Avaliação da modulação na neurotransmissão colinérgica como resposta aos efeitos causados pela exposição ao agrotóxico endosulfan utilizando zebrafish (Danio rerio) como organismo modelo

• Ano de defesa: 2012
• Autor(a) principal: Pereira, Vanessa Maynart
• Orientador(a): Bogo, Maurício Reis
• Tipo de documento: Dissertação
• Tipo de acesso: Acesso aberto
• Idioma: por
• Instituição de defesa: Pontifícia Universidade Católica do Rio Grande do Sul; Porto Alegre
• Palavras-chave em Português: BIOLOGIA CELULAR; NEUROBIOLOGIA; PESTICIDAS; PEIXES; ACETILCOLINESTERASE; EXPERIMENTAÇÃO ANIMAL; TOXICIDADE; COMPORTAMENTO
• Link de acesso: http://hdl.handle.net/10923/1297

Endosulfan is a broad spectrum organochlorine pesticide that is still widely used in many developing countries. Following application endosulfan can get to watercourses through surface runoff from agricultural fields and disturb the nontarget aquatic animals including freshwater fish species. Given that the activity of the enzyme acetylcholinesterase (AChE) is one of the most recurrently used biomarkers of exposure to pesticides and there are controversial results concerning the effects of endosulfan exposure and AChE activity in fish, the aim of the present study was to evaluate the effects of endosulfan in brain AChE activity and its gene expression pattern using adult zebrafish (Danio rerio) as an animal model. Moreover, we have analyzed the effects of endosulfan exposure in different parameters of zebrafish swimming activity and in long-term memory formation. After 96 hours of exposition, fish in the 2. 4 μg endosulfan/L group presented a significant decrease in AChE activity (9. 44 ± 1. 038 μmol SCh. h-1. mg protein-1; p = 0. 0205) when compared to the control group (15. 87 ± 1. 768 μmol SCh. h-1. mg protein-1; p = 0. 0205). The downregulation of brain AChE activity is not directly related with the transcriptional control as demonstrated by the RT-qPCR analysis. Our results reinforce AChE activity inhibition as a pathway of endosulfan-induced toxicity in brain of fish species. In addition, exposure to 2. 4 μg endosulfan/L during 96 hours impaired all exploratory parameters evaluated: decreased line crossings (273. 7 ± 28. 12 number of line crossings compared to the control group 344. 6 ± 21. 30, p=0. 0483), traveled distance (23. 44 ± 2. 127 meters compared to the control group 29. 39 ± 1. 585, p=0. 0281), mean speed (0. 03 ± 0. 003 meters/seconds compared to the control group 0. 04 ± 0. 002, p=0. 0275) and body turn angle (69,940 ± 4,871 absolute turn angle compared to the control group 88,010 ± 4,560 p=0. 0114). These results suggest that endosulfan exposure significantly impairs animals' exploratory performance, and potentially compromises their ecological and interspecific interaction. Our results also showed that the same endusulfan exposure did not compromise animals' performance in the inhibitory avoidance apparatus. These findings provide further evidence of the deleterious effects of endosulfan exposure in the nervous system.