A further characterization of acridine-photosensitized inhibition of mast cell degranulation.
The purpose of this study was to further characterize acridine-photosensitized inhibition of mast cell degranulation. Acridine plus UVA radiation (320-400 nm) inhibited degranulation in response to antigen in IgE-sensitized rat serosal mast cells and in response to concanavalin A, which acts by a mechanism similar to antigen-IgE challenge. Removing oxygen from the incubation medium prevented the acridine-photosensitized inhibition of mast cell degranulation in response to 48/80. Acridine plus UVA radiation did not decrease mast cell ATP content, thus excluding inhibition of ATP production as a mechanism for photosensitized inhibition of mast cell degranulation. Although the viability of mast cells, as determined by uptake of trypan blue, was not affected 3 h after treatment with acridine plus UVA radiation, viability decreased by 6 h, and by 22 h 44% of the cells were nonviable. These results indicate that degranulation of mast cells by a variety of agents is inhibited by UVA plus acridine treatment, and that photosensitization requires oxygen and occurs before cytotoxicity.
Wellman Laboratories, Department of Dermatology, Harvard Medical School, Massachusetts General Hospital, Boston.
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D000166:Acridines / Q000494:pharmacology*; D000255:Adenosine Triphosphate / Q000032:analysis; D000818:Animals; D015550:Cell Degranulation / Q000187:drug effects / Q000528:radiation effects*; D002463:Cell Membrane Permeability / Q000187:drug effects / Q000528:radiation effects; D002470:Cell Survival / Q000187:drug effects / Q000528:radiation effects; D002478:Cells, Cultured; D003208:Concanavalin A / Q000494:pharmacology; D007073:Immunoglobulin E / Q000276:immunology; D008297:Male; D008407:Mast Cells / Q000187:drug effects / Q000502:physiology*; D051381:Rats; D011919:Rats, Inbred Strains; D014466:Ultraviolet Rays
D000166:Acridines; D003208:Concanavalin A; D007073:Immunoglobulin E; D000255:Adenosine Triphosphate