ABSTRACT
Background: Phototherapy is believed to be a safe method for the management of hyperbilirubinemia. However, there are some controversial issues regarding the genotoxic effects of phototherapy on DNA. The aim of this study was to investigate morphologically both phototherapy-induced DNA double-strand breaks [DSBs] and apoptosis in lymphocytes derived from jaundiced and non-jaundiced neonates
Methods: Newborns were divided into three groups, including phototherapy-treated [PT, n=30] jaundiced newborns with total serum bilirubin [TSB] levels >15 mg/dl, non-treated jaundiced newborns [C+, n=27], as positive, as well as healthy negative [C-, n=30] controls with TSB levels ranging from 10 and 15 mg/dl and less than 5 mg/dl, respectively. Lymphocytes were isolated from whole blood samples by Ficoll-isopaque density gradient centrifugation and then assessed for DNA damage and apoptosis before and 24 hours after incubation at 37 degree C in 5% CO2 using the neutral comet assay
Results: DSB levels were significantly much higher in the PT group compared to the controls before incubation but decreased remarkably after the incubation period. As expected, no statistical differences were found between the two control groups before and after incubations. The frequency of apoptotic cells showed no significant differences among all the three groups before incubation; however, it was significantly increased in the PT group after incubation
Conclusion: It seems that phototherapy in jaundiced infants is able not only to induce apoptosis in newborn lymphocytes but also to affect indirectly DNA integrity
ABSTRACT
Impaired DNA repair mechanism is one of the main causes of tumor genesis. Study of intrinsic radiosensitivity of cancer patients in a non-target tissue [e.g. peripheral blood] might show the extent of DNA repair deficiency of cells in affected individuals and might be used a predictor of cancer predisposition. Initial radiation-induced DNA damage [ratio of Tail DN A/Head DNA], dose-response curves and kinetics of DNA repair in leukocytes from healthy volunteers and prostate cancer patients were assessed using alkaline comet assay after exposure to [60]Co gamma rays. Results showed that higher levels of baseline and gamma rays induced DNA damage in leukocytes of prostate cancer cases than in controls. A similar dose response was obtained for both groups. After a repair time of 24 h following in vitro irradiation, samples from the healthy individuals showed no residual DNA damage in their leukocytes, whereas prostate cancer patients revealed more than 20%. Although similar initial radiosensitivity was observed for both groups, the repair kinetics of radiation induced DNA damage of leukocytes from prostate cancer cases and healthy subjects were statistically different. These results support the hypothesis that men affected by prostate cancer may have a constitutional genomic instability