Background: Endothelial nitric oxide synthase (eNOS) could be a candidate gene for coronary artery disease (CAD). This study investigated the relationship of the eNOS Glu 298 3 Asp and T 786 3 C polymorphisms with the presence and severity of CAD in the Italian population. Methods: We enrolled 415 unrelated individuals who underwent coronary angiography. The severity of CAD was expressed by means of the Duke score. The eNOS Glu 298 3 Asp and T 786 3 C variants were analyzed by PCR. Results: There was significant linkage disequilibrium between the two eNOS polymorphisms (P <0.0001). Both variants were significantly associated with the occurrence and severity of CAD (P ؍ 0.01 and 0.004 for Glu 298 3 Asp and T 786 3 C, respectively). The risk of CAD was increased among individuals homozygous for the C allele of the T 786 3 C polymorphism compared with individuals homozygous for the T allele (odds ratio ؍ 2.5; P <0.01) and was independent of the other common risk factors (P ؍ 0.04). Moreover, individuals with both the Asp/Asp genotype of the Glu 298 3 Asp polymorphism and at least one C allele of the T 786 3 C variant in the promoter region of the eNOS gene had an increased risk of CAD (odds ratio ؍ 4.0; P <0.001) and a significantly higher mean Duke score (26.2 ؎ 2.9 vs 45.2 ؎ 3.7; P ؍ 0.002) compared with individuals with the TT genotype and the Glu allele.
Conclusions:The present study provides evidence that the Glu 298 3 Asp and T 786 3 C polymorphisms of the eNOS gene are associated with the presence and sever-
These data indicate an overall elevation of oxidative DNA damage in CAD patients correlated with the severity of the disease and some atherogenic risk factors, suggesting a possible role of oxidative genetic damage in the pathogenesis of atherosclerosis.
Interventional cardiologists who work in cardiac catheterization laboratories are exposed to low doses of ionizing radiation that could pose a health hazard. DNA damage is considered to be the main initiating event by which radiation damage to cells results in development of cancer and hereditary disease. The aim of the present study was to assess the effects of chronic low-dose X-ray radiation exposure on somatic DNA damage of interventional cardiologists working in high-volume cardiac catheterization laboratories. For this analysis, we used peripheral lymphocytes and the assay for micronuclei (MNs), which is considered to be a reliable biological dosimeter for radiation exposure. We obtained peripheral blood from 62 physicians (mean age+/-se = 40.6+/-1.5 years): 31 interventional cardiologists (group I, exposed) and 31 age- and sex-matched clinical cardiologists (group II, nonexposed). Interventional cardiologists showed higher MN values (group I=20.5+/-1.6 vs. group II=12.8+/-1.3, P=0.001), although some overlap was apparent in the individual subject analysis. A correlation between years of professional activity and MN frequency value was detectable for interventional cardiologists (r=0.428, P=0.02) but not for clinical cardiologists (r=0.253, P=0.17). The results indicated that, overall, interventional cardiologists working in a high-volume catheterization laboratory have higher levels of somatic DNA damage when compared with clinical cardiologists working outside the catheterization laboratory. The amount of this damage varies and is only weakly related to the duration of professional exposure, which suggests that a dominant modulation of the underlying genetic substrate by environmental factors has a role in determining the harm in individual physicians.
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