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The Effects of the Broadband UVA Radiation on Myeloid Leukemia Cells: The Possible Role of Protein Kinase C in Mediation of UVA-lnduced Effects
Authors:Dariusz Leszczynski  Susanna Fagerholm  Kirsti Leszczynski
Institution:Radiobiology Laboratory, Finnish Centre for Radiation and Nuclear Safety, Helsinki, Finland;Non-lonizing Radiation Laboratory, Finnish Centre for Radiation and Nuclear Safety, Helsinki, Finland
Abstract:Abstract— We examined the effects of broadband UVA radiation (320–400 nm) on a rat myeloid leukemia cell line–chlo-roma (ChL). A Phillips face tanner model HB 171/A was used as a light source. Chloroma were irradiated through a 5 mm thick glass Alter that cut off all of the UVB contamination. The irradiances were measured, from 250 to 400 nm, with a well-characterized and calibrated double-grating spectroradiometer Optronic 742. The overall uncertainty of dose evaluation was estimated to be <15% (2s?). The cells were irradiated with UVA doses of 4 and 8 J/cm2 and cultured thereafter for 24 h. After this period of time, a marked decline up to 50% was observed in cell proliferation in UVA-irradiated ChL cultures. The cell proliferation decline was found to be caused by simultaneously occurring G2/M phase cell cycle arrest and apoptosis in part of the UVA-irradiated ChL population. Concomitantly, with the decline in cell proliferation, an increase was observed in the expression of the major histocompatibility (MHC) class I and II antigens. Because protein kinase C (PKC) is known to regulate cell proliferation, apoptosis and expression of MHC antigens, and because UVA was shown to regulate PKC activity/expression, we therefore examined whether UVA irradiation has any effect on the expression of isozymes of PKC. Western blots revealed that ChL express α, βI, δ, α, γ, and π isozymes of PKC and that expression of all isozymes declined 24 h after UVA irradiation (8 J/cm2). Finally, PKC activation in ChL by exposure to phorbol ester caused cell cycle arrest in G1 phase but did not induce apoptosis. This suggests that the previously shown UVA-induced PKC activation in ChL might be responsible for the induction of MHC antigens but the simultaneously observed ChL apoptosis is likely to be mediated by PKC down-regulation. All together, our results suggest that UVA, at irradiance levels that resemble the outdoor exposure, may have profound effects on the immune-related properties of leukocytes. Thus, we speculate that in vivo the immune functions of leukocytes passing through dermal capillaries might be altered by exposure to solar UVA radiation.
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