Light-induced cytotoxicity and genotoxicity of a sunscreen agent, 2-phenylbenzimidazole in Salmonella typhimurium TA 102 and HaCaT keratinocytes

防晒剂2-苯基苯并咪唑对鼠伤寒沙门氏菌TA 102和HaCaT角质形成细胞的光诱导细胞毒性和遗传毒性

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Abstract

2-phenylbenzimidazole (PBI) is an ingredient found in sunscreen agents. PBI can absorb the UV portion of the solar light and undergo a series of light-induced reactions to cause adverse effects in humans. Therefore, chemical and photochemical toxicity of PBI were investigated in the bacteria Salmonella typhimurium TA 102 and human skin keratinocyte cells. There is no appreciable bacteria death due to the exposure to PBI alone, indicating that PBI is not chemically toxic to the bacteria at a dose as high as 625 microM. However, exposure to PBI and a solar simulator light (300-W Xe/Hg lamp, 30 min, 18.6 J/cm2, equivalent to 30 min outdoor sunlight) causes significant bacteria death: 35% at 25 microM and 55% at 625 microM PBI. Exposure of the bacteria to light and PBI at doses 5-25 microM causes the bacteria to revert, an indication of mutation. In the presence of PBI but without light irradiation, the number of revertant bacteria colonies is around 200 due to spontaneous mutation. Combination of light irradiation and PBI causes the number of revertant TA 102 colonies to increase in a dose dependent manner, reaching a maximum of around 1700 revertant colonies at 25 microM PBI. At higher PBI concentrations, the number of revertant colonies remains constant. This result clearly indicates that PBI is photomutagenic in TA 102. Exposure of the human skin HaCaT keratinocytes in aqueous solution in the presence of PBI causes the cell to lose its viability with or without light irradiation. There is no significant difference in cell viability for the light irradiated or non-irradiated groups, indication PBI is not photocytotoxic. However, exposure of the cells to both PBI and light irradiation causes cellular DNA damage, while exposure to PBI alone does not cause DNA damage.

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