Photodynamically-induced Apoptosis Due to Ultraviolet A in the Presence of Lomefloxacin in Human Promyelocytic Leukemia Cells

Abstract

Lomefloxacin (LFX) is a widely used fluoroquinolone antimicrobial agent that plays an important role in the treatment of human and animal infections; however, it has been reported to cause phototoxicity. In this study, we investigated the induction of apoptosis due to ultraviolet A (UVA) light in the presence and absence of LFX in HL-60 human promyelocytic leukemia cells. HL-60 cells were exposed to UVA at an intensity of 1.1 mW/cm² for 20 min in the presence and absence of LFX, and the induction of apoptosis was examined by analyzing cell morphology, DNA fragmentation, and caspase-3 activity. Cells treated with 100 μM LFX and UVA clearly showed membrane blebbing and cell shrinkage. The proportion of apoptotic cells was significantly higher in cells treated with both UVA and LFX than in those treated with UVA or LFX alone. In addition, DNA ladder formation and caspase-3 activation were observed in cells treated with both UVA and LFX. A significant reduction in the number of UVA-induced apoptotic cells and caspase-3 activation was observed when histidine was present, which suggested that photodynamically-generated singlet oxygen is an important mediator of apoptosis. These results indicate that the combination of UVA and LFX induces apoptosis in HL-60 cells.

Keywords: Apoptosis; HL-60; caspase-3; lomefloxacin; reactive oxygen species; ultraviolet A.