Please use this identifier to cite or link to this item: https://doi.org/10.1016/j.bbrc.2006.07.089
Title: Action of diclofenac on kidney mitochondria and cells
Authors: Ng, L.E.
Vincent, A.S.
Halliwell, B. 
Wong, K.P.
Keywords: ATP biosynthesis
Diclofenac
Malate-aspartate shuttle
Mitochondrial membrane potential
NAD(P)H
NSAIDs
Issue Date: 2006
Citation: Ng, 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
Abstract: The 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.
Source Title: Biochemical and Biophysical Research Communications
URI: http://scholarbank.nus.edu.sg/handle/10635/28502
ISSN: 0006291X
10902104
DOI: 10.1016/j.bbrc.2006.07.089
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