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Oxidative Medicine and Cellular Longevity
Volume 2013, Article ID 612784, 16 pages
Research Article

A Regulatory Role of NAD Redox Status on Flavin Cofactor Homeostasis in S. cerevisiae Mitochondria

1Istituto di Biomembrane e Bioenergetica, CNR, Via Orabona 4, 70126 Bari, Italy
2Centro Integrato di Ricerca, Università Campus Bio-Medico di Roma, Via Alvaro del Portillo 21, 00128 Roma, Italy
3Dipartimento di Bioscienze, Biotecnologie e Biofarmaceutica, Università degli Studi di Bari “Aldo Moro”, Via Orabona 4, 70126 Bari, Italy

Received 21 May 2013; Accepted 18 July 2013

Academic Editor: Cristina Mazzoni

Copyright © 2013 Teresa Anna Giancaspero et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Flavin adenine dinucleotide (FAD) and nicotinamide adenine dinucleotide (NAD) are two redox cofactors of pivotal importance for mitochondrial functionality and cellular redox balance. Despite their relevance, the mechanism by which intramitochondrial NAD(H) and FAD levels are maintained remains quite unclear in Saccharomyces cerevisiae. We investigated here the ability of isolated mitochondria to degrade externally added FAD and NAD (in both its reduced and oxidized forms). A set of kinetic experiments demonstrated that mitochondrial FAD and NAD(H) destroying enzymes are different from each other and from the already characterized NUDIX hydrolases. We studied here, in some detail, FAD pyrophosphatase (EC, which is inhibited by NAD+ and NADH according to a noncompetitive inhibition, with values that differ from each other by an order of magnitude. These findings, together with the ability of mitochondrial FAD pyrophosphatase to metabolize endogenous FAD, presumably deriving from mitochondrial holoflavoproteins destined to degradation, allow for proposing a novel possible role of mitochondrial NAD redox status in regulating FAD homeostasis and/or flavoprotein degradation in S. cerevisiae.