RESUMO
Bee pollen as a plant-derived food is consumed as nutritional/functional supplements by humans. But it might confer foodborne allergenicity in susceptible populations, limiting its extensive application. In this study, five potential allergens including profilin, cystatin, prolamin, expansin, and alcohol dehydrogenase in bee pollen derived from Brassica campestris (BP-Bc), were identified through mass spectrometry-based proteomic analysis. Moreover, different types of enzymes (cellulases, pectases, and papains) serve biological roles in pollen wall breaking and expansion, but also promote allergen release and degradation. Proteomic analysis showed that profilin, cystatin, and alcohol dehydrogenase were significantly reduced in BP-Bc following joint treatment with three enzymes. Metabolomic characterization of potential enzymatic hydrolysates of these significantly-decreased allergens was performed, which showed nine major oligopeptides and six amino acids at significantly higher levels in the enzyme-treated BP-Bc. These findings clarified the culprit responsible for bee pollen allergy and the mechanism of enzymatic desensitization for its further development.
Assuntos
Alérgenos , Hipersensibilidade Alimentar , Álcool Desidrogenase , Alérgenos/química , Animais , Abelhas , Hipersensibilidade Alimentar/metabolismo , Metabolômica/métodos , Pólen/química , Profilinas/química , Proteômica/métodosRESUMO
Recent studies have shown that lead (Pb) could disrupt the prooxidant/antioxidant balance of tissue which leads to biochemical and physiological dysfunction. Epigallocatechin-3-gallate (EGCG), a catechin polyphenols component, is found to be an effective antioxidant. The present study investigated whether EGCG administration could reverse the changes on redox states in rat hippocampus caused by lead exposure. The association between redox status changes and long-term potentiation (LTP) in CA1 area of hippocampus were also examined. Wistar rats exposed to lead from postnatal day 1 were followed by 10 days of EGCG (10, 25 and 50 mg/kg) administration through intraperitoneally (ip), and the rats were sacrificed for experiments at the age of 21-23 days. The experimental results showed that glutathione (GSH) and superoxide dismutase (SOD) activity decreased accompanied with LTP amplitude decrease in CA1 area of hippocampus in the lead-exposed group. EGCG supplementation following lead intoxication resulted in increases in the GSH and SOD levels and increases in the LTP amplitude. Malondialdehyde (MDA) levels, a major lipid peroxidation byproduct, increased following lead exposure and decreased following EGCG treatment. In hippocampal neuron culture model, lead exposure (20 microM) significantly inhibited the viability of neurons which was followed by an accumulation of ROS and a decrease of mitochondrial membrane potential (delta Psi m). Treatment by EGCG (10-50 microM) effectively increased cell viability, decreased ROS formation and improved delta Psi m in hippocampal neurons exposed to lead. These observations suggest that EGCG is a potential complementary agent in the treatment of chronic lead intoxication through its antioxidative character.
Assuntos
Antioxidantes/farmacologia , Catequina/análogos & derivados , Hipocampo/efeitos dos fármacos , Compostos Organometálicos/toxicidade , Estresse Oxidativo/efeitos dos fármacos , Animais , Animais Recém-Nascidos , Catequina/farmacologia , Sobrevivência Celular/efeitos dos fármacos , Células Cultivadas , Relação Dose-Resposta a Droga , Antagonismo de Drogas , Feminino , Glutationa/metabolismo , Hipocampo/metabolismo , Hipocampo/fisiopatologia , Injeções Intraperitoneais , Lactação , Peroxidação de Lipídeos/efeitos dos fármacos , Potenciação de Longa Duração/efeitos dos fármacos , Malondialdeído/metabolismo , Exposição Materna , Potencial da Membrana Mitocondrial/efeitos dos fármacos , Neurônios/efeitos dos fármacos , Neurônios/metabolismo , Ratos , Ratos Wistar , Espécies Reativas de Oxigênio/metabolismo , Superóxido Dismutase/metabolismoRESUMO
This study evaluates the interaction of selenium (Se) and mercury (Hg) in the accumulations and oxidative stress of rat tissues. Rats were divided into five groups including one control (n=9) and four treated groups including M-Hg (n=9), L-Hg+Se (n=11), M-Hg+Se (n=10), and H-Hg+Se (n=10) group. Treated groups of rats were instilled with different amounts of mercuric chloride (HgCl(2)) and dl-selenomethionine (SeMet) by gavage since pregnancy of their mothers. Atomic fluorescence spectroscopy (AFS) was applied for mercury and selenium quantification. Glutathione (GSH), malondialdehyde (MDA), and total superoxide dismutase (SOD) activity of tissues were detected using biochemical methods. Results showed that Hg was deposited mainly in kidney. Se could decrease Hg content in kidney but increase it in blood and liver. Hg decreased GSH and SOD and increased MDA levels in most detected tissues, while Se took on a counteraction effect in same tissues. This study suggests that interactions of Se and Hg affect their accumulation and Se may antagonize Hg-induced inhibition on organic activities.