived neurotrophic factors, could prevent or halt the progress of neurodegeneration in PD.
The present study was designed to assess the motor behaviour with apomorphine injection and level of enzymatic and non-enzymatic antioxidants after transplantation of Human Amniotic Epithelial HAE cells in 2,4,5 trihydroxyphenylethylamine 6-OHDA lesioned striatum in rats. The present result suggest that increased free radicals and the decrease in the antioxidant defence system possibly lead to structural and functional alterations in membrane-related events and play significant role of the 6-OHDA induced neurotoxicity.
These alterations were found to be recovered after the HAE cells graft during long term. The 6-OHDA induced neurotoxicity by the generation of free radicals was pronounced by indication of the increased LPO level, decrease in antioxidants and alteration in the dopamine and its metabolites. Unfortunately, the actions of all these agents are compromised as they also elicit dyskinesia when given even with low doses of L-DOPA.
Radical stress, caused by the production of reactive oxygen species ROS , is thought to be a critical factor in the modest neuronal degeneration that occurs with aging. Superoxide radicals, hydrogen peroxide H 2 O 2 , and hydroxyl radicals are oxygen-centered reactive species that have been implicated in several neurotoxic disorders.
