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《Redox report : communications in free radical research》2013,18(2):53-60
AbstractApoptosis is an important cell death system that deletes damaged and mutated cells, preventing the induction of cancer. We previously have reported that UV irradiation inhibited the apoptosis induced by serum starvation and cell detachment. This phenomenon is suitable for clarifying the relationship between cancer and the dysregulation of apoptosis by UV irradiation. Here, we have studied the factors responsible for this inhibition of apoptosis, focusing on reactive oxygen species (ROS) and DNA damage. Treatment with xanthine oxidase in the presence of hypoxanthine, which is known to produce superoxide anion (O2??) and hydrogen peroxide (H2O2), inhibited the induction of apoptosis. The xanthine oxidase-induced anti-apoptotic effect was suppressed in the presence of an H2O2-eliminating enzyme, catalase, but not in the presence of an O2??-eliminating enzyme, superoxide dismutase. Treatment with H2O2 itself significantly inhibited the induction of apoptosis. Furthermore, the effect of the inhibition of cell death by UVB irradiation and by H2O2 treatment decreased in H2O2-resistant cells. Although both UVB and H2O2 are known to induce DNA damage, other DNA damaging agents, like γ-irradiation and treatment with cisplatin and bleomycin, showed no inhibition of apoptosis. These findings suggested that H2O2 was essential to the inhibition of apoptosis, in which DNA damage had no role. 相似文献
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M. Tomita 《Redox report : communications in free radical research》2013,18(1):19-24
SUMMARYThe beginning of the cell death process initiated by paraquat is caused by oxygen-free radicals produced through the redox cycle. We examined the next step driven by the radicals focusing on changes in deoxyribonucleic acid (DNA) utilizing flow cytometry. A significant decrease in the proportion of cells was observed in the G0/G1 phase, while a remarkable accumulation of cells was noted in the S phase. Forward light scattering (FSC) and side light scattering (SSC) histograms of the particles from cells treated with paraquat showed a change in the size, the refractive index and the granularity of the nucleoids. By contrast, leakage of lactate dehydrogenase (LDH) was not observed during the period in which changes in DNA occurred. These results suggest that paraquat-induced DNA damage constitutes one of the next steps driven by free radicals, leading to the process of cell death. 相似文献
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Comparison of UVB and UVC Effects on the DNA Damage‐Response Protein 53BP1 in Human Pancreatic Cancer
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