Abstract
Ultraviolet A (UVA) radiation is harmful for living organisms but in low doses may stimulate cell proliferation. Our aim was to examine the relationships between exposure to different low UVA doses, cellular proliferation, and changes in cellular reactive oxygen species levels. In human colon cancer (HCT116) and melanoma (Me45) cells exposed to UVA doses comparable to environmental, the highest doses (30–50 kJ/m2) reduced clonogenic potential but some lower doses (1 and 10 kJ/m2) induced proliferation. This effect was cell type and dose specific. In both cell lines the levels of reactive oxygen species and nitric oxide fluctuated with dynamics which were influenced differently by UVA; in Me45 cells decreased proliferation accompanied the changes in the dynamics of H2O2 while in HCT116 cells those of superoxide. Genes coding for proteins engaged in redox systems were expressed differently in each cell line; transcripts for thioredoxin, peroxiredoxin and glutathione peroxidase showed higher expression in HCT116 cells whereas those for glutathione transferases and copper chaperone were more abundant in Me45 cells. We conclude that these two cell types utilize different pathways for regulating their redox status. Many mechanisms engaged in maintaining cellular redox balance have been described. Here we show that the different cellular responses to a stimulus such as a specific dose of UVA may be consequences of the use of different redox control pathways. Assays of superoxide and hydrogen peroxide level changes after exposure to UVA may clarify mechanisms of cellular redox regulation and help in understanding responses to stressing factors.
Highlights
Ultraviolet radiation is the non-ionizing part of the electromagnetic radiation spectrum with a wavelength of 100–400 nm, invisible to human sight
HCT116 and Me45 cells were exposed to a range of Ultraviolet A (UVA) radiation doses (0.05, 0.1, 0.25, 0.5, 1, 5, 10, 15, 20, 30, 40, or 50 kJ/m2) and their proliferation was studied by clonogenic tests
We assumed that the increase of surviving fraction observed upon exposition to some doses of UVA reflect induction of cell proliferation, rather than decrease in apoptosis as the basal apoptotic fraction in studied cells was very small (< 6%) and its decrease would not cause change significant enough to be detected by clonogenic survival assay
Summary
Ultraviolet radiation is the non-ionizing part of the electromagnetic radiation spectrum with a wavelength of 100–400 nm, invisible to human sight. The sun is a natural emitter of UV divided into three main fractions UVA (315–400 nm), UVB (280–315 nm), and UVC (100– 280 nm), but most of this radiation is blocked by the atmosphere [1,2]. UVA constitutes the largest part (*95%) of UV radiation that reaches the Earth’s surface [3], whereas UVB represents only 4–5% [1]. Specific cell responses to UVA and ROS regulation no direct impact on DNA, but it can influence cellular structures indirectly by induction of reactive oxygen species (ROS) which can damage macromolecules [1, 4]. For a long time UV was regarded as damaging for cells and organisms [5], but since a few decades it is known that low doses can stimulate proliferation of cells; the mechanisms underlying this phenomenon are not completely understood [1, 3, 6, 7]
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