Background Oxidative effects of phototherapy on cell membranes and cell components may have a wide range of potential adverse effects, including .DNA damage. Apoptosis is an indispensable mechanism for maintaining many cellular functions, including cell replication, and removal of damaged cells with high burden of genetic mutations. Many genes function as apoptosis regulatory genes. Examples of these genes include the BCL2 gene which is an anti-apoptotic oncogene, and the BAX gene which acts as a promoter of apoptosis.
Objectives Assess the effect(s) of phototherapy on DNA and on rate of apoptosis in full term neonates with hyperbilirubinemia. It comprised 35 neonates with indirect hyperbilirubinemia who received phototherapy for 48 hours, and 20 apparently healthy full term neonates with normal serum bilirubin level, as a control group. DNA damage was assessed by DNA fragmentation and micronucleus assay. Determination of the anti-apoptotic, (BCL2) protein, and Bax gene expression status.
Results The frequency of micronuclei in circulating lymphocytes of neonates who received phototherapy has significantly increased before and after phototherapy compared to controls. DNA fragmentation in circulating lymphocytes, was significantly higher among cases before and after phototherapy compared to controls. The plasma BCL2 protein was significantly lower in the cases before and after phototherapy compared to controls .and Bax gene expression was significantly high among cases before and after phototherapy compared to controls.
Conclusions Phototherapy induces more DNA damage and enhances apoptosis of exposed cells, probably through down regulation of BCL2 expression and upregulation of bax gene expression in neonates with hyperbilirubinemia.
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