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Oxidative Medicine and Cellular Longevity
Volume 2012 (2012), Article ID 498914, 14 pages
Research Article

Detailed Analysis of Apoptosis and Delayed Luminescence of Human Leukemia Jurkat T Cells after Proton Irradiation and Treatments with Oxidant Agents and Flavonoids

1Department of Biophysics, “Carol Davila” University of Medicine and Pharmacy, 8 Eroii Sanitari, 050474 Bucharest, Romania
2Istituto Nazionale di Fisica Nucleare, Laboratori Nazionali del Sud, via S. Sofia, 95125 Catania, Italy
3Dipartimento di Fisica e Astronomia, Università di Catania, Viale A. Doria 6, 95125 Catania, Italy
4Sezione di Biochimica e Biologia Molecolare, Dipartimento di Scienze Chimiche, Università di Catania, 6 A. Doria, 95125 Catania, Italy
5“Horia Hulubei” National Institute for Physics and Nuclear Engineering (IFIN-HH), 30 Reactorului, 077125 Bucharest, Romania
6Università degli Studi di Enna “Kore”, Facoltà di Ingegneria, Architettura e delle Scienze Motorie, Cittadella Universitaria, 94100 Enna, Italy

Received 9 March 2012; Accepted 14 May 2012

Academic Editor: Cristina Angeloni

Copyright © 2012 Irina Baran 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.


Following previous work, we investigated in more detail the relationship between apoptosis and delayed luminescence (DL) in human leukemia Jurkat T cells under a wide variety of treatments. We used menadione and hydrogen peroxide to induce oxidative stress and two flavonoids, quercetin, and epigallocatechin gallate, applied alone or in combination with menadione or H2O2. 62 MeV proton beams were used to irradiate cells under a uniform dose of 2 or 10 Gy, respectively. We assessed apoptosis, cell cycle distributions, and DL. Menadione, H2O2 and quercetin were potent inducers of apoptosis and DL inhibitors. Quercetin decreased clonogenic survival and the NAD(P)H level in a dose-dependent manner. Proton irradiation with 2 Gy but not 10 Gy increased the apoptotic rate. However, both doses induced a substantial G2/M arrest. Quercetin reduced apoptosis and prolonged the G2/M arrest induced by radiation. DL spectroscopy indicated that proton irradiation disrupted the electron flow within Complex I of the mitochondrial respiratory chain, thus explaining the massive necrosis induced by 10 Gy of protons and also suggested an equivalent action of menadione and quercetin at the level of the Fe/S center N2, which may be mediated by their binding to a common site within Complex I, probably the rotenone-binding site.