Participation of Mast Cells and Complement in the Immediate Phase of Hematoporphyrin-Induced Phototoxicity

We have investigated the roles of mast cells and the complement system in the immediate phase of hematoporphyrin-induced phototoxicity in guinea pigs. Clinically, i.v. injection of hematoporphyrin, followed by irradiation with a light source containing 400–405 nm wavelength, resulted in the immediate onset of erythema and edema, which subsided partially in 30–60 min. This was followed by the appearance of delayed erythema and edema, which peaked at 6–12 h after irradiation. Histologic examination of the response of the immediate phase, using a 1 μ-thick section, revealed eosinophil infiltration and mast cell degranulation. The immediate phase of the clinical response was further quantitated by the extravasation of intravenously injected [1251] bovine serum albumin. Pretreatment of the guinea pig skin with the intradermal injection of compound 48/80 significantly suppressed the increase in vascular permeability induced by hematoporphyrin and irradiation (p < 0.05). This hematoporphyrin-induced alteration in vascular permeability was also significantly inhibited by antihistamines, either H1 receptor antagonist alone (p < 0.05) or a combination of H1 and H2 receptor antagonists (P < 0.05). Guinea pigs depleted of complement also showed significantly less vascular permeability changes (p & 0.05). These results indicate that functionally intact mast cells, and the complement system, are required for the full development of the immediate phase of phototoxicity induced by hematoporphyrin