Nitric oxide and mechanisms of vascular and tissue damage. new hope for research and therapy of multiple sclerosis
Mayer, M.
Der Nervenarzt 65(12): 819-827
1994
ISSN/ISBN: 0028-2804 PMID: 7854502 Document Number: 423161
Nitric oxide (NO) was recently recognized as a--from a biological point of view rather unusual--signalling molecule and ubiquitous mediator. Soon after the discovery of the significance of NO for intercellular communication and intracellular regulations, it became apparent that the NO-dependent processes play a part also in the immune and inflammatory mechanisms of vascular and tissue damage, including affections of the CNS. In higher concentrations, NO acts directly as a toxic factor and co-factor, and in lower concentrations it has rather more regulatory and even protective properties. In the present article the role played by NO in some mechanisms that, according to present knowledge, participate in the pathogenesis of multiple sclerosis is reviewed. These are as follows: The production and action of cytokines, especially interferon-gamma, tumour necrosis factor and interleukins; Interactions between leukocytes, thrombocytes and endothelial cells; The arachidonic acid cascade, metabolism and effects of reactive oxygen species and actions of corticosteroids; Glia-dependent cytotoxic and immunopathological events; Virus-host interactions. It has become increasingly clear that the research focused on NO and related problems brings significant progress in our understanding of the pathogenesis of many neurological diseases and, moreover, may provide new stimuli in the search for novel therapeutic approaches in multiple sclerosis.