Please use this identifier to cite or link to this item: https://doi.org/10.1016/j.bbrc.2006.07.089
DC FieldValue
dc.titleAction of diclofenac on kidney mitochondria and cells
dc.contributor.authorNg, L.E.
dc.contributor.authorVincent, A.S.
dc.contributor.authorHalliwell, B.
dc.contributor.authorWong, K.P.
dc.date.accessioned2011-11-23T02:25:35Z
dc.date.available2011-11-23T02:25:35Z
dc.date.issued2006
dc.identifier.citationNg, L.E., Vincent, A.S., Halliwell, B., Wong, K.P. (2006). Action of diclofenac on kidney mitochondria and cells. Biochemical and Biophysical Research Communications 348 (2) : 494-500. ScholarBank@NUS Repository. https://doi.org/10.1016/j.bbrc.2006.07.089
dc.identifier.issn0006291X
dc.identifier.issn10902104
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/28502
dc.description.abstractThe mitochondrial membrane potential measured in isolated rat kidney mitochondria and in digitonin-permeabilized MDCK type II cells pre-energized with succinate, glutamate, and/or malate was reduced by micromolar diclofenac dose-dependently. However, ATP biosynthesis from glutamate/malate was significantly more compromised compared to that from succinate. Inhibition of the malate-aspartate shuttle by diclofenac with a resultant decrease in the ability of mitochondria to generate NAD(P)H was demonstrated. Diclofenac however had no effect on the activities of NADH dehydrogenase, glutamate dehydrogenase, and malate dehydrogenase. In conclusion, decreased NAD(P)H production due to an inhibition of the entry of malate and glutamate via the malate-aspartate shuttle explained the more pronounced decreased rate of ATP biosynthesis from glutamate and malate by diclofenac. This drug, therefore affects the bioavailability of two major respiratory complex I substrates which would normally contribute substantially to supplying the reducing equivalents for mitochondrial electron transport for generation of ATP in the renal cell. © 2006 Elsevier Inc. All rights reserved.
dc.description.urihttp://libproxy1.nus.edu.sg/login?url=http://dx.doi.org/10.1016/j.bbrc.2006.07.089
dc.sourceScopus
dc.subjectATP biosynthesis
dc.subjectDiclofenac
dc.subjectMalate-aspartate shuttle
dc.subjectMitochondrial membrane potential
dc.subjectNAD(P)H
dc.subjectNSAIDs
dc.typeArticle
dc.contributor.departmentBIOCHEMISTRY
dc.description.doi10.1016/j.bbrc.2006.07.089
dc.description.sourcetitleBiochemical and Biophysical Research Communications
dc.description.volume348
dc.description.issue2
dc.description.page494-500
dc.description.codenBBRCA
dc.identifier.isiut000240275000024
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