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

2017 ◽  
Vol 2017 ◽  
pp. 1-8 ◽  
Author(s):  
Linda Turnu ◽  
Alessandro Di Minno ◽  
Benedetta Porro ◽  
Isabella Squellerio ◽  
Alice Bonomi ◽  
...  

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 (p=0.035). A significant burst was detected at T1 (p=0.019), while at T2, 8-oxodG levels were significantly lower than those measured at T0 (p<0.0001) and comparable to those found in CTR (p=0.73). 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 (r=0.323, p=0.002). 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.

2012 ◽  
Vol 9 (8) ◽  
pp. 621-626 ◽  
Author(s):  
Yüksel KAYA ◽  
Ayşegül ÇEBİ ◽  
Nihat SÖYLEMEZ ◽  
Halit DEMİR ◽  
Hamit Hakan ALP ◽  
...  

2008 ◽  
Vol 56 (7) ◽  
pp. 925-930 ◽  
Author(s):  
Selen Yurdakul ◽  
Beste Ozben ◽  
Ahmet Kaya Bilge ◽  
Umit Mutlu Turkoglu ◽  
Selda Arkaya ◽  
...  

BackgroundOxidative DNA damage was increased in patients with coronary artery disease (CAD) and correlated with the severity of the disease. Endothelial dysfunction plays a major role in atherosclerotic process. The aim of this study was to explore a relation between oxidative DNA damage and endothelial function in patients with CAD.MethodsForty patients with CAD and 20 age- and sex-matched healthy controls were included. Endothelial function was assessed by brachial artery ultrasonography. The DNA damage was determined by comet method.ResultsThe DNA damage scores after incubation with repair enzymes were found significantly higher in the patients with CAD (P = 0.04). There was a significant negative correlation between oxidized DNA damage scores and flow-mediated dilation (FMD) measures in the patients with CAD (r = −0.41; P = 0.009). Oxidized DNA damage scores were significantly and independently associated with FMD (standardized β = −0.455; P = 0.009) when adjusted by age, sex, smoking status, blood pressure, and cholesterol levels.ConclusionsThe DNA damage scores were significantly inversely correlated with FMD measures. To our knowledge, this is the first study showing the presence of a relation between DNA damage scores and FMD.Abbreviations: CAD, coronary artery disease, 8-Ohgua, 7, 8-Dihydro-8-oxo-guanine; Endo III, endonuclease III; FMD, flow-mediated dilation; Fpg, formamidopyrimidine glycosylase; NTG, nitroglycerin


2002 ◽  
Vol 13 (5) ◽  
pp. 269-274 ◽  
Author(s):  
Nicoletta Botto ◽  
Serena Masetti ◽  
Lucia Petrozzi ◽  
Cristina Vassalle ◽  
Samantha Manfredi ◽  
...  

1980 ◽  
Vol 43 (02) ◽  
pp. 137-140 ◽  
Author(s):  
Jan Erikssen ◽  
Erik Thaulow ◽  
Helge Stormorken ◽  
Ole Brendemoen ◽  
Arvid Hellem

SummaryThe view based on epidemiological and laboratory data that blood group A subjects (=A) have clinically significant higher thrombotic potential than blood group 0 subjects (= O), is supported by the present finding of a significantly higher platelet retention in A than 0.The completely normal ABO distribution found among 71 cases of proven latent CHD, and the disproportionate excess of 0 vs. A in a consecutive series of 191 coronary artery bypass candidates apparently conflict with epidemiological data indicating a higher risk of achieving CHD in A than 0. The conflict may be solved by suggestinga) that the »thrombotic proneness« in A compared with 0 causes a poorer prognosis in CHD among the former, leaving a disproportionate excess of 0 among longterm CHD survivors, and b) that AB0-related factors have had an insignificant, independent impact on the evolution of preclinical coronary artery disease in our 71 men with latent CHD.


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