Abstract

BackgroundGeneration of reactive oxygen species (ROS), triggered by ultraviolet radiation (UVR), is associated with carcinogenesis of the skin. UV irradiation induced superoxide anion (O2•−) is the key ROS involved in the cellular damage. The cytoprotective efficacy of an unknown anti-oxidant compound can be evaluated by analyzing the production of O2•− from treated cells.MethodsIn this study, a glass carbon electrode functionalized with nanotube@DNA-Mn3(PO4)2 composite was applied to quantitative determination of generation of highly unstable O2•− from the melanoma A375 cell line following UVR(UV, UVA and UVB). In addition, the cytoprotective efficacy of anti-oxidant α-tocopherol was evaluated by quantifying the production of O2•−.ResultsThe results showed that, UVR triggers generation of O2•− in melanoma A375 cells, and α-tocopherol is effective in diminishing the production of O2•− following UV irradiation. By comparing the conventional cell-survival assays results, we found that our simple and quick electrochemical sensing method can quantify O2•− generation through the biological activity of an anti-oxidant compound (α-tocopherol).ConclusionOur label-free electrochemical quantification method for ROS (O2•− major) in cells facing UVR stress demonstrates its potential application for high-throughput screening of anti-oxidation compounds.

Highlights

  • Generation of reactive oxygen species (ROS), triggered by ultraviolet radiation (UVR), is associated with carcinogenesis of the skin

  • A carbon nanotube@DNAMn3(PO4)2compositefunctionalized glass carbon electrode was applied for quantitative determination of O2−generation from melanoma cell A375 following UV, Ultraviolet A (UVA), Ultraviolet B (UVB) irradiation

  • The dismutation of superoxide ion was catalyzed by Mn3(PO4)2 sheets, but the carbon nanotubes (CNTs) allows quick shifts of electrons to maximize its sensitivity, specificity and reproducibility for O2− detection [34]

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Summary

Introduction

Generation of reactive oxygen species (ROS), triggered by ultraviolet radiation (UVR), is associated with carcinogenesis of the skin. UV irradiation induced superoxide anion (O2−) is the key ROS involved in the cellular damage. It is well documented that UVR can stimulate the production of a series of ROS [3,4,5], which may cause cellular oxidative stress injury that is believed to be one of the key. UVC (100–290 nm) is absorbed by ozone (O3) in the upper atmosphere but UVB and UVA reach to earth surface, are the major fractions linked to skin diseases. Since UV fractions reach different biological layers of skin and lead to skin pathology via different cellular pathways. Petersen et al reported that superoxide anion (O2−) production in HaCaT cells was probably linked to DNA damage induced by UVA [13]. UVB can induce the formation of ROS, leading to cellular damage [14,15,16]

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