Endogenous sodium potassium ATPase inhibition related biochemical cascade and the acquired immunodeficiency syndrome--neural regulation of viral replication and immune response to the virus.

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dc.contributor.authorRavikumar, Aen_US
dc.contributor.authorKurup, P Aen_US
dc.date.accessioned2009-05-28T08:10:08Z
dc.date.available2009-05-28T08:10:08Z
dc.date.issued2001-11-01en_US
dc.description.abstractThe isoprenoid pathway and its metabolites - digoxin, dolichol and ubiquinone were assessed in acquired immunodeficiency syndrome. Digoxin is an endogenous regulator of membrane Na+-K+ ATPase secreted by the human hypothalamus. The HMG CoA reductase activity was increased with increased digoxin and dolichol levels and reduced ubiquinone levels in AIDS. Membrane Na+-K+ ATPase activity and serum magnesium levels were reduced. The tryptophan catabolites were increased and the tyrosine catabolites were reduced. The glycoconjugate metabolites were increased and lysosomal stability was reduced. There was reduced incorporation of glycoconjugates into membranes and increased membrane cholesterol: phospholipid ratio. Lipid peroxidation products and NO were increased while free radical scavenging enzymes and reduced glutathione were reduced. The role of the isoprenoid pathway related cascade in the pathogenesis of AIDS is discussed.en_US
dc.description.affiliationDept. of Biochemistry, University of Kerala, Trivdndrum, India.en_US
dc.identifier.citationRavikumar A, Kurup PA. Endogenous sodium potassium ATPase inhibition related biochemical cascade and the acquired immunodeficiency syndrome--neural regulation of viral replication and immune response to the virus. Indian Journal of Dermatology, Venereology and Leprology. 2001 Nov-Dec; 67(6): 312-6en_US
dc.identifier.urihttps://imsear.searo.who.int/handle/123456789/52209
dc.language.isoengen_US
dc.source.urihttps://www.ijdvl.comen_US
dc.titleEndogenous sodium potassium ATPase inhibition related biochemical cascade and the acquired immunodeficiency syndrome--neural regulation of viral replication and immune response to the virus.en_US
dc.typeJournal Articleen_US
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