2024-03-29T10:39:33Zhttp://digital.csic.es/dspace-oai/requestoai:digital.csic.es:10261/1505682018-09-19T11:29:06Zcom_10261_31891com_10261_2col_10261_31892
DIGITAL.CSIC
author
Martinez, Caroline S.
author
Miguel, Marta
author
Wiggers, Giulia Alessandra
funder
Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (Brasil)
funder
Conselho Nacional de Desenvolvimento Científico e Tecnológico (Brasil)
funder
Fundação de Amparo à Pesquisa e Inovação do Espírito Santo
funder
Universidade Federal do Pampa
funder
Governo do Estado de São Paulo
2017-05-29T09:53:25Z
2017-05-29T09:53:25Z
2017
Neurotoxicity Research 31(1): 20-30 (2017)
http://hdl.handle.net/10261/150568
10.1007/s12640-016-9656-y
http://dx.doi.org/10.13039/501100002322http://dx.doi.org/10.13039/501100003593http://dx.doi.org/10.13039/501100010598
Aluminum (Al) is a significant environmental contaminant. While a good deal of research has been conducted on the acute neurotoxic effects of Al, little is known about the effects of longer-term exposure at human dietary Al levels. Therefore, the purpose of this study was to investigate the effects of 60-day Al exposure at low doses for comparison with a model of exposure known to produce neurotoxicity in rats. Three-month-old male Wistar rats were divided into two major groups: (1) low aluminum levels, and (2) a high aluminum level. Group 1 rats were treated orally by drinking water for 60 days as follows: (a) control—received ultrapure drinking water; (b) aluminum at 1.5 mg/kg b.w., and (c) aluminum at 8.3 mg/kg b.w. Group 2 rats were treated through oral gavages for 42 days as follows: (a) control—received ultrapure water; (b) aluminum at 100 mg/kg b.w. We analyzed cognitive parameters, biomarkers of oxidative stress and acetylcholinesterase (AChE) activity in hippocampus and prefrontal cortex. Al treatment even at low doses promoted recognition memory impairment seen in object recognition memory testing. Moreover, Al increased hippocampal reactive oxygen species and lipid peroxidation, reduced antioxidant capacity, and decreased AChE activity. Our data demonstrate that 60-day subchronic exposure to low doses of Al from feed and added to the water, which reflect human dietary Al intake, reaches a threshold sufficient to promote memory impairment and neurotoxicity. The elevation of oxidative stress and cholinergic dysfunction highlight pathways of toxic actions for this metal.
eng
closedAccess
Cholinergic dysfunction
Cognitive dysfunction
Aluminum
Oxidative stress
Aluminum Exposure at Human Dietary Levels for 60 Days Reaches a Threshold Sufficient to Promote Memory Impairment in Rats
libro
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URL
https://digital.csic.es/bitstream/10261/150568/1/accesoRestringido.pdf
File
MD5
42637ae8545636bc41605c1740a9a84e
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application/pdf
accesoRestringido.pdf