4.4 Article

Endosulfan exposure inhibits brain AChE activity and impairs swimming performance in adult zebrafish (Danio rerio)

期刊

NEUROTOXICOLOGY
卷 33, 期 3, 页码 469-475

出版社

ELSEVIER
DOI: 10.1016/j.neuro.2012.03.005

关键词

Organochlorines; Endosulfan; Neurotoxicity; Acetylcholinesterase; Altered-behavior; Zebrafish

资金

  1. Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq)
  2. DECIT/SCTIEMS through CNPq
  3. Fundacao de Amparo a Pesquisa do Estado do Rio Grande do Sul (FAPERGS) [FAPERGS 10/0036-5-PRONEX]
  4. Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior (CAPES)

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Endosulfan is a broad spectrum organochlorine pesticide that is still widely in use in many developing countries. Following application, endosulfan can get to watercourses through surface runoff from agricultural fields and disturb the non-target 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 h of exposition, fish in the 2.4 mu g endosulfan/L group presented a significant decrease in AChE activity (9.44 +/- 1.038 mu mol SCh h(-1) mg protein(-1): p = 0.0205) when compared to the control group (15.87 +/- 1.768 mu mol SCh h(-1) mg protein(-1); p = 0.0205) which corresponds to approximately 40%. The down-regulation 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 mu g endosulfan/L during 96 h impaired all exploratory parameters evaluated: decreased line crossings (approximate to 21%, 273.7 +/- 28.12 number of line crossings compared to the control group 344.6 +/- 21.30, p = 0.0483), traveled distance (approximate to 20%, 23.44 +/- 2.127 m compared to the control group 29.39 +/- 1.585, p = 0.0281), mean speed (approximate to 25%, 0.03 +/- 0.003 m/s compared to the control group 0.04 +/- 0.002, p = 0.0275) and body turn angle (approximate to 21%, 69.940 +/- 4871 absolute turn angle compared to the control group 88.010 +/- 4560, 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 endosulfan 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. (c) 2012 Elsevier Inc. All rights reserved.

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