Long-wave ultraviolet radiation causes increase of membrane-bound fraction of protein kinase C in rat myeloid leukemia cells.

We examined the effect of long-wave ultraviolet radiation (UVA) on protein kinase C (PKC) and on the proliferation of rat myeloid leukemia cell line (ChL). Exposure of cells to a single dose of UVA (8 J/cm2 at 372 +/- 10 nm) caused a rapid increase in the quantity of the membrane-bound PKC, as assessed by 3H-phorbol ester (3H-PMA) binding assay (performed at 4 degrees C). Within 2 h of UVA irradiation, three peaks of increased 3H-PMA binding to the ChL cells (by 70-100%) were observed at ca. 20, 60 and 95 min post-irradiation. The exposure of ChL to UVA caused also a rapid, but transient, decline in the cell proliferation rate (by 18% within 24 h). However, the statistically significant decrease in cell numbers was observed only 3 days later (down by 22%). The inhibition of ChL proliferation was not due to alteration of cell viability as determined by trypan blue exclusion assay, and neither was it caused by cell cycle arrest or apoptosis, as determined by flow cytometry analysis of propidium iodide-labelled cells and cell morphology in May-Grünvald-Giemsa-stained cell smears. Phorbol-ester-induced activation of PKC (performed at 37 degrees C) caused inhibition of ChL proliferation similar to that caused by UVA. This suggests that a UVA-induced increase of the membrane-bound fraction of PKC may be responsible for the UVA-induced inhibition of ChL proliferation.