Isoprenoid pathway and free radical generation and damage in neuropsychiatric disorders.

dc.contributor.authorRavikumar, Aen_US
dc.contributor.authorArun, Pen_US
dc.contributor.authorDevi, K Ven_US
dc.contributor.authorAugustine, Jen_US
dc.contributor.authorKurup, P Aen_US
dc.date.accessioned2009-05-28T12:42:41Z
dc.date.available2009-05-28T12:42:41Z
dc.date.issued2000-05-29en_US
dc.description.abstractTwo substances which are products of the isoprenoid pathway, can participate in lipid peroxidation. One is digoxin, which by inhibiting membrane Na(+)-K+ ATPase, causes increase in intracellular Ca2+ and depletion of intracellular Mg2+, both effects contributing to increase in lipid peroxidation. Ubiquinone, another products of the pathway is a powerful membrane antioxidant and its deficiency can also result in defective electron transport and generation of reactive oxygen species. In view of this and also in the light of some preliminary reports on alteration in lipid peroxidation in neuropsychiatric disorders, a study was undertaken on the following aspects in some of these disorders (primary generalised epilepsy, schizophrenia, multiple sclerosis, Parkinson's disease and CNS glioma)--1) concentration of digoxin, ubiquinone, activity of HMG CoA reductase and RBC membrane Na(+)-K+ ATPase 2) activity of enzymes involved in free radical scavenging 3) parameters of lipid peroxidation and 4) antioxidant status. The result obtained indicates an increase in the concentration of digoxin and activity of HMG CoA reductase, decrease in ubiquinone levels and in the activity of membrane Na(+)-K+ ATPase. There is increased lipid peroxidation as evidenced from the increase in the concentration of MDA, conjugated dienes, hydroperoxides and NO with decreased antioxidant protection as indicated by decrease in ubiquinone, vit E and reduced glutathione in schizophrenia, Parkinson's disease and CNS glioma. The activity of enzymes involved in free radical scavenging like SOD, catalase, glutathione peroxidase and glutathione reductase is decreased in the above diseases. However, there is no evidence of any increase in lipid peroxidation in epilepsy or MS. The role of increased operation of the isoprenoid pathway as evidenced by alteration in the concentration of digoxin and ubiquinone in the generation of free radicals and protection against them in these disorders is discussed.en_US
dc.description.affiliationDepartment of Neurology, Medical College, Thiruvananthapuram 695 011, India.en_US
dc.identifier.citationRavikumar A, Arun P, Devi KV, Augustine J, Kurup PA. Isoprenoid pathway and free radical generation and damage in neuropsychiatric disorders. Indian Journal of Experimental Biology. 2000 May; 38(5): 438-46en_US
dc.identifier.urihttps://imsear.searo.who.int/handle/123456789/58451
dc.language.isoengen_US
dc.source.urihttps://www.niscair.res.in/ScienceCommunication/ResearchJournals/rejour/ijeb/ijeb0.aspen_US
dc.subject.meshCentral Nervous System Neoplasms --metabolismen_US
dc.subject.meshDigoxin --metabolismen_US
dc.subject.meshEpilepsy, Generalized --metabolismen_US
dc.subject.meshFree Radicals --metabolismen_US
dc.subject.meshGlioma --metabolismen_US
dc.subject.meshHumansen_US
dc.subject.meshLipid Peroxidationen_US
dc.subject.meshMultiple Sclerosis --metabolismen_US
dc.subject.meshNervous System Diseases --metabolismen_US
dc.subject.meshParkinson Disease --metabolismen_US
dc.subject.meshSchizophrenia --metabolismen_US
dc.subject.meshUbiquinone --metabolismen_US
dc.titleIsoprenoid pathway and free radical generation and damage in neuropsychiatric disorders.en_US
dc.typeJournal Articleen_US
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