Materials and Methods: Twenty-five enamel slabs were divided into three treatment groups: light-activated bleaching, laser-activated bleaching, and control. The baseline data were recorded for enamel microhardness (Vickers microhardness [VMH]) and surface roughness (Roughness average, Ra). The specimens were cured for 10 min upon hydrogen peroxide application for the light-activated bleaching group and activated with a laser source, 8 cycles, 10 s per cycle for the laser-activated group. The changes in VMH and Ra at days 1, 7, and 28 were evaluated. Kruskal-Wallis, Friedman, Wilcoxon, and Mann-Whitney tests were used to analyze both VMH and Ra between the treatment groups at different time intervals.
Results: There were a significant reduction in VMH values and significant differences between days 1, 7, and 28 against the baseline in the light-activated bleaching group (P = 0.001). The Ra values revealed significant differences in both light- (P = 0.001) and laser-activated (P = 0.033) groups.
Conclusion: Light activation of a bleaching agent caused a reduction in enamel microhardness and an increase in surface roughness when compared to laser activation.
RESULTS: By using MAR/SAR recognition signature (MRS), potential MAR/SAR sites were predicted in the AF9 gene. The predicted MAR/SAR sites precisely match to the experimentally determined MAR/SARs. Hydrogen peroxide (H2O2) was used to induce apoptosis in normal nasopharyngeal epithelial cells (NP69) and NPC cells (HK1). Nested inverse polymerase chain reaction was employed to identify the AF9 gene cleavages. In the SAR region, the gene cleavage frequency of H2O2-treated cells was significantly higher than that of the non-treated cells. A few chromosomal breakages were detected within the AF9 region which was previously found to be involved in the mixed lineage leukaemia (MLL)-AF9 translocation in an acute lymphoblastic leukaemia patient. As for the non-SAR region, no significant difference in the gene cleavage frequency was found between the untreated control and H2O2-treated cells. Furthermore, H2O2-induced cleavages within the SAR region were reduced by caspase-3 inhibitor, which indirectly inhibits CAD.
CONCLUSIONS: These results reaffirm our previous findings that oxidative stress-induced apoptosis could be one of the potential mechanisms underlying chromosome breakages in nasopharyngeal epithelial cells. MAR/SAR may play a vital role in defining the location of chromosomal breakages mediated by oxidative stress-induced apoptosis, where CAD is the major nuclease.