The action of quercetin on the mitochondrial NADH to NAD(+) ratio in the isolated perfused rat liver

It has been suggested that active forms of quercetin ( o-semiquinones) are able to oxidize NADH in mammalian cells. The purpose of this study was to investigate this proposition by measuring the beta-hydroxybutyrate to acetoacetate ratio as an indicator of the mitochondrial NADH/NAD (+) redox ratio...

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Bibliographic Details
Published in:	Planta medica Vol. 71; no. 12; p. 1118
Main Authors:	Buss, Gisele D, Constantin, Jorgete, de Lima, Leonardo C, Teodoro, Graziele R, Comar, Jurandir F, Ishii-Iwamoto, Emy L, Bracht, Adelar
Format:	Journal Article
Language:	English
Published:	Germany 01-12-2005
Subjects:	Animals Liver - cytology Liver - drug effects Liver - metabolism Mitochondria - drug effects Mitochondria - metabolism NAD - metabolism Oxygen - metabolism Perfusion Quercetin - pharmacology Rats
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Summary:	It has been suggested that active forms of quercetin ( o-semiquinones) are able to oxidize NADH in mammalian cells. The purpose of this study was to investigate this proposition by measuring the beta-hydroxybutyrate to acetoacetate ratio as an indicator of the mitochondrial NADH/NAD (+) redox ratio in the isolated perfused rat liver. The NADH to NAD (+) ratio was reduced by quercetin; half-maximal reduction occurred at a concentration of 32.6 microM. Additionally, quercetin (25 to 300 microM) stimulated the Krebs cycle ( (14)CO (2) production) and inhibited oxygen uptake (50 to 300 microM). Low quercetin concentrations (25 microM) stimulated oxygen uptake. The results of the present work confirm the hypothesis that quercetin is able to participate in the oxidation of NADH in mammalian cells, shifting the cellular conditions to a more oxidized state (prooxidant activity). Stimulation of the Krebs cycle was probably caused by the increased NAD (+) availability whereas the decreased NADH availability and the inhibition of mitochondrial energy transduction could be the main causes for oxygen uptake inhibition.
ISSN:	0032-0943
DOI:	10.1055/s-2005-873174