Environmental health perspectives · 2008
Activated toxicity of diesel particulate extract by ultraviolet a radiation in mammalian cells: role of singlet oxygen.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Bao Lingzhi, Xu An, Tong Liping, Chen Shaopeng, Zhu Lingyan, Zhao Ye, Zhao Guoping, Jiang Erkang, Wang Jun, Wu Lijun
Аннотация
BACKGROUND: Diesel exhaust [diesel exhaust particles (DEPs) and their extracts (DPE)] and ultraviolet A radiation (UVA) are two ubiquitous environmental factors that have been identified as essential risk factors for various benign or malignant human diseases, either alone or in combination with other agents.
OBJECTIVES: We aimed to investigate the synergistic effects of DPE and UVA at low-dose exposures in human-hamster hybrid (AL) cells and their underlying mechanisms.
METHODS: We exposed exponentially growing AL cells to DPE and/or UVA radiation with or without reactive oxygen species (ROS) quenchers and then assayed the cells for survival, mutation induction, apoptosis, and micronucleus generation. In addition, using a singlet oxygen (1O2) trapping probe, 2,2,6,6-tetramethyl-4-piperidone, coupled with electron paramagnetic resonance spectroscopy, we determined the production of 1O2.
RESULTS: Treatment of AL cells with DPE+UVA induced significant cytotoxic and genotoxic damage. In contrast, we found no significant damage in cells treated with either UVA or DPE alone at the same doses. Mutation spectra of CD59- mutants showed that treatment with DPE+UVA easily induces multilocus deletions. Sodium azide significantly inhibited both cellular and DNA damage induced by DPE+UVA treatment, whereas other ROS inhibitors had little protecting effect. Furthermore, we found a significant increase of 1O2 in the cells that received DPE+UVA treatment.
CONCLUSION: These findings suggest that UVA activated the genotoxicity and cytotoxicity of DPE in mammalian cells and that 1O2 played an important role in these processes.
OBJECTIVES: We aimed to investigate the synergistic effects of DPE and UVA at low-dose exposures in human-hamster hybrid (AL) cells and their underlying mechanisms.
METHODS: We exposed exponentially growing AL cells to DPE and/or UVA radiation with or without reactive oxygen species (ROS) quenchers and then assayed the cells for survival, mutation induction, apoptosis, and micronucleus generation. In addition, using a singlet oxygen (1O2) trapping probe, 2,2,6,6-tetramethyl-4-piperidone, coupled with electron paramagnetic resonance spectroscopy, we determined the production of 1O2.
RESULTS: Treatment of AL cells with DPE+UVA induced significant cytotoxic and genotoxic damage. In contrast, we found no significant damage in cells treated with either UVA or DPE alone at the same doses. Mutation spectra of CD59- mutants showed that treatment with DPE+UVA easily induces multilocus deletions. Sodium azide significantly inhibited both cellular and DNA damage induced by DPE+UVA treatment, whereas other ROS inhibitors had little protecting effect. Furthermore, we found a significant increase of 1O2 in the cells that received DPE+UVA treatment.
CONCLUSION: These findings suggest that UVA activated the genotoxicity and cytotoxicity of DPE in mammalian cells and that 1O2 played an important role in these processes.