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.
D000818:Animals; D002199:Capillary Permeability; D002746:Chlorpromazine / Q000633:toxicity*; D003167:Complement Activation; D003165:Complement System Proteins / Q000502:physiology*; D005260:Female; D006168:Guinea Pigs; D006801:Humans; D007123:Immunoelectrophoresis, Two-Dimensional; D010787:Photosensitivity Disorders / Q000209:etiology*; D014466:Ultraviolet Rays
D003165:Complement System Proteins; D002746:Chlorpromazine