Disinfection with UVC light may significantly reduce environmental bacterial contamination and thereby protect the next patient housed in an isolation room. UVC disinfection may not be used alone but is a good addition to chemical disinfection.
The effects of UVA (365 nm) and UVB (297/302 nm) radiation on cellular proliferation, cell cycle progression, aneuploidy and multinucleus induction have been studied in two different fibroblast cell lines; V79 Chinese hamster lung fibroblasts and 3T3 Swiss albino mouse fibroblasts. UVA and UVB were found to inhibit proliferation of the cells in a fluence-dependent manner. This inhibition was due to a temporary accumulation of cells in the S phase of the cell cycle, as determined by flow cytometry of UV-irradiated V79 cells. The UVA- and UVB-induced S phase delay was observed a few hours after irradiation and by 48 h post-irradiation the cells had recovered from cell cycle arrest. For UVA, but not for UVB, the elongation of S phase was followed by a small accumulation of cells in the G2 phase. After exposure to UVA and a post-irradiation time long enough for the cells to recover from cell cycle arrest, a large proportion of the cells were polyploid, with two or more nuclei. Multinucleated cells were not, however, induced by UVB irradiation.
The effects of UVA (365 nm) radiation on the cellular distribution of F-actin and formation of binucleated cells have been studied using 3T3 Swiss albino mouse fibroblasts and V79 Chinese hamster fibroblasts. Ultraviolet A at biologically relevant fluences was found to disintegrate the actin filaments in the cells shortly (5 min) after irradiation, concomitant with the formation of cells with two nuclei. In 76-100% of the bi- and multinucleated cells the distribution of F-actin was clearly altered. Cells in GI phase of the cell cycle were most probably involved in the formation of binucleated cells. The disintegration of F-actin was presumably not due to depolymerization of F-actin to G-actin, as the amount of F-actin in the cells was unaltered after UVA exposure but rather due to direct breakage of the actin filaments. Ultraviolet B (297/302 nm) had no effect on the cellular distribution of microfilaments, not even at highly lethal fluences.
The effects of ultraviolet (UV) radiation on gap junctional intercellular communication (GJIC) in V79 Chinese hamster fibroblasts were studied by means of a dye transfer assay. Intercellular communication was shown to be altered by UVB (297/302 nm) and UVA (365 nm) radiation, the effect depending on the wavelength of exposure and time between irradiation and microinjection of the dye in the dye transfer assay. Exposure to 297/302 nm radiation induced a reduction in intercellular communication 6 min after exposure. Incubation of the cells post-irradiation reversed the inhibition of GJIC. From 2 to 24 h after exposure an increase in GJIC over the control cells was seen, with a maximum at 8 h post-irradiation. UVA (365 nm) radiation, on the other hand, induced an increase in the intercellular communication 6 min after irradiation. Incubation of the cells post-irradiation led to a decrease in the number of communicating cells, with a minimum seen 4 h after exposure. The reduction in communication observed after exposure to UVB and UVA was not correlated with similar modifications in the gap junction protein connexin43 as found when exposing the cells to the tumour promoter 12-O-tetradecanoyl-phorbol-13-acetate. For the higher fluences of UVA, a decrease in immunorecognizable connexin43 was seen, concomitant with a markedly increased background of higher mol. wt compounds. This may be due to UVA-induced crosslinking of connexin43. No correlation was found between changes in communication induced by UV radiation and levels of cyclic AMP.
When cells growing in monolayers are exposed to ultraviolet radiation (UV) their binding to the substratum is increased in strength. An action spectrum for such UV-induced binding was determined, using the time needed for trypsin-EDTA to detach the cells as a measure of the binding strength. This action spectrum was significantly different from the action spectrum for cell inactivation, which was also determined. At the shortest wavelengths (297/302, 313 nm) lethal fluences were needed to induce measurable binding while at the longest wavelengths (365, 405 nm) completely nonlethal fluences induced strong and persistent binding. Thus, different chromophores are involved in the two processes: while DNA may be the main chromophore for cell inactivation, other and unidentified chromophores may be more important for induction of increased cell binding to the substratum.
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