COMPARATIVE ACTION SPECTRUM FOR ULTRAVIOLET-LIGHT KILLING OF MOUSE MELANOCYTES FROM DIFFERENT GENETIC COAT COLOR BACKGROUNDS

The photobiology of mouse melanocyte lines with different pigment geno types was studied by measuring colony-forming ability after irradiatio n. The cell lines were wildtype black (melan-a) and the mutants brown (melan-b) and albino (melan-c). Four lamps emitting various UV wavelen gths were used. These were germicidal (UVC, 200-280 nm), 82.3% output at 254 nm, TL01 (UVB, 280-320 nm), 64.2% at 310-311 nm, FS20, broadban d with peak output at 312 nm and Alisun-S (WA, 320-400 nm), broadband with peak output at 350-354 nm. Appropriate filtration reduced the con taminating UVC to nonlethal levels for the longer waverange lamps, Wil d-type melan-a was resistant to UVC and UVA compared to the other two cell lines, but the differences were small. The melan-c cell line was more resistant to UVB and markedly more resistant to FS20 than the pig mented lines. With the exception of FS20 responses, melan-b was more s ensitive than melan-a to killing by the various UV lamps. There were m ore pyrimidine dimers (cyclobutane dimers and 6-4 photoproducts) produ ced in melan-a than in melan-c cells by UVC, UVB and FS20 lamps. Unlik e melan-c, melan-a and melan-b showed a strong free radical signal of melanin character with a detectable contribution of pheomelanin-like c enters. The contribution of pheomelanin was higher in melan-b than in melan-a, while the total melanin content in these two cell lines was c omparable. The abundant melanin granules of wild-type melan-a melanocy tes were well melanized and ellipsoidal, whereas those of melan-b mela nocytes tended to be spherical. In the albino line (melan-c) the melan ocytes contained only early-stage melanosomes, all of which were devoi d of melanin. The results indicate that pigment does not protect again st direct effect DNA damage in the form of pyrimidine dimers nor does it necessarily protect against cell death. High pigment content is not very protective against killing by UVC and UVA, and it may photosensi tize in UVB the very wavelength range that is of greatest concern with respect to the rising incidence in skin cancer, especially melanoma. It is clear from these studies that, in pigment cells, monochromatic r esults cannot predict polychromatic responses and that cell death from solar irradiations is a complex phenomenon that depends on more than DNA damage.