Cytotoxicity and Mutagenicity of Narrowband UVB to Mammalian Cells.

Dylan J Buglewicz,Jacob T Mussallem,Cathy Su,Takamitsu A Kato,Alexis H Haskins,Junko Maeda

doi:10.3390/genes11060646

Dylan J Buglewicz, Jacob T Mussallem + Show 4 more

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https://doi.org/10.3390/genes11060646

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Journal: Genes	Publication Date: Jun 11, 2020
Citations: 10	License type: CC BY 4.0

Affiliation: Colorado State University

Abstract

Phototherapy using narrowband ultraviolet-B (NB-UVB) has been shown to be more effective than conventional broadband UVB (BB-UVB) in treating a variety of skin diseases. To assess the difference in carcinogenic potential between NB-UVB and BB-UVB, we investigated the cytotoxicity via colony formation assay, genotoxicity via sister chromatid exchange (SCE) assay, mutagenicity via hypoxanthine phosphoribosyltransferase (HPRT) mutation assay, as well as cyclobutane pyrimidine dimer (CPD) formation and reactive oxygen species (ROS) generation in Chinese hamster ovary (CHO) and their NER mutant cells. The radiation dose required to reduce survival to 10% (D10 value) demonstrated BB-UVB was 10 times more cytotoxic than NB-UVB, and revealed that NB-UVB also induces DNA damage repaired by nucleotide excision repair. We also found that BB-UVB more efficiently induced SCEs and HPRT mutations per absorbed energy dosage (J/m2) than NB-UVB. However, SCE and HPRT mutation frequencies were observed to rise in noncytotoxic dosages of NB-UVB exposure. BB-UVB and NB-UVB both produced a significant increase in CPD formation and ROS formation (p < 0.05); however, higher dosages were required for NB-UVB. These results suggest that NB-UVB is less cytotoxic and genotoxic than BB-UVB, but can still produce genotoxic effects even at noncytotoxic doses.

Highlights

As ultraviolet C (UVC) is blocked by the earth’s atmosphere, it is ultraviolet A (UVA) and ultraviolet B (UVB) radiation that are responsible for the effects of ultraviolet radiation (UVR) on the epidermal layer of the skin, but can be used to treat skin diseases
We examined the cytotoxicity via cell survival, genotoxicity via sister chromatid exchange (SCE) frequency, mutagenicity via hypoxanthine phosphoribosyltransferase (HPRT) mutation frequency, as well as Cyclobutane Pyrimidine Dimer (CPD) formation and reactive oxygen species (ROS) generation of narrowband UVB (NB-UVB) in comparison to broadband UVB (BB-UVB) in mammalian Chinese hamster ovary (CHO) and their nucleotide excision repair (NER) mutant cells
Our results indicate that at cytotoxic dosages of NB-UVB, far lower than the dosages used in that study, we were able to observe a significant increase in CPD formation (Figure 5d)

Summary

Introduction

As ultraviolet C (UVC) is blocked by the earth’s atmosphere, it is ultraviolet A (UVA) and ultraviolet B (UVB) radiation that are responsible for the effects of ultraviolet radiation (UVR) on the epidermal layer of the skin, but can be used to treat skin diseases. Unlike UVB, UVA is relatively ineffective for treatment of skin diseases unless used with the light-sensitizing medication psoralen, which is administered topically or orally. NB-UVB has become favored over BB-UVB, as it has been demonstrated to be more effective in the treatment of psoriasis [2], as well as effective in treating polymorphic light eruption [5], atopic eczema [6], and many other inflammatory dermatoses. It is considered safer and/or more practicable than P-UVA in the management of psoriasis [7]

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