8-oxo-7,8-dihydro-2'-deoxyguanosine as a biomarker of oxidative damage in oesophageal cancer patients: lack of association with antioxidant vitamins and polymorphism of hOGG1 and GST

8-oxodG was analysed in peripheral blood mononuclear cells (PBMCs) by High Performance Liquid Chromatography with Electrochemical Detection (HPLC-ED). Analysis of gene polymorphisms in GSTM1 and GSTT1 was performed by multiplex PCR and in GSTP1 and hOGG1 by a PCR-RFLP method. Reversed-phase HPLC with UV detection at 294 nm was used to measure vitamins A and E in serum from the same blood samples.We observed that in our combined population (cases and control, n = 60), there was no statistically significant correlation between the levels of 8-oxodG and (i) the serum concentration of antioxidant vitamins, vitamin A (P = 0.290) or vitamin E (P = 0.813), or (ii) the incidence of the Ser326Cys polymorphic variant (P = 0.637) of the hOGG1 gene. Also, the levels of 8-oxodG were not significantly associated with polymorphisms in metabolite-detoxifying genes, such as GSTs, except for the positive correlation with Val/Val GST P1 allele (P < 0.0001).The weakness of our cohort size notwithstanding, vitamins levels in serum and genetic polymorphisms in the hOGG1 or GST genes do not appear to be important modulators of 8-oxodG levels.Oesophageal cancer remains an important public health concern worldwide with an estimated burden of 500, 000 new cases in 2005 [1]. The two major histological types of oesophageal cancers, squamous cell carcinoma (SCC) and adenocarcinoma (ADC) differ substantially in their underlying patterns of incidence and key etiologic factors. Alcoholism and smoking are the major established risk factors for SCC, whereas Barrett's oesophagus or gastro-oesophageal reflux disease (GORD) are consistently associated with an increased risk of ADC.Oxidative stress and reactive oxygen species (ROS) are thought to play a role in oesophageal carcinogenesis. ROS may result from external factors such as smoking, and alcohol metabolism, or may be produced endogenously via inflammatory conditions such as oesophagitis or GORD or may also be due to precancerous lesions (Barrett