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      Electrochemical oxidation, adsorption and quantification of 1,2-benzopyrone employing a glassy carbon electrode

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          Abstract

          The electrooxidation of 1,2-benzopyrone (BP) was assessed via linear voltammetry and electrochemical impedance spectroscopy on a glassy carbon electrode in dibasic potassium phosphate buffer. The oxidation process for BP requires one electron and forms a ketone. This oxidation product was adsorbed by the electrode surface to form a film that blocks active sites and increases in thickness over consecutive measurements. The oxidation conditions were optimized using factorial design and Doehlert matrices. This electrochemical method was compared to high performance liquid chromatography (HPLC), which has a detection limit of 26.4 µmol L-1 for BP. The voltammetric results were statistically similar to those from HPLC; however, the method was faster, simpler, more easily acquired, more sensitive, and required less organic solvent.

          Translated abstract

          O processo de eletrooxidação da 1,2-benzopirona (BP) foi avaliado através de medidas de voltametria linear e espectroscopia de impedância eletroquímica sobre o eletrodo de carbono vítreo em tampão fosfato dibásico de potássio. O número de elétrons envolvidos na eletrooxidação é um e o produto formado é uma cetona. O produto da oxidação fica adsorvido na superfície do eletrodo formando um filme, o qual bloqueia os sítios ativos e a espessura do filme aumenta após medidas consecutivas. As condições de analise foram otimizadas usando planejamento fatorial e matriz Doehlert. A metodologia eletroquímica foi comparada com a cromatografia líquida de alta eficiência (HPLC) com um limite de detecção para a BP de 26,4 µmol L-1. Os resultados voltamétricos foram estatisticamente semelhantes aos obtidos por HPLC, mas o método proposto é mais rápido, simples, de fácil aquisição e de alta sensibilidade, e não exige grandes quantidades de solventes orgânicos.

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          Most cited references33

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          Electrochemical methods: Fundamentals and applications

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            Possible role of zinc in the selective degeneration of dentate hilar neurons after cerebral ischemia in the adult rat.

            The fluorescent dye 6-methoxy-8-p-toluene sulfonamide quinoline (TSQ) was used to monitor the distribution of zinc in the hippocampus and fascia dentata of adult rats subjected to 20 min of cerebral ischemia. In normal brains TSQ stains only neuropil, in particular the mossy fiber layers in the dentate hilus (CA4) and CA3, but within 2 h after ischemia, TSQ-fluorescent cells were observed in the dentate hilus. At longer survival times TSQ-positive cells stained positively with acid fuchsin, a sign of cellular degeneration. At the same time a decrease in the TSQ fluorescence of the mossy fiber terminals in the dentate hilus (CA4) and the CA3 mossy fiber layer was noted. The observations suggest that zinc many play a role in the selective death of dentate hilar neurons after cerebral ischemia.
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              Minocycline blocks nitric oxide-induced neurotoxicity by inhibition p38 MAP kinase in rat cerebellar granule neurons.

              Minocycline, a semisynthetic second-generation tetracycline, was reported to have neuroprotective effects in models of global and focal cerebral ischemia, the R6/2 mouse model of Huntington disease, as well as glutamate-induced neurotoxicity in mixed neuronal/glial cultures. It was suggested that neuroprotective effects of minocycline resulted from inhibition of microglial/astroglial activation 'Proc. Natl. Acad. Sci. USA 95 1998 15769'. To determine whether or not minocycline is able to directly protect neurons against injury insults and to delineate its neuroprotective mechanism(s), we treated cultured rat cerebellar granule neurons (CGN) with nitric oxide (NO) in the presence or absence of minocycline. We found that minocycline protected neurons against NO-induced neuronal death in a concentration-dependent fashion. Consistent to other reports, NO was able to induce p38 MAP kinase phosphorylation at 3-6 h and such an induction could be significantly inhibited by minocycline. Furthermore, SB 203580, a p38 MAP kinase inhibitor, almost completely attenuated NO-induced neuronal death of CGN as well. These results suggest that minocycline is able to block NO-induced neurotoxicity in CGN by inhibiting NO-induced phosphorylation of p38 MAP kinase. Our finding may explain the neuroprotective mechanism of minocycline in those neurodegenerative models.
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                Author and article information

                Contributors
                Role: ND
                Role: ND
                Role: ND
                Role: ND
                Journal
                jbchs
                Journal of the Brazilian Chemical Society
                J. Braz. Chem. Soc.
                Sociedade Brasileira de Química (São Paulo )
                1678-4790
                March 2014
                : 25
                : 3
                : 469-477
                Affiliations
                [1 ] Universidade Federal de Alfenas Brazil
                [2 ] Universidade Estadual de Campinas Brazil
                Article
                S0103-50532014000300009
                10.5935/0103-5053.20140004
                a26ed02c-e81f-47db-8f1c-8f923cb018b2

                http://creativecommons.org/licenses/by/4.0/

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                SciELO Brazil

                Self URI (journal page): http://www.scielo.br/scielo.php?script=sci_serial&pid=0103-5053&lng=en
                Categories
                CHEMISTRY, MULTIDISCIPLINARY

                General chemistry
                1,2-benzopyrone,guaco,adsorption process,multivariate optimization
                General chemistry
                1,2-benzopyrone, guaco, adsorption process, multivariate optimization

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