Phototherapy (PT) is the most widely used form of treatment for unconjugated 
hyperbilirubinemia. One possible harmful consequence of PT is of a genetic 
nature. High levels of bilirubin may lead to oxidative damage in newborns: 
photochemical reactions may produce toxic photoproducts, probably peroxides. In 
order to investigate this hypothesis further under in vivo conditions, DNA 
strand-break frequency was examined by means of the comet assay in peripheral 
lymphocytes of icteric newborns undergoing PT treatment, and the levels of 
catalase, an antioxidant enzyme, were determined. We analyzed 20 term 
non-hemolitic hyperbilirubinemic jaundiced neonates before PT ('before PT' 
group) and just prior to ending PT ('after PT' group) and compared comet scores 
of these patients with those of 20 healthy term neonates who all had bilirubin 
levels in the physiological range. Comet scores (tail length, tail moment and 
%DNA in tail) of the group 'before phototherapy' were 23.5 +/- 16.3, 7.41 
(0.97-40.7), 33.0 +/- 12.1, respectively and scores of after phototherapy group 
were 3.2 +/- 1.8, 0.29 (0.3-3.2), 10.7 +/- 3.7, respectively. Comet scores of 
the control group were 3.0 +/- 2.9, 0.25 (0.03-3.22), 10.9 +/- 4.5, 
respectively. Comet scores and plasma catalase activities in hyperbilirubinemic 
newborns were significantly higher before phototherapy, compared with the values 
after phototherapy and in the control groups (p < 0.001). There was no 
statistical difference between the 'after phototherapy' group and the controls 
(p > 0.05). These results indicate that high serum bilirubin level has genotoxic 
effects as is evident from the high rate of DNA strand-breaks in jaundiced 
newborns. Also PT does not cause an increase in DNA oxidation or induce the 
genotoxic effects of bilirubin. The counteracting effect of higher catalase 
activities in hyperbilirubinemic newborns may be responsible for the 
inactivating toxic and DNA-damaging effects of PT.