REACTIVITY AND SELECTIVITY OF NITRENIUM IONS DERIVED FROM ESTER DERIVATIVES OF CARCINOGENIC N-(4-BIPHENYLYL)HYDROXYLAMINE AND THE CORRESPONDING HYDROXAMIC ACID

N-Acetyl-N-(sulfonatooxy)-4-aminobiphenyl (1a) and N-(4-biphenylyl)-O- pivaloylhydroxylamine (1c) decompose in 5% CH3CN/H2O, mu = 0.5 M, at 2 0-degrees-C via rate-limiting N-O bond heterolysis to generate the nit renium ion intermediates 2a and 2b, respectively. Addition of Cl- (les s-than-or-equal-to 0.5 M) or N3- (less-than-or-equal-to 0.05 M) causes a marked decrease in the yields of all hydrolysis products derived fr om 1a and 1c, except the rearrangement products 10a and 11, without an y change in the hydrolysis rate constants. At 0.5 M Cl- more than 75% of the trappable hydrolysis products of 1a are replaced by the chloro adduct 7a without any observable change in the hydrolysis rate constan t, and at 0.025 M N3- 96% of the trappable hydrolysis products of 1a a re replaced by the azide adduct 8a, again, without an observable chang e in the hydrolysis rate constant. Similar results are obtained for 1c . The nucleophile/solvent selectivity ratios, k(Cl)/k(s) and k(az)/k(s ) are 7.4 +/- 0.3 M-1 and (1.02 +/- 0.04) x 10(3) M-1, respectively, f or 2a. For 2b k(Cl)/k(s) is 15.7 +/- 0.8 M-1 and k(az)/k(s) is (2.9 +/ - 0.2) x 10(3) M-1. If k(az) is at the diffusion controlled limit of 5 x 10(9) M-1 s-1, k(s) for 2a is 4.9 x 10(6) s-1, and k(s) for 2b is 1 .7 x 10(6) s-1. Both of these ions are considerably less labile to sol vent attack than 1-phenylethyl or cumyl carbocations with a 4-phenyl s ubstituent. Surprisingly, 2a and 2b differ in their reactivity to solv ent by only a factor of 3, while the estimated rate constants for thei r generation from starting materials with identical leaving groups dif fer by a factor of 10(6). This phenomenon is similar to the situation previously observed by Richard for 1-aryl-2,2,2-trifluoroethyl and 1-a rylethyl carbocations and may be due to similar factors. A detailed me chanism for the hydrolysis of 1a and 1c, which is consistent with all available experimental data, is presented. The implications of these r esults for the mechanisms of chemical carcinogenesis by N-arylhydroxyl amine derivatives are discussed.