DNA damage repair and genetic polymorphisms: Assessment of individual sensitivity and repair capacity

The Influence of Individual Genome Sensitivity in DNA Damage Repair Assessment in Chronic Professional Exposure to Low Doses of Ionizing Radiation

“…After 60 minutes from the exposure, the values did not significantly differ from the control values before irradiation in both control and exposed group. Those results were different that the ones found by Cornetta et al (2006) during DNA repair assessment after the exposure to the dose of 2 Gy. They have shown that even after 60 minutes from the exposure, TI were still significantly higher than before radiation.…”

“…The analysis of comet assay parameters did not give consistent results. Immediately after the irradiation with the dose of 2 Gy, values for tail intensity, which is recently considered the most reliable parameter for DNA damage estimation (Collins, 2004), were higher than the values of other authors for the same dose (Cornetta et al, 2006). The exposed and control group also had significantly higher TL and TM for all observed time intervals when compared to the control values before irradiation in both groups.…”

“…The results could be explained by the difference in the repair of single stranded and double stranded DNA breaks. Single stranded DNA breaks are usually formed after the exposure to gamma or X-ray (90 %), while only small part of damage is created by double stranded breaks (10 %) (Cornetta et al, 2006). The repair of double stranded breaks after the exposure to ionising radiation usually lasts 12 or 16 hours (Vodicka et al, 2004), that is considerably longer than the repair of single stranded breaks.…”

Meat-derived carcinogens, genetic susceptibility and colorectal adenoma risk

“…DNA adducts are repaired primarily by components of the nucleotide excision repair pathway (NER: xeroderma pigmentosum group A (XPA) and XPD) and to a lesser extent by components in the base excision repair pathway (BER: X-ray repair cross-complementing group 1 (XRCC1)) (Yeh et al 2005). Left unrepaired, DNA adducts can induce DNA damage; specifically, micronucleus formation, DNA strand breaks and sister chromatid exchanges are markers of DNA damage that have been associated with PhIP and MeIQx exposures, and associations have been observed between these markers and components of the NER (XPD and XPC), BER (XRCC1 and ADP-ribosyltransferase (ADPRT)) and homologous repair (XRCC3) pathways (Cornetta et al 2006;Godderis et al 2006;Wang et al 2010).…”

XRCC1 rs1799782 polymorphism and objective response rate in NSCLC patients treated with platinum-based chemotherapy

“…The XRCC1 gene codes for a DNA-repair enzyme that is involved in base excision repair of oxidative DNA damage as well as single-strand break repair. Evidence has shown that polymorphisms in DNA repair genes could influence individual DNA repair capacity [4]. Lu et al suggested that XRCC1 Arg194Trp polymorphism was associated with increased risk for glioma, especially in Asians [5].…”