Ultraviolet light-emitting diode irradiation induces reactive oxygen species production and mitochondrial membrane potential reduction in HL-60 cells

Objective Ultraviolet light-emitting diode (UV LED) irradiation at 280 nm has been confirmed to induce apoptosis in cultured HL-60 cells, but the underlying mechanisms remain unclear. This study aimed to investigate the effects of 280 nm UV LED irradiation on reactive oxygen species (ROS) production and mitochondrial membrane potential (MMP) in HL-60 cells. Methods HL-60 cells were irradiated with 0, 8, 15, or 30 J/m(2) of 280 nm UV LED and incubated for 2 hours. The intracellular ROS levels were assessed using the fluorescent probe 2MODIFIER LETTER PRIME-7MODIFIER LETTER PRIME-dichlorodihydrofluorescein diacetate (DCFH-DA) and a fluorescence plate reader. MMP was determined by flow cytometry using 5,5MODIFIER LETTER PRIME,6,6MODIFIER LETTER PRIME-tetrachloro-1,1MODIFIER LETTER PRIME,3,3MODIFIER LETTER PRIME-tetraethylbenzimidazol-carbocyanine iodide (JC-1) staining. The apoptosis-related proteins Bax and Bcl-2 were evaluated by western blot. Results UV LED irradiation at 280 nm induced a dose-dependent increase in ROS production and loss of MMP, and it activated apoptosis at irradiation doses of 8 to 30 J/m(2). These results were consistent with a previous apoptosis study from the authors' group. Conclusion Enhanced ROS production and mitochondrial depolarization are two distinct but interacting events, and both are involved in UV LED-induced apoptosis in HL-60 cells.

Automated summary

UV LED irradiation at 280 nm induces ROS production and loss of MMP in HL-60 cells, leading to apoptosis, suggesting that enhanced ROS production and mitochondrial depolarization are important events in UV LED-induced apoptosis.