Photocatalytic Degradation of Textile dye Orange-122 Via Electrospray Mass Spectrometry

Abstract This work reports the study of the potential application of Zn/TiO2 catalysts, obtained by the sol-gel method, in processes of environmental decontamination through the reactions of photodegradation of textile dye, followed by electrospray mass spectrometry. The catalysts synthesis was performed according to a 2² factorial design with repetition at the central point. The characterization techniques used were: N2 adsorption measurements (BET method), scanning electron microscopy with energy dispersive X-ray (MEV/EDS), X-ray diffraction and point of zero charge (PZC). The photocatalytic tests were performed in batch in the presence of sunlight, and to evaluate the degradation kinetics study, a rapid direct injection electrospray mass spectrometry (DI-ESI-MS) method has been developed. By the photocatalytic tests, the calcination temperature of 400 °C has shown the best results of discoloration for the reactive Orange-122 dye (99.76%) in a reaction time of 2h. The discoloration kinetics were a pseudo-first order, and a statistical analysis was performed to investigate the effects of the variables and to optimize the conditions of discoloration to the dye. After the reactional time of 2 h, an ion of m/z 441.5 was detected by ESI-MS, indicating that the photocatalytic process was effective for the degradation of the dye to secondary compounds.

Homeopathic drugs Natrum sulphuricum and Carcinosin prevent azo dye-induced hepatocarcinogenesis in mice.

The study was undertaken to examine whether Carcinosin-200 (Car-200) could provide additional ameliorative effect, if used intermittently with Natrum sulphuricum-30 (Nat Sulph-30) against hepatocarcinogenesis induced by chronic feeding of p-dimethylaminoazobenzene (p-DAB) and phenobarbital (PB) in mice (Mus musculus). Mice were randomly divided into seven sub-groups: (i) normal untreated; (ii) normal + succussed alcohol; (iii) p-DAB (0.06%) + PB (0.05%); (iv) p-DAB + PB + succussed alcohol, (v) p-DAB + PB + Nat Sulph-30, (vi) p-DAB + PB + Car-200, and (vii) p-DAB + PB + Nat Sulph-30 + Car-200. They were sacrificed at 30, 60, 90 and 120 days for assessment of genotoxicity through cytogenetical end-points like chromosome aberrations, micronuclei, mitotic index and sperm head anomaly and cytotoxicity through assay of widely accepted biomarkers and pathophysiological parameters. Additionally, electron microscopic studies and gelatin zymography for matrix metalloproteinases (MMPs) were conducted in liver at 90 and 120 days. Results showed that administration of Nat Sulph-30 alone and in combination with Car-200 reduced the liver tumors with positive ultra-structural changes and in MMPs expression, genotoxic parameters, lipid peroxidation, -glutamyl transferase, lactate dehydrogenase, blood glucose, bilirubin, creatinine, urea and increased GSH, glucose-6-phosphate dehydrogenase, superoxide dismutase, catalase, glutathione reductase activities and hemoglobin, cholesterol, and albumin levels. Thus, intermittent use of Car-200 along with Nat Sulph-30 yielded additional benefit against genotoxicity, cytotoxicity, hepatotoxicity and oxidative stress induced by the carcinogens during hepatocarcinogenesis.

Identification of a sensitive index during fish bioassay of an azo dye methyl red (untreated and treated).

Acute and chronic toxicity of methyl red (untreated) was examined on a freshwater fish Poecilia reticulata, using indices viz; mortality, reduction in RBC counts and their morphological abnormality (poikilocytosis and anisocytosis). Similar studies (acute toxicity) were also made in physicochemically and biologically treated methyl red. Data comparison of these four indices revealed poikilocytosis as the most sensitive index, since it measured higher toxicity of methyl red when fish mortality was either minimum at its low concentration (5 ppm) during both acute and chronic toxicity or even nil in the biologically treated 100 ppm methyl red, during acute toxicity. Mortality was next to poikilocytosis though it ranked 1st at higher concentration of methyl red during acute toxicity. The reduction in RBC counts however, was found to be the most sensitive parameter only in case of prolonged exposure (4 weeks) to 5 ppm methyl red. Amongst the four indices used for quantifying toxicity; anisocytosis was found to be the least expressive. Based on these findings we recommend quantification of data on fish mortality and poikilocytosis during acute toxicity whereas reduction in RBC counts and poikilocytosis during chronic exposure to methyl red.

Evaluation of protective potentials of a potentized homeopathic drug, Chelidonium majus, during azo dye induced hepatocarcinogenesis in mice.

Several cytogenetical and enzymatic protocols were used to test if two microdoses of Chelidonium majus, namely Chelidonium-30 (Ch-30) and Chelidonium-200 (Ch-200), used as homeopathic drugs, showed anti-tumor activity and also favorably modulated genotoxic damages produced by an azo dye in mice at several intervals of fixation. Different sets of healthy mice were fed: (i) hepatocarcinogen, p-dimethylaminoazobenzene (p-DAB, initiator) + phenobarbital (PB, promoter), (ii) only p-DAB, (iii) only PB, and (iv) neither p-DAB nor PB (normal control). Mice fed with p-DAB + PB were divided into different sets that were also fed either Ch-30 (v) or Ch-200 (vi) or diluted alcohol (vii), the "vehicle" of the microdoses of Chelidonium. All mice of group (i), a few of group (ii) and group (vii) and none of groups (iii) and (iv) developed tumors in liver at the longer intervals of fixation. The frequencies of chromosome aberrations (CA), micronucleated erythrocytes (MN), mitotic index (MI) and sperm head abnormality (SHA) were much higher in groups (i) and (vii) mice than in groups (ii), (iii) and (iv) mice at all fixation intervals. However, in mice of both groups (v) and (vi), the frequencies of CA, MN, SHA were strikingly less than those of groups (i) and (vii), and moderately less than those of groups (ii) and (iii). Both Ch-30 and Ch-200 also modulated favourably some toxicity marker enzymes like acid and alkaline phosphatases, peroxidases, glutamate oxaloacetate and glutamate pyruvate transaminases in liver, kidney and spleen tissues of the carcinogen fed mice. The microdoses of Chelidonium having no visible ill effects of their own, may be strong candidates for use in delaying/protecting liver cancer.

Dose related promoter effect of metanil yellow on the development of hepatic pre-neoplastic lesions induced by N-nitrosodiethylamine in rats.

The dose-dependent effect of mentanil yellow (MY) on the development of preneoplastic hepatic lesions during N-nitrosodiethylamine (DEN) induced hepatocarcinogenesis was studied in comparison with phenobarbitone (PB), in male Wistar (WR) rats. Rats were administered 200 ppm DEN through drinking water for a period of 1 month. After an interval of 2 wk, the animals were administered MY at concentrations of 0.1, 0.5 and 1.0 per cent in the diet for a period of 7 months. PB at 500 ppm served as the standard tumour promoter. The dose-dependent tumour promoter effects of MY were monitored on the basis of morphological appearance of the livers, liver weight profile, histological pattern, appearance of gamma-glutamyl transpeptidase (GGT) positive foci, total GGT activity and the induction of glycogen-deficient islands. All the three doses of MY were found to enhance liver carcinogenesis when compared with either the corresponding controls or only the DEN treated animals. MY at 0.1 per cent was found to be more effective as an enhancer of DEN-induced carcinogenesis than 0.5 and 1.0 per cent. In the present study a dose-related enhancing effect of MY on DEN-induced hepatic preneoplasia in rats has been demonstrated.