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Role of nitric oxide and reactive oxygen species in arthritis

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Nitric Oxide and Inflammation

Part of the book series: Progress in Inflammation Research ((PIR))

Abstract

The free radical nitric oxide (NO) is synthesized from the guanidino group of L-arginine by a family of enzymes termed NO synthases (NOS). Three isoforms have been described and cloned: endothelial cell NOS (ecNOS, or type 3), brain NOS (bNOS, nNOS, or type 1), and inducible macrophage type NOS (iNOS, or type 2). The cytotoxic effects of NO (in high local concentrations) involve the inhibition of key mitochondrial Fe-S enzymes, including NADH:ubiquinone oxidoreductase, NADH:succinate oxidoreductase, and aconitase [1], cGMP-independent activation by NO of other enzymes, such as cyclooxygenase, has also been described. This action may be related to the reaction of NO with the iron-heme center at the active site of the enzyme [2]. Administration of NOS inhibitors reduces blood flow to most organs.

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Cuzzocrea, S. (2001). Role of nitric oxide and reactive oxygen species in arthritis. In: Salvemini, D., Billiar, T.R., Vodovotz, Y. (eds) Nitric Oxide and Inflammation. Progress in Inflammation Research. Birkhäuser, Basel. https://doi.org/10.1007/978-3-0348-8241-5_9

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  • DOI: https://doi.org/10.1007/978-3-0348-8241-5_9

  • Publisher Name: Birkhäuser, Basel

  • Print ISBN: 978-3-0348-9488-3

  • Online ISBN: 978-3-0348-8241-5

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