Abstract— –Photohemolysis of erythrocytes. from patients with erythropoietic protoporphyria results from damage to the cell membrane following photoexcitation of the protoporphyrin molecule by 400 nm radiation. Photochemical reactions were assessed for their roles in initiating cell destruction in an in vitro model in which erythrocytes from patients with erythropoietic protoporphyria were irradiated. Electron transfer properties were demonstrated using 2,3,6‐trichloroindophenol as an electron acceptor. Photohemolysis of these abnormal cells is due to cell membrane damage initiating colloid osmotic hemolysis. Additional data are offered demonstrating that this type of photohemolysis is oxygen‐dependent, associated with peroxide formation, and preceded by increased osmotic fragility. An hypothesis explaining the interrelationship of the photochemistry of protoporphyrin with the photobiologic observation of hemolysis is offered.

Skin tumors were induced in hairless mutant mice following a single exposure to ultraviolet radiation (UV). Tumors were first noted as early as 7 weeks following irradiation. The UV, emitted by FS20/40T12 fluorescent lamps, was principally in the 280-320 nm spectral region with a peak at 3 13 nm. Single (skin surface) doses of 3 x lo' J/m2 to 24 x lo' J/m2 were delivered in 3 h or less. The higher doses resulted in more severe acute damage as well as greater tumor yield.Most of the tumors were benign hyperplastic epithelial papillomas; 4 out of 96 tumors examined histologically proved to be squamous cell carcinomas. This appears to be the first report of experimental carcinogenesis due to a single UV exposure, not requiring exogenous chemical promotion.

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