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Inhalation Toxicology
International Forum for Respiratory Research
Volume 22, 2010 - Issue 11
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Original Article

Pre and post-natal exposure to ambient level of air pollution impairs memory of rats: the role of oxidative stress

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Pages 910-918 | Received 14 Dec 2009, Accepted 16 May 2010, Published online: 22 Jun 2010
 

Abstract

The aims of this study were to evaluate whether air pollution during pre-natal and post-natal phases change habituation and short-term discriminative memories and if oxidants are involved in this process. As secondary objectives, it was to evaluate if the change of filtered to nonfiltered environment could protect the cortex of rats against oxidative stress as well as to modify the behavior of these animals. Wistar, male rats were divided into four groups (n = 12/group): pre and post-natal exposure until adulthood to filtered air (FA); pre-natal period to nonfiltered air (NFA-FA); until (21st post-natal day) and post-natal to filtered air until adulthood (PND21); pre-natal to filtered air until PND21 and post-natal to nonfiltered air until adulthood (FA-NFA); pre and post-natal to nonfiltered air (NFA). After 150 days of air pollution exposure, animals were tested in the spontaneous object recognition test to evaluate short-term discriminative and habituation memories. Rats were euthanized; blood was collected for metal determination; cortex dissected for oxidative stress evaluation. There was a significant increase in malondialdehyde (MDA) levels in the NFA group when compared to other groups (FA: 1.730 ± 0.217; NFA-FA: 1.101 ± 0.217; FA-NFA: 1.014 ± 0.300; NFA: 5.978 ± 1.920 nmol MDA/mg total proteins; p = 0.007). NFA group presented a significant decrease in short-term discriminative (FA: 0.603 ± 0.106; NFA-FA: 0.669 ± 0.0666; FA-NFA: 0.374 ± 0.178; NFA: −0.00631 ± 0.106 sec; p = 0.006) and an improvement in habituation memories when compared to other groups. Therefore, exposure to air pollution during both those periods impairs short-term discriminative memory and cortical oxidative stress may mediate this process.

Acknowledgements

The authors would like to thank Dr. Elia Caldini, MSc. Nilsa Damaceno Rodrigues (Cell Biology Laboratory, Medical School, University of São Paulo); Dr. Mariangela Macchione, Dr. Mariana Matera Veras (Laboratory of Experimental Pollution, University of São Paulo). Lucas Sagrillo Fagundes, Lucianna Schmitt, Marcella Ody Piva, Maria Fernanda Hornos Carneiro, Roberto Marques Damiani (Laboratory of Oxidative Stress and Atmospheric Pollution, Basic Health Sciences Department, Federal University of Health Sciences of Porto Alegre, Rio Grande do Sul, Brazil) for their technical support.

Declaration of interest

This work was supported by University of São Paulo, Federal University of Health Sciences of Porto Alegre, Fundação de Amparo a Pesquisa do Estado de São Paulo (FAPESP) and FINEP. A.C. Zanchi is supported by a fellowship from FAPESP, Dr. P.H.N. Saldiva and Dr. C.R. Rhoden supported by—Conselho Nacional de Desenvolvimento Científico e Tecnológico—CNPq. Dr. P.H.N. Saldiva and Dr. A.C. Valle are support by FAPESP.

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