The aim of this study is to investigate the mechanism of skin adaptation to low-dose ultraviolet A (UVA), changes in mitochondrial reactive oxygen species (ROS) levels, and mitochondrial DNA 4977-bp deficiency (ΔmtDNA4977) in fibroblasts, keratinocytes, and melanocytes.
Background:
The mechanisms related to the adaptive response of low doses of UVA in the skin remain to be studied, which could provide a basis for light avoidance and treatment.
Methods:
Skin cells were cultured with different doses of UVA. Laser confocal scanning microscopy was used to observe mitochondrial fluorescence intensity following MitoTracker Red CMX Ros and MitoTracker Red CM-H2X Ros staining. Additionally, the effects of different cumulative UVA irradiation doses on the mitochondrial number and ROS levels were determined. The total mtDNA mutation level and incidence of ΔmtDNA4977 were comparatively quantified using the real-time polymerase chain reaction.
Results:
Cells exposed to low-dose UVA showed changes in cell aging, and acute toxic reactions were observed in cells exposed to high-dose UVA. The acute toxic reactions were less severe in the adaptive response group than in the high-dose group. UVA irradiation could induce mitochondrial ROS production. Intracellular ROS levels increased swiftly following high-dose UVA irradiation, while low-dose UVA irradiation induced a steady low-level increase in intracellular ROS compared with the sham irradiation group (p < 0.01).
Conclusions:
Low-dose UVA irradiation exposure induced a sustained low level of mitochondrial ROS production. Besides signal transduction, the adaptive response may be triggered and maintained by ΔmtDNA4977, resulting in a low level of mitochondrial ROS.
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