The changes in protein conformation resulting from protein oxidation are deduced from the relevant EPR parameter.Oxidative stress has been widely believed to be an important pathogenetic mechanism of neuronal apoptosis in PD can lead to oxidative damage in the brain of PD, as shown by increased lipid peroxidation and DNA damage in the substantia nigra.Increased protein oxidation is also apparent in many areas of the brain, whereas substantia nigra is particularly vulnerable is rapidly and nonenzymatically oxidized by molecular oxygen to form hydrogen peroxide to form the reactive and damaging hydroxyl free radical.The latter then undergoes an intramolecular cyclization, followed by a purchase Norepinephrine cascade of oxidative reactions resulting in the formation of an insoluble polymeric pigment related to neuromelanin. ROS generated from the respiratory chain in mitochondria, ischemiaactivated xanthinehypoxanthine oxidase, and lipid fatty acid metabolism play an important role in the brain ischemiareperfusion process. Because of the high rate of oxidative metabolic activity, high content of polyunsaturated fatty acids, relatively low antioxidant capacity, low repair activity, and nonreplicating nature of the neuronal cells, the brain is very susceptible to the damage caused by oxygen radicals generated during ischemiareperfusion. In the cerebral circulation system, the burst in the production of ROS damages the endothelium cell and smooth muscle cell, induces blood platelet aggregation and vascular permeability changes, and results in edema. Efforts have been made to investigate the effects of antioxidants on preventing the abovementioned diseases, which involve oxidative stress.Here, we discuss the effects of natural antioxidants, including vitamins E and C, polyphenols, and avonoids in preventing neurodegenerative diseases.The treatment was found to delay functional deterioration in moderately impaired AD patients. Exposure of neuronal cells to a NO donor led to a decrease in the mitochondrial transmembrane potential and intracellular ATP content, which suggested that NO treatment caused mitochondrial dysfunction.In other study, we found that EPCK could scavenge hydroxyl radicals, alkyl radicals, and lipid radicals.EPCK was a moderate scavenger on hydroxyl radicals and alkyl radicals, a potent scavenger on lipid radicals, and an effective inhibitor on lipid peroxidation.To determine the potential protective mechanisms of avonoids in cell death, the mouse hippocampal cell line HT was used as a model.Many, but not all, avonoids protect HT cells and rat primary neurons from glutamate toxicity as well as from ve other oxidative injuries.Three structural requirements of avonoids for protection from glutamate are the hydroxylated C, an unsaturated C ring, and hydrophobicity.Three distinct mechanisms of protection were also found.These data show that the mechanism of protection from oxidative insults by avonoids is highly specic for each compound, which contains avonoids and biolobalids, has been reported to protect the brain against hypoxic damage and inhibit ROS formation in cerebellar neurons.It was found that the order parameter and the ratio of strong immobilized component to weak immobilized component, indicating that the membrane uidity attacked by the free radical was lower than that of the control.The lactic dehydrogenase activity and cell apoptosis attacked by the hydroxyl radical were higher than that of the control was found to have a protective effect on the cells attacked by free radicals.