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Zhang, JR; Vrecko, K; Nadlinger, K; Tomic, DS; Birkmayer, GD; Reibnegger, G.
The Reduced Coenzyme Nicotinamide Adenine-Dinucleotide (NADH) Repairs DNA-Damage of PC12 Cells Induced by Doxorubicin
J TUMOR MARKER ONCOLOGY. 1998; 13: 5-17.
Web of Science

Co-authors Med Uni Graz: Reibnegger Gilbert; Vrecko Karoline
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Abstract:: The effect of NADH on DNA repair was investigated on PC12 cells, damaged by doxorubicin. PC12 cells were incubated in medium without and with NADH before and after exposure to the DNA damaging agent doxorubicin. The changes of the cell proliferation genes (c-myc, c-erbB-2), the apoptosis inhibition gene bcl-2 and p53 (tumor suppressor gene), cell apoptosis gene (c-fos) and the proliferating cell nuclear antigen (PCNA) were investigated using a cytotoxicity assay and immunofluorescence flow cytometric analysis. Doxorubicin induced DNA damage in PC 12 cells by inhibiting the expression of the cell proliferation genes and by triggering apoptotic processes in the cells. This was shown by down regulating the expression of c-erb-2, c-myc, bcl-2 and upregulating the expression of PCNA and c-fos of the PC 12 cells. NADH did not only increase the resistance of PC 12 cells to the doxorubicin induced DNA damage but also repaired the damage partially. NADH promoted survival and differentiation by regulating the c-myc oncogene protein. Furthermore it supported the process of DNA repair by regulating the expression of p53 bcl-2 on the PC12 cells damaged by doxorubicin. NADH also down regulated expression of the cell apoptosis gene c-fos on the PC12 cells. The expression of c-erbB-2 oncogene protein and PCNA on the PC12 cells did not show a significant change in the group of cells incubated with NADH in comparison to the group incubated with medium alone. In addition, an abnormal proliferation effect of NADH on PC12 cells has not been observed in these experiments. For these results we conclude that NADH may be considered as a therapeutic adjunct for cancer patients to protect normal cells from the toxic effect of chemotherapeutic agents such as doxorubicin or cisplatin by stimulating the DNA repair system and by promoting normal cellular biosynthetic responses after chemotherapy.