Alkali-induced decomposition of (2-hydroxyalkyl)cobaloximes

Article abstract of DOI:10.1021/om00130a001

The mechanism by which (2-hydroxyethyl)(pyridine)cobaloxime decomposes in alkaline solution yielding acetaldehyde and cobaloxime(I) anion has been reinvestigated. The reaction is characterized by a complex hydroxide ion dependence, varying from second order in weakly basic solution to apparent first order near 0.2 N sodium hydroxide, with an extrapolation to zeroeth order in strongly alkaline solution. The reaction exhibits a negligible kinetic deuterium isotope effect [for (2-hydroxypropyl)(pyridine)cobaloxime-2-d] and is inhibited by excess pyridine or by cyanide ion. (Formylmethyl)cobaloxime is unreactive in alkaline solution and is therefore not an intermediate. A mechanistic pathway is suggested by the conversion of (3-hydroxypropyl)(pyridine)cobaloxime in (CD₃)₂SO-D₂O-NaOD into a cis-cobaloxime, with intramolecular ligation of the propyloxy substituent to cobalt, as observed by NMR spectroscopy. It is concluded that the hydride migration-displacement mechanism previously proposed for alkaline decomposition of (2-hydroxyethyl)(pyridine)cobaloxime is incorrect. Present evidence suggests that the rate-limiting step is conversion to a cis-cobaloxime, with a rapid subsequent σ- to π-complex conversion, ultimately yielding the enol of acetaldehyde. The reaction is actually second order in hydroxide but is simultaneously subject to first-order hydroxide inhibition.