Abstract
Roles of nitric oxide (·N=O, NO) in decreasing vascular tone, decreasing platelet adhesion and aggregation, increasing the cytotoxic response of macrophages and neutrophils, and serving as a retrograde neurotransmitter in normal biochemically-mediated physiological responses have been reviewed by Moncada, Palmer, and Higgs (1), Lancaster (2). These reviews also present pathological consequences of excess synthesis of NO by Nitric Oxide Synthase (NOS) which include: pain, inflammations, gastrointestinal ulcers, seizures, neoplasias, diabetes, ischemia-reperfusion injuries, and radiation injuries. Synthesis of NO involves an NADPH-dependent diaphorase which supplies reducing equivalents for the conversion L-Arginine to NO.
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Sorenson, J.R.J. (1996). Down-Regulation of Nitric Oxide Synthase May Account for the Antiinflammatory Activities of Copper Chelates. In: Nève, J., Chappuis, P., Lamand, M. (eds) Therapeutic Uses of Trace Elements. Springer, Boston, MA. https://doi.org/10.1007/978-1-4899-0167-5_20
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DOI: https://doi.org/10.1007/978-1-4899-0167-5_20
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