A Mechanistic Study on the Oxidative Degradation of Dibenzazepine Derivatives by Manganese(III) Complexes in Acidic Sulfate Media

Abstract

ABSTRACTThe oxidative degradation of tricyclic antidepressants (TCA) was studied in the presence of a large excess of the oxidizing agent manganese(III) and its reduced form manganese(II) sulfate in acidic media. The products were detected and identified using UV–vis, ESI‐MS, IR, and EPR methods. The mechanism of the reaction was studied for the following two classes of TCA: 10,11‐dihydro‐5H‐dibenz[b, f]azepines and dibenz[b, f]azepines. The oxidative degradation between dibenz[b, f]azepines and the manganese(III) ions resulted in the formation of substituted acridine with the same substituent as in the origin dibenz[b, f]azepine derivative. The pseudo–first‐order rate constants (kobs) were determined for the degradation process. The dependences of the observed rate constants on the [MnIII] with a zero intercept were linear. The reaction between 10,11‐dihydro‐5H‐dibenz[b, f]azepines, and the manganese(III) sulfate ion resulted in oxidative dehydrogenation, which proceeded via the formation of the following two intermediates: a free organic radical and a dimer. Further oxidation of the second intermediate led to a positively charged radical dimer as the single final product. Linear dependences of the pseudo–first‐order rate constants (kobs) on the [MnIII] with a zero intercept were established for the degradation of 10,11‐dihydro‐5H‐dibenz[b, f]azepines. The observed rate constants were dependent on the [H+] and independent of the [TCA] within the excess concentration range of the manganese(III) complexes used in the isolation method. The radical product of the degradation of 10,11‐dihydro‐5H‐dibenz[b, f]azepines was not stable in the aqueous solution and was subsequently transformed to a nonradical dimer in the next slower step. The observed rate constants were independent of the [MnIII], independent of the [H+] and increased slightly with increasing TCA concentrations when TCA was used in excess. The mechanistic consequences of all of these results are discussed.