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

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.

Glutamatergic neurons in rodent models respond to nanoscale particulate urban air pollutants in vivo and in vitro

“…Inhalation by mice of ambient vehicle-derived PM from an urban freeway for 2-6 weeks induced glial responses with elevations of interleukin-1α (IL-1α), tumor necrosis factor-α (TNFα), nuclear factor κB, and several protein kinases (Campbell et al 2005(Campbell et al 2009Kleinman et al 2008). These inflammatory changes, together with increased lipid oxidation (Zanchi et al 2010), suggest that chronic inhalation of vehiclederived PM can cause inflammation and oxidative stress in the brain.…”

“…Also, a prospective study of children showed associations of lower IQ with prenatal exposure to vehicle-derived polycyclic aromatic hydrocarbons (PAHs) (Perera et al 2009), and autism prevalence was associated with residential proximity at birth to urban freeways (Volk et al 2010). Rodent models also show varying memory impairment after exposure to ozone (Avila-Costa et al 1999;Dorado-Martinez et al 2001;Guerrero et al 1999;Rivas-Arancibia et al 2010) and vehiclederived air pollutants (Zanchi et al 2010).…”

Neurotoxicity of a modelled complex environmental heavy metal exposure in rats

“…For Mn 2+ , a similar mechanism (blocked membrane Ca-channels and increased intracellular Ca release at the same time) was reported by Kita et al (1981). In rats exposed to traffic-generated dust containing Pb and Cd, shortterm memory was impaired (Zanchi et al, 2010), and memory formation and consolidation is known to depend on Ca-regulated neuronal events.…”

Nervous system effects and oxidative stress in rats treated with metal oxide nanoparticles

“…Kumar et al (1996) described membrane damage and increase of intracellular Ca 2+ on Cd treatment of rats but without further functional implications. Also in a paper on the effect on rats of traffic-generated dust, containing Pb and Cd, (Zanchi et al, 2010) impaired short-term memory and oxidative stress as its possible cause was just mentioned. In our experiments, as shown by Figures 8 and 14, the measured oxidative stress parameters were much less strongly associated to the metal levels than the neuro-functional parameters so that, except for the significant correlation of ECoG index and brain GSH level in the Mn-treated rats, any connection between the two could not be directly demonstrated.…”