Hydroxyl radical induced oxidation of theophylline in water: a kinetic and mechanistic study

Oxidative destruction and mineralization of emerging organic pollutants by hydroxyl radicals ((OH)-O-center dot) is a well established area of research. The possibility of generating hazardous by-products in the case of (OH)-O-center dot reaction demands extensive investigations on the degradation mechanism. A combination of pulse radiolysis and steady state photolysis (H2O2/UV photolysis) followed by high resolution mass spectrometric (HRMS) analysis have been employed to explicate the kinetic and mechanistic features of the destruction of theophylline, a model pharmaceutical compound and an identified pollutant, by (OH)-O-center dot in the present study. The oxidative destruction of this molecule, for intermediate product studies, was initially achieved by H2O2/UV photolysis. The transient absorption spectrum corresponding to the reaction of (OH)-O-center dot with theophylline at pH 6, primarily caused by the generation of (T8-OH)(center dot), was characterised by an absorption band at 330 nm (k(2) = (8.22 +/- 0.03) x 10(9) dm(3) mol(-1) s(-1))" A significantly different spectrum (lambda(max): 340 nm) was observed at highly alkaline pH (10.2) due to the deprotonation of this radical (pK(a) similar to 10.0). Specific one electron oxidants such as sulphate radical anions (SO4 center dot-) and azide radicals (N-3(center dot)) produce the deprotonated form (T(-H center dot)) of the radical cation (T center dot+) of theophylline (pK(a) 3.1) with k(2) values of (7.51 +/- 0.04) x 10(9) dm(3) mol(-1) s(-1) and (7.61 +/- 0.02) x 10(9) dm(3) mol(-1) s(-1) respectively. Conversely, oxide radicals (O center dot-) react with theophylline via a hydrogen abstraction protocol with a rather slow k(2) value of (1.95 +/- 0.02) x 10(9) dm(3) mol(-1) s(-1). The transient spectral studies were complemented by the end product profile acquired by HRMS analysis. Various transformation products of theophylline induced by (OH)-O-center dot were identified by this technique which include derivatives of uric acids (i, iv & v) and xanthines (ii, iii & vi). Further breakdown of the early formed product due to (OH)-O-center dot attack leads to ring opened compounds (ix-xiv). The kinetic and mechanistic data furnished in the present study serve as a basic frame work for the construction of (OH)-O-center dot induced water treatment systems as well as to understand the biological implications of compounds of this kind.