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Oxidative Medicine and Cellular Longevity
Volume 2017 (2017), Article ID 9715898, 8 pages
Research Article

Assessing Free-Radical-Mediated DNA Damage during Cardiac Surgery: 8-Oxo-7,8-dihydro-2′-deoxyguanosine as a Putative Biomarker

1Centro Cardiologico Monzino, IRCCS, Milan, Italy
2Dipartimento di Chirurgia Cardiaca, IRCCS Policlinico San Donato, Milan, Italy

Correspondence should be addressed to Benedetta Porro

Received 3 March 2017; Accepted 9 April 2017; Published 4 June 2017

Academic Editor: Michael Bukrinsky

Copyright © 2017 Linda Turnu 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.


Coronary artery bypass grafting (CABG), one of the most common cardiac surgical procedures, is characterized by a burst of oxidative stress. 8-Oxo-7,8-dihydro-2′-deoxyguanosine (8-oxodG), produced following DNA repairing, is used as an indicator of oxidative DNA damage in humans. The effect of CABG on oxidative-induced DNA damage, evaluated through the measurement of urinary 8-oxodG by a developed and validated liquid chromatography-tandem mass spectrometry (LC-MS/MS) method in 52 coronary artery disease (CAD) patients, was assessed before (T0), five days (T1), and six months (T2) after CABG procedure. These results were compared with those obtained in 40 subjects with cardiovascular risk factors and without overt cardiovascular disease (CTR). Baseline (T0) 8-oxodG was higher in CAD than in CTR (). A significant burst was detected at T1 (), while at T2, 8-oxodG levels were significantly lower than those measured at T0 () and comparable to those found in CTR (). A similar trend was observed for urinary 8-iso-prostaglandin F2α (8-isoPGF2α), a reliable marker of oxidative stress. In the whole population baseline, 8-oxodG significantly correlated with 8-isoPGF2α levels (, ). These data argue for CABG procedure in CAD patients as inducing a short-term increase in oxidative DNA damage, as revealed by 8-oxodG concentrations, and a long-term return of such metabolite toward physiological levels.