The Open Leukemia Journal

2013, 5 : 1-6
Published online 2013 May 3. DOI: 10.2174/1876816420130418001
Publisher ID: TOLEUKEMIAJ-5-1

RESEARCH ARTICLE
Mitochondrial DNA Alterations and Oxidative Stress in Acute Leukemia

Mouna Saadaoui1,4 , Lamia Aissaoui2 , Véronique Salaun3 , Mohamed Manai4 and Stéphane Allouche, * ,1
1 Université de Caen, Laboratoire de Biologie Moléculaire et Cellulaire de la Signalisation, UPRES-EA 3919, IFR 146 ICORE, avenue côte de Nacre, 14032 Caen, France
2 Service d'Hématologie. CHU Aziza Othmana, Tunis, Tunisie
3 Service d'Hématologie Biologique, Avenue côte de Nacre, CHU de Caen, France
4 Unité de Biologie Moléculaire et de Biochimie, Faculté des Sciences de Tunis, Tunisie

* Address correspondence to this author at the Service de Biochimie, Centre Hospitalier et Universitaire, Avenue côte de nacre, 14033 Caen Cedex, France; Tel: +33 231065419; Fax: +33231065172; E-mail: allouche-s@chu-caen.fr

ABSTRACT

Mitochondrial DNA (mtDNA) alterations were reported in many cancers but their roles in oncogenesis are still debated. We aimed to examine qualitative and quantitative mtDNA modifications and oxidative stress in normal and cancer cells. 23 leukemia patients and 18 healthy subjects were recruited from the hospital of Azziza Othmana (Tunisia). Mitochondrial D-loop was sequenced, mtDNA level was determined by Q-PCR, the oxidative stress was assessed by a fluorescent probe and the mitochondrial transcription factor A (mTFA) level was quantified. No somatic mutation was evidenced in leukemia cells compared to non-malignant cells. However, a significant higher level of mtDNA associated with an increase of mTFA expression and reactive oxygen species (ROS) production were measured in patients’ cells compared to non-malignant cells. In conclusion, our results don’t support the role of mtDNA mutations in leukemogenesis but increase of mtDNA and ROS levels would be molecular signatures of leukemia.

Keywords:

Mitochondrial DNA, leukemia, reactive oxygen species (ROS), mitochondrial transcription factor A (mTFA).