a b s t r a c tBackground: There are evidences of association between occupational radiation exposure, cytogenetic alterations and the increase in cancer rates. It is known that the probability of carcinogenesis is greater in populations exposed to radiation, since ionizing radiation can raise the frequency of chromosomal aberration and spontaneous mutations.Objective: Our purpose was to assess the role of chromosomal aberrations and oxidative DNA adduct 8-hydroxy-2-deoxyguanosine (8-OHdG) as biomarkers of radiation injury in individuals occupationally exposed to ionizing radiation.Subjects: and Methods: Blood samples were collected from 60 radiation workers and 30 healthy volunteers age and sex matched as control group who had never worked in radiation-related jobs. Chromosomal aberrations in peripheral blood lymphocytes were assayed by conventional cytogenetic technique and serum levels of 8-OHdG was measured by enzyme linked immunossorbent assay (ELISA).Results: The incidence of all types of chromosomal aberrations was significantly higher in all exposed groups than in controls with the highest rate of chromosomal aberrations in the industrial radiographers. Serum 8-OHdG in all radiation workers was significantly higher than in control group. There was a significant higher values among industrial radiographers compared to diagnostic radiologists or radiotherapists. Significantly lower mean corpuscular volume (M.C.V) was found among radiation workers versus the controls reflecting erythrocyte microcytosis.Conclusions: Scoring of chromosome aberrations such as breaks, fragments and dicentrics is a reliable method to detect previous exposure to ionizing radiation. This type of monitoring may be used as a biological dosimeter instead of physical dosimetry.8-OHdG is a useful oxidative DNA marker among radiation workers and those exposed to environmental carcinogens.

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Despite being one of the most common congenital defects in boys, the etiology of hypospadias remains largely unknown. In this study we evaluated a spectrum of potential risk factors for hypospadias in which we focused on both paternal and maternal factors and chromosomal aberrations. Cases were selected from the Genetic Clinic, Medical Research Institute, University of Alexandria. A total of 176 cases with hypospadias were included in this study, and a matching control group of normal 300 boys for the association study. All cases were subjected to detailed family, pregnancy, genetic histories, clinical examination, and pedigree study. Chromosome analysis was performed using peripheral blood lymphocyte cultures by trypsin G-banding technique. Hormonal assays, abdominal and pelvic ultrasound were carried out according to case presentation. Both parents of cases and the control group completed written questionnaires. Abnormal karyotyes were detected in 23 cases (13.07%) associated with other anomalies, sex chromosome abnormalities were present in 69.56% and autosomal aberrations in 30.43%. Patients with chromosomal abnormalities were excluded from the association study. Logistic regression analysis was used to assess the independent contribution of different factors to the risk of hypospadias. Our data did not support an association with increased parental age. The most profound result was the increased risk of hypospadias for boys with positive family history (n=23; OR=26.36; 95% CI: 5.90-164.23). Strong indications for an increased risk of hypospadias were also found with low birth weight (n=45; OR=13.47; 95% CI=6.09-30.70), preterm birth (n=6; OR=12.20; 95% CI=1.45-271.47), twin or triplet pregnancy (n=4; OR=8.03; 95% CI=0.84-190.23), and when mothers had preeclampsia (n=16; OR=11.56; 95% CI=3.11-50.77). Associations with pregnancy achieved with fertility treatment, and mother used iron supplements were also found. In conclusion, routine karyotype screening permits the diagnosis of chromosomal anomalies especially in those with the most severe forms of hypospadias and additional anomalies. Several risk factors have been identified for hypospadias which support the idea that genetic predisposition, placental insufficiency, and substances that interfere with natural hormones before conception or during fetal development play a role in the etiology of hypospadias.

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