The Mechanism of Quinone Formation from Carcinogenic Benzo[a]Pyrene Mediated by Lipid Peroxidation in Liposomal Suspension

Polycyclic aromatic hydrocarbons, including benzo[a]pyrene (B[a]P), are widely distributed in the environment and some of them are known to possess potent carcinogenicity. B[a]P is metabolized to ultimate or proximate carcinogenic form by subcellular mixed function oxidase system. Lipid peroxides and their derived radicals are suggested to play a role in the metabolic activation of B[a]P. Earlier works showed that B[a]P quinones were formed as main products when B[a]P was cooxidized by nonenzymatic lipid peroxidation of polyunsaturated fatty acids1 or of liver microsomal membrane2. The contribution of quinone formation to the carcinogenic activation of B[a]P is suggested by the following observations: (i) Intermediates in quinone formation can bind to DNA and cause DNA strand scission. (ii) B[a]P quinone possesses mutagenicity. (iii) B[a]P quinone generates active oxygen species by the reduction and oxidation cycle involving quinone, hydroquinone and molecular oxygen. Such active oxygens are recently recognized to act as potent promoters in carcinogenesis. The purpose of this work is to know the mechanism of lipid peroxidation-mediated quinone formation from B[a]P in biomembranes by using a water-soluble azo compounds as the free radical initiator in a liposomal suspension3.