ANTIOXIDANTS IN PERIPHERAL-NERVE

Oxidative stress and antioxidants have been related in a wide variety of ways with nervous tissue, This review attempts to gather the most r elevant information related to a) the antioxidant status in non pathol ogic nervous tissue; b) the hypothesis and evidence for oxidative stre ss (considered as the disequilibrium between prooxidants and antioxida nts in the cell) as the responsible mechanism of diverse neurological diseases; and c) the correlation between antioxidant alterations and n eural function, in different experimental neuropathies. Decreased anti oxidant availability has been observed in different neurological disor ders in the central nervous system, for example, Parkinson's disease, Alzheimer's disease, epilepsy, amyotrophic lateral sclerosis, cerebral ischaemia, etc. Moreover, the experimental manipulation of the antiox idant defense has led in some cases to interesting experimental models in which electrophysiological alterations are associated with the met abolic modifications induced. In view of the electrophysiological and biochemical effects of some protein kinase C inhibitors on different n eural experimental models, special attention is dedicated to the role of this kinase in peripheral nervous tissue. The nervous tissue, centr al as well as peripheral, has two main special features that are certa inly related to its antioxidant metabolism: the lipid-enriched membran e and myelin sheaths, and cellular excitability. The former explains t he importance of the glutathione (GSH)-conjugating activity towards 4- hydroxy-nonenal, a biologically active product of lipid peroxidation, present in nervous tissue and in charge of its inactivation, The impai rment of the latter by oxidative damage or experimental manipulation o f antioxidant metabolism is discussed. Work on different experimental neuropathies from author's laboratory has been primarily used to provi de information about the involvement of free radical damage and antiox idants in peripheral nerve metabolic and functional impairment.