Light-Induced Cytotoxicity and Genotoxicity of a Sunscreen Agent, 2-Phenylbenzimidazole in Salmonella typhimurium TA 102 and HaCaT Keratinocytes

Charity N Mosley,Stephanie Gilley,Hongtao Yu,Shuguang Wang,Lei Wang

doi:10.3390/ijerph2007040006

Charity N Mosley, Stephanie Gilley + Show 3 more

Open Access

https://doi.org/10.3390/ijerph2007040006

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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.

Highlights

There has been a shift in the paradigm of the American lifestyle
The aim of this study is to investigate the phototoxic and photomutagenic effect of PBI in the bacteria, Salmonella typhimurium strain TA 102 and human skin HaCaT keratinocytes upon concomitant exposure to PBI and light radiation
Dimethyl sulfoxide (DMSO), 8-methoxypsoralen (8MOP), and PBI were purchased from Sigma-Aldrich Chemical Company (Milwaukee, WI)

Summary

Introduction

In today’s society, the development of leisure activities, holiday habits, along with tanning through sunbathing or artificial tanning devices for cosmetic purposes, has caused an increase in ultraviolet radiation (UVR) exposure [1, 2]. Unnecessary sunlight exposure is known to induce acute and chronic modifications in the skin such as erythema, immune suppression, premature skin aging, and skin cancer [1, 35]. Natural sunlight includes UVA (320-400 nm), UVB (280-320 nm), UVC (200-280 nm), and visible (400-700 nm) radiation. UVA irradiation can penetrate into the dermal layer of the skin. UVB radiation, commonly referred to as the erythema band, is largely absorbed in the epidermis with a small portion reaching the upper dermal layer. The UVC radiation or the “germicidal radiation” does not reach the earth’s surface [4,5,6]

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