[Pathophysiology of oxystress-induced tissue damage in cerebrovascular disease].

The electron transport system required for energy transduction in mitochondria releases free electrons to generate superoxide, which is converted to hydrogen peroxide either spontaneously or by superoxide dismutase (SOD). In the presence of catalase and/or peroxidases, hydrogen peroxide is converted to water and hypochlorite (when metabolized by myeloperoxidase). In the absence of SOD, hydrogen peroxide can be converted to highly toxic hydroxyl radicals, in particular, in the presence of transition metals such as the free form of iron. Superoxide also reacts rapidly with nitric oxide (NO) to form peroxynitrite, thereby regulating the biological activities of NO. Oxidative stress caused by such reactive species functions as redox regulator for cells as well as hazardous metabolites, which oxidize a wide variety of cellular constituents, including critical amino acid residues (cysteine, histidine, tyrosine, tryptophan, etc.) in proteins and low-molecular weight constituents. Thus, oxidative stress functions as a double-edged sword in living organisms, including mammals. The present work describes the pathophysiological roles of oxidative stress in and around blood vessels and in the etiology of vasogenic brain injury.