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The primary selectivity denoted by S is determined, in fact, by the sum of selectivities of each cytochrome-dependent reaction. Primary selectivity (S) = axrxPx + a2r2P2 + · · •/ßi'"i + Wi + (1) In Eq. (1), rl9 r2, and so on are the total rates of carcinogen metabolism at the separate forms, and Pl9 P2, and so on are the respective fractions metabolized to a carcinogenic precursor. 2. 43 Integration of Xenobiotic Metabolism The partition of the metabolism of precursor P between activation to an electrophile U and detoxication can be represented by the diversionary detoxication factor D.

S. , and Okita, R. T. (1979). /« "Enzymatic Basis of Detoxication" (W. B. ), Vol. 1, pp. 183-199. Academic Press, New York. 31. Lu, A. Y. , and Coon, M. J. (1968). Role of hemoprotein P-450 in fatty acid omegahydroxylation in a soluble enzyme system from liver microsomes. J. Biol. Chem. 243, 1331-1332. 32. Kawalek, J. , Thomas, P. , and Lu, A. Y. H. (1975). Purification of liver microsomal cytochrome P-448 from 3-methylcholanthrene-treated rabbits. Mol. Pharmacol. 11, 874-878. 1. Metabolic Formation of Toxic Metabolites 25 33.

A. (1977). Thioacetamide-induced hepa­ tic necrosis. I. Involvement of the mixed-function oxidase enzyme system. J. Phar­ macol. Exp. Ther. 200, 439-448. 128. Porter, W. , Gudzinowicz, M. , and Neal, R. A. (1979). Thioacetamide-induced hepatic necrosis. II. Pharmacokinetics of thioacetamide and thioacetamide S-oxide in the rat. J. Pharmacol. Exp. Ther. 208, 386-391. 129. Boyd, M. , and Neal, R. A. (1976). Studies on the mechanism of toxicity and of development of tolerance to the pulmonary toxin, α-naphthylthioureau (ANTU).

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