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1.
Braz. J. Pharm. Sci. (Online) ; 58: e19221, 2022. tab, graf
Artigo em Inglês | LILACS | ID: biblio-1374557

RESUMO

Abstract The purpose of the current work was to assess a possible role of cytochrome P450 1A2 (CYP1A2) and N-acetyltransferase 2 (NAT2) in the metabolic activation of 2,6-dimethylaniline (2,6-DMA) and also clarify the function of DNA repair in affecting the ultimate mutagenic potency. Two cell lines, nucleotide excision repair (NER)-deficient 5P3NAT2 and proficient 5P3NAT2R9 both expressing CYP1A2 and NAT2, were treated with 2,6-DMA for 48 h or its metabolites for 1 h. Cell survival determined by trypan blue exclusion and MTT assays, and 8-azaadenine-resistant mutants at the adenine phosphoribosyltransferase (aprt) gene locus were evaluated. 5P3NAT2 and 5P3NAT2R9 cells treated with 2,6-DMA and its metabolites showed a dose-dependent increase in cytotoxicity and mutant fraction; N-OH-2,6-DMA and 2,6-DMAP in serum-free α-minimal essential medium (MEM) are more potent than 2,6-DMA in complete MEM. 5P3NAT2 cells was more sensitive to the cytotoxic and mutagenic action than 5P3NAT2R9 cells. H2DCFH-DA assay showed dose-dependent ROS production under 2,6- DMAP treatment. These findings indicate that the genotoxic effects of 2,6-DMA are mediated by CYP1A2 activation via N-hydroxylation and the subsequent esterification by the phase II conjugation enzyme NAT2, and through the generation of ROS by hydroxylamine and/or aminophenol metabolites. NER status is also an important contributor


Assuntos
Células/classificação , Citocromo P-450 CYP1A2/análise , Genotoxicidade , Linhagem Celular/classificação , Hidroxilamina/agonistas , Reparo do DNA
2.
Acta sci., Biol. sci ; 37(2): 159-167, abr.- jun. 2015. ilus
Artigo em Inglês | LILACS | ID: biblio-847748

RESUMO

The mechanisms of photosynthetic electron transport can be elucidated by inhibition of electron flow through the use of specific substances that, when combined with the chlorophyll chlorophyll a fluorescence emission was measured to investigate the effect of several inhibitors of the photosynthetic electron transport chain in canola leaf discs. Leaf discs were incubated in the dark for 2 hours in different solutions: (a) water ­ control; (b) DCMU at 500 µM; (c) phenanthroline at 10 mM; and (d) hydroxylamine at 10, 50, 100 and 200 mM. Similar effects were observed between DCMU and phenanthroline, the initial fluorescence value was altered, but not the maximum fluorescence, with the disappearance of the IP phase. Hydroxylamine interacted and inhibited the oxygen evolving complex and caused an imbalance between the rate of QA reduction by photosystem II and the rate of QA oxidation by photosystem I.


Os mecanismos de transporte de elétrons podem ser elucidados pela inibição do fluxo de elétrons pelo uso de substâncias específicas que, juntamente com a técnica de fluorescência da clorofila, torna-se uma ferramenta importante para detalhar a cadeia de transporte de elétrons. Neste trabalho, a emissão da fluorescência da clorofila foi mensurada para investigar o efeito dos diferentes inibidores da cadeia de transporte de elétrons fotossintéticos de discos foliares de canola. Os discos foliares foram incubados no escuro durante 02 h em diferentes soluções: (a) água - controle, (b) 500 uM de DCMU, (c) 10 mM de fenantrolina, e (d) 10, 50, 100 e 200 mM de hidroxilamina. Foram observados efeitos similares entre DCMU e fenantrolina, o valor da fluorescência inicial foi alterado, contudo a fluorescência máxima não se alterou, havendo o desaparecimento da fase de IP. Hidroxilamina interagiu e inibiu o complexo de evolução de oxigênio e causou desequilíbrio entre a taxa de redução QA pelo fotossistema II e a taxa de oxidação QA pelo fotossistema I.


Assuntos
Brassica napus , Clorofila , Diurona , Hidroxilamina , Oxigênio , Fenantrolinas
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