Role of Cell Oxidant Status and Redox State in Controlling Cell Proliferation and Apoptosis in Two Models of Wallerian Degeneration of Rat Sciatic Nerve

After peripheral nerve lesion, the role of reactive oxygen species has not been clarified during Wallerian degeneration. The present study examined the participation of oxidant stress after rat sciatic nerve injury induced by two experimental models (crush and transection). Here, biochemical parameters indicative of oxidant stress, nitric oxide (NO) metabolism, cell proliferation, apoptosis and bioenergetics were determined in injured and contralateral sciatic nerves, and caudofemoralis muscle, by measuring production of ROS by-products and conjugated dienes, H2DCF-DA reacting by-products content, production of free radicals detected by chemiluminescence, rate of protein oxidation (carbonyl groups), NO metabolism, parameters indicative of cell proliferation, activity of caspase-3, changes in the cell redox state (cytoplasmic), mitochondrial cytochrome oxidase activity in crushed and transected sciatic nerves. The results show a different response pattern of injury between transected and crushed nerves during Wallerian degeneration and between contralateral nerves as well. The contralateral nerves also had changes in these parameters, but in a differential manner depending on the type of nerve lesion. In conclusion, present data strongly suggest that changes in the patterns of lipid peroxidation are not merely consequences of cell damage and death but rather are exerting a controlling role in the progression of Wallerian degeneration.