Avaliação da toxicidade do chumbo em parâmetros bioquímicos e comportamentais: efeito preventivo do zinco e N-acetilcisteína

• Ano de defesa: 2017
• Autor(a) principal: Pedroso, Taíse Fonseca
• Tipo de documento: Dissertação
• Tipo de acesso: Acesso aberto
• Idioma: por
• Instituição de defesa: Universidade Federal de Santa Maria; Brasil; Bioquímica; UFSM; Programa de Pós-Graduação em Ciências Biológicas: Bioquímica Toxicológica; Centro de Ciências Naturais e Exatas
• Palavras-chave em Português: Filhotes; Desenvolvimento; Porfobilinogênio-sintase; Acetilcolinesterase; Prevenção; Pups; Development; Porphobilinogen synthase; Acetylcholinesterase; Prevention; CNPQ::CIENCIAS BIOLOGICAS::BIOQUIMICA
• Link de acesso: http://repositorio.ufsm.br/handle/1/12772

Lead (Pb) is a toxic metal without biological function, which can cause various undesirable changes in organism. Developing animals are more sensitive to external aggressions, and exposure to Pb may cause pronounced and even irreversible damage. Studies show detoxifyng action by zinc chloride (ZnCl2) and N-acetylcysteine (NAC), suggesting same protective effect against intoxication with Pb. Therefore, we investigated the toxic effect of lead acetate (AcPb) on biochemical and behavioral parameters, in developing animals, and the possible protective effect of ZnCl2 and NAC. For this young Wistar rats received subcutaneously: saline, ZnCl2 (27 mg/kg), NAC (5 mg/kg) or more NAC ZnCl2 from the 3rd to 7 th; and AcPb (7 mg/kg) or saline from the 8th to 12th day of age. The animals were subjected to behavioral tasks: negative geotactismo, the tail immersion test beaker and open field to assess neurological damage and motors. They were sacrificed at 33 days and the biological samples were stored for further analysis. We assessed the body weight, the activity of porphobilinogen synthase (PBG synthase) in blood, acetylcholinesterase (AChE) in brain and cerebellum, hemoglobin (Hb) in whole blood, serum urea and creatinine, and blood, cerebrum and cerebellum levels. Pups exposed to AcPb presented a decrease of blood PBG-synthase activity, without changes in Hb content. ZnCl2 pre-exposure partially prevented the PBG-synthase inhibition. Pb caused a decrease in the activity of brain AChE, while the treatment with ZnCl2, NAC and ZnCl2 more NAC prevented this change. In addition, animals exposed to AcPb presented Pb accumulation in blood and brain; all preventive treatments decreased Pb levels. In summary, the results show that there was an accumulation of Pb and inhibition of the activity of two enzymes, which are important biomarkers of toxicity. As preventive treatments, the protector effect of ZnCl2 may related to its capacity of to induce the biosyntese of metal ligant proteins. As to NAC, it is probable that its protective effect is related to chelating effects.