title: DNA damage in children with scoliosis following X-ray exposure.
abstract: OBJECTIVE
  It has been suggested that cancer incidence is high in subjects with scoliosis who are relatively more often exposed to X--ray for diagnosis and follow--up. X--ray is a kind of ionizing radiation and leads to formation of oxygen free radicals which are capable of damage to DNA, thus altered gen expression and mutation. p53 tumor suppressor gene plays a crucial role in the damage response. It controls the checkpoint of cell cycle and redirects the cell metabolism to either repair of damaged DNA or apoptosis as response to DNA damage. The aim of the present study was to examine serum levels of 8--Hydroxydeoxyguanosine (8--OHdG), a strongly mutagenic product of oxidative DNA damage, p53, superoxide dismutase (SOD) and glutathione peroxidase (G--Px), as antioxidant activity, in children with scoliosis who had got whole spine radiograph two times during the last year.
  
  
  METHODS
  A total of 31 children with adolescent idiopathic scoliosis and age--matched 21 healthy children were included in the study. Serum levels of 8--OHdG and p53 were measured with ELISA kits. SOD and G--Px activities were determined with spectrophotometric assays.
  
  
  RESULTS
  Serum levels of 8--OHdG and p53 were found to be higher (P<0.001 and P<0.01, respectively), SOD activity was found to be lower (P<0.001) in the children with scoliosis as compared to age--matched controls. There was no significant difference between the groups for G--Px activity.
  
  
  CONCLUSIONS
  Our data show that X--ray exposure causes increased 8--OHdG level, and decreased SOD activity, which both may reflect a tumor promoting condition. Increased p53 level may be interpreted as a compensatory effort of cell to X--ray mediated DNA damage.
authors.affiliation: Biruni University, Health Sciences Faculty, Department of Nutrition and Dietetics - yldz.dincer@gmail.com.
authors.forename: S
authors.initials: S
authors.lastname: Himmetoglu
authors.forename: M F
authors.initials: MF
authors.lastname: Guven
authors.forename: N
authors.initials: N
authors.lastname: Bilsel
authors.forename: Y
authors.initials: Y
authors.lastname: Dincer