Toxicity of metoprolol (MET) alone and in mixtures with its photocatalytic degradation intermediates obtained by using TiO2 Wackherr and Degussa P25 under UV irradiation in the presence of O2 was evaluated in vitro in a panel of three histologically different cell lines: rat hepatoma (H-4-II-E), human colon adenocarcinoma (HT-29) and human fetal lung (MRC-5). Both catalysts promoted a time-dependent increase in the toxicity of the photodegradation products, and those obtained using Degussa P25 photocatalyst were more toxic. The most pronounced and selective toxic action of MET and products of its photodegradation was observed in the hepatic cell line. The higher toxicity of the mixtures obtained using Degussa P25 catalyst could be explained by a different mechanism of MET degradation, i.e. by the presence or higher concentrations of some intermediates. Although the concentrations of intermediates obtained using TiO2 Wackherr catalyst were higher, they did not affect significantly the growth of the examined cell lines, indicating their lower toxicity. This suggests that a treatment aiming at complete mineralization should be performed bearing in mind that the type of catalyst, the concentration of target molecule, and the duration of the process are significant factors that determine the nature and toxicity of the resulting mixtures. Although the EC50 values of MET obtained in mammalian cell lines were higher compared to the bioassays for lower trophic levels, the time-dependent promotion of toxicity of degradation mixtures should be attributed to the higher sensitivity of mammalian cell bioassays.
Keywords: H-4-II-E; HT-29; MRC-5; Metoprolol; Photodegradation; Toxicity.
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