Efeitos bioquímicos e comportamentais resultantes da exposição aguda à aflatoxina B1 em ratos

• Ano de defesa: 2016
• Autor(a) principal: Souto, Naieli Schiefelbein
• Tipo de documento: Dissertação
• Tipo de acesso: Acesso aberto
• Idioma: por
• Instituição de defesa: Universidade Federal de Santa Maria; Brasil; Ciência e Tecnologia dos Alimentos; UFSM; Programa de Pós-Graduação em Ciência e Tecnologia dos Alimentos; Centro de Ciências Rurais
• Palavras-chave em Português: Micotoxina; Intoxicação aguda; Sistema nervoso central; Estresse oxidativo; Proteína quinase; Mycotoxin; Acute intoxication; Central nervous system; Oxidative stress; Protein kinase; CNPQ::CIENCIAS AGRARIAS::CIENCIA E TECNOLOGIA DE ALIMENTOS
• Link de acesso: http://repositorio.ufsm.br/handle/1/18154

Aflatoxins are mainly produced by Aspergillus flavus and A. parasiticus. Aflatoxin B1 (AFB1) is the most common mycotoxin and highly toxic, causing carcinogenic, mutagenic and teratogenic effects. This mycotoxin has been detected in important crops worldwide, including corn, peanuts, beans, rice, wheat, cotton, sorghum, fruits and also in animal feed. The AFB1 is converted in the liver into 8,9-epoxide, a metabolite which react with cellular macromolecules, including proteins, RNA and DNA. In addition, it changes hematologic parameters and promotes an imbalance in the oxidative system, especially in antioxidant enzymes. Therefore, the aim of our study was to evaluate the acute effects caused by oral administration of AFB1 on behavioral tests and biochemical parameters. Were used young male Wistar rats that received an administration of AFB1 (250 μg / kg) and after 48 hours were submitted to behavioral analysis, determination of biochemical parameters on cerebral cortex as antioxidant enzymes superoxide dismutase (SOD) and glutathione S-transferase (GST), protein carbonyls and levels of 3-nitrotyrosine, Na+, K+-ATPase activity, determination of ascorbic acid, determination of non-protein sulfhydryl groups (NPSH) and lipoperoxidation, (TBARS) as well as changes in immunoreactivity of protein kinase A (PKA-Ser96) and protein kinase C (PKC-Ser957). The results show that the acute intoxication by AFB1 causes neurotoxic effects, evidenced by significant reduction in the levels of ascorbic acid and non-protein sulfhydryl groups, accompanied by the increase in immunoreactivity ratio of protein kinase C phosphorylated/total (p-PKC α Ser957/PKC α). In this acute protocol AFB1 was able to cause toxic effects in the central nervous system without any behavioral alteration.