Abstract
Reactive oxygen metabolites have been demonstrated to play a significant pathobiologic role in a number of clinical and experimental models of both immune and non immune glomerular diseases.1,2 In some forms of these diseases, resident glomerular cells, in addition to recruited inflammatory cells, can be the source of reactive oxygen metabolites. Recent evidence demonstrated a prooxidant role of nitric oxide (NO) as well. Enhanced expression and enzyme activity of the inducible nitric oxide synthase (iNOS) in various forms of glomerulonephritis was described.3 Activation of iNOS results in a sustained high output production of nitric oxide (NO) which can cause oxidative injury either in its own or by interacting with the superoxide anion to form the relatively stable prooxidant peroxynitrite (ONOO-).4
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Datta, P.K., Lianos, E.A. (2002). Regulation and Role of Heme Oxygenase-1 in Glomerulonephritis. In: Abraham, N.G. (eds) Heme Oxygenase in Biology and Medicine. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-0741-3_21
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DOI: https://doi.org/10.1007/978-1-4615-0741-3_21
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