Please use this identifier to cite or link to this item: http://nopr.niscpr.res.in/handle/123456789/23791
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dc.contributor.authorRavikumar, A-
dc.contributor.authorAugustine, Jyothi-
dc.contributor.authorKurup, P A-
dc.date.accessioned2013-11-19T08:39:35Z-
dc.date.available2013-11-19T08:39:35Z-
dc.date.issued2001-06-
dc.identifier.issn0975-1009 (Online); 0019-5189 (Print)-
dc.identifier.urihttp://hdl.handle.net/123456789/23791-
dc.description537-541en_US
dc.description.abstractThe human hypothalamus produces an endogenous membrane Na+-K‑+ ATPase inhibitor digoxin. Digox in is a steroidal glycoside and could be synthesised by the isoprenoid pathway. The other metabolites of the isoprenoid pathway are Cholesterol, dolichol and ubiquinone. We have tried to find out the extent of incorporation of 14C acetate into digoxin in rat brain. The effects of digoxin administration on the rat brain was also studied. The results show that the percentage incorporation of 14C acetate into digoxin is low but detectable. The maximum incorporation was observed for cholesterol, followed by dolichol and finally ubiquinone. The histopathological changes observed after digoxin administration were focal degeneration of the ganglion cells in the cerebrum and cerebellum. The carbohydrate components of the glycoproteins were reduced and the concentration of serotonin, dopamine, and epinephrine showed a significant increase. The role of digoxin in mediating neuronal cell death is discussed. en_US
dc.language.isoen_USen_US
dc.publisherNISCAIR-CSIR, Indiaen_US
dc.rights CC Attribution-Noncommercial-No Derivative Works 2.5 Indiaen_US
dc.sourceIJEB Vol.39(06) [June 2001]en_US
dc.titleStudies on digoxin - 14C-acetate incorporation in to digoxin and degenerative changes in the brain in rats administered digoxin en_US
dc.typeArticleen_US
Appears in Collections:IJEB Vol.39(06) [June 2001]

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