Estudo da atividade quimioprotetora in vitro e in vivo da Eugenia dysenterica dc. (Myrtaceae) após exposição ao cromo hexavalente

• Autor(a) principal: Marcelino, Renato Ivan de Ávila
• Data de Publicação: 2013
• Tipo de documento: Dissertação
• Idioma: por
• Título da fonte: Repositório Institucional da UFG
• Texto Completo: http://repositorio.bc.ufg.br/tede/handle/tede/3679
• topic: Eugenia dysenterica; Myrtaceae; Cromo; Metais pesados; Espécies de oxigênio reativas; Macrófagos alveolares; Apoptose; Toxicidade aguda; Falência hepática; Insuficiência renal; Eugenia dysenterica; Myrtaceae; Chromium; Heavy metals; Reactive oxygen species; Alveolar macrophages; Apoptosis; Acute toxicity; Hepatic insufficiency; Renal insufficiency; CIENCIAS BIOLOGICAS::FARMACOLOGIA

Hexavalent chromium [Cr(VI)] is a toxic metal that triggers toxicity events in the body, penetrating cell membranes and increasing reactive oxygen species (ROS). These products, in turn, damage cellular macromolecules, inhibiting their functions and enhancing cell death via apoptosis. Therefore, it has been suggested that the use of antioxidants can minimize the damage induced by this metal. In this context, the Eugenia dysenterica DC. (Myrtaceae) plant species, native from Cerrado biome, has been studied because it presents high levels of polyphenols, substances with known antioxidant potential. Moreover, it is traditionally used in folk medicine and presents food and economic importance. In this work, in vitro and in vivo effects of the Eugenia dysenterica DC. leaf hydroalcoholic extract (EDE) on AMJ2-C11 cell line and mice exposed to Cr(VI), respectively, were investigated. In parallel, the antioxidant activity of EDE was also investigated by the methods of 2,2-Diphenyl-1-picrylhydrazyl (DPPH•) free radical capturing and co-oxidation of β-caroteno/linoleic acid. In vitro, pre-treatment of AMJ2-C11 cells with EDE (20, 40 ou 80 μg/mL) followed by exposure to Cr(VI) (100, 250 ou 500 μM) resulted in a concentration-dependent increase of cell viability. Furthermore, mechanistic studies of flow cytometry (cell cycle, annexin V, active caspases, ROS and rhodamine 123) and cell morphology showed that the EDE protected the cells from apoptosis triggered by Cr(VI), and reduced the ROS intracellular levels and prevented the loss of mitochondrial membrane potential. Additionally, significant antioxidant potential of EDE was observed. In vivo, prophylactic treatment for 10 days with EDE (50, 100 ou 200 mg/kg/day) and subsequent exposure to a sublethal dose of Cr(VI) (30 mg/kg) induced a decrease in Cr levels in the kidneys, liver and plasm, besides preventing liver and kidney changes caused by this metal. Moreover, treatment of animals with EDE (50, 100, 125, 200, 250 ou 500 mg/kg/day) followed by exposure to a lethal dose of Cr(VI) (50 mg/kg) induced an increase in the survival of exposed animals, especially at the doses of 50, 100 and 125 mg/kg. Therefore, the present study demonstrated that the EDE showed in vitro and in vivo effect against Cr(VI)-induced oxidative toxicity.