Role of complement in chlorpromazine-induced phototoxicity

To evaluate the role of the complement system in inflammation induced by chlorpromazine (CPZ) and ultraviolet-A (UVA) irradiation, the phototoxic response in guinea pigs decomplemented by cobra venom factor was compared with that in saline-treated animals. Phototoxic lesions were induced in animals by intradermal injections of CPZ solution, followed by UVA irradiation. Clinically, the normal animals developed erythema and induration which showed a maximal response at 10 h with a mean value of 1.6 on a scale of 0 to 3+. The complement-depleted animals showed a weaker clinical response than the normal animals 6-24 h postirradiation (p less than 0.05). These clinical changes were associated with increased vascular permeability, as demonstrated by extravasation of i.v. injected Evans blue in saline-treated animals. In vitro UVA irradiation of serum containing CPZ resulted in a dose-dependent diminution of total complement activity. Such irradiated serum showed immunoelectrophoretic C3 conversion. These results suggest that the complement system is involved in the development of CPZ-induced phototoxic lesions.