Urban Air Pollution Induces Oxidative Stress, Inflammation And Mitochondrial Disfunction In Mice Brain Cortex And Olfactory bulb

CALABRÓ V; GARCÉS M; MARCHINI T; MAGNANI N; FREIRE A; CACERES L; VICO T; VANASCO V; BERDASCO C; MÉNDEZ DIODATI N; MARTINEFSKI M; BUCHHOLZ B; TRIPODI V; GOLDSTEIN J; GELPI RJ; BERRA A; ALVAREZ S; EVELSON P

Conferencia; 27th Annual Conference of the Society for Redox Biology and Medicine; 2020

Society for Redox Biology and Medicine

Previous reports indicate that the central nervous system (CNS) is a target of air pollution, causing tissue damage and functional alterations. Oxidative stress and neuroinflammation have been point out as possible mechanisms mediating these effects. The aim of this work was to study the chronic effects of urban air pollution on mice brain cortex (CX) and olfactory bulb (OB), focusing on oxidative and inflammatory markers, and mitochondrial function. Male 8-week-old BALB/c mice were exposed to filtered air (FA, control) or urban air (UA) inside whole-body inhalation chambers located in a highly polluted area of Buenos Aires City, for up to 4 weeks. Glutathione levels, assessed as GSH/GSSG ratio, were decreased in CX after 1 and 2 w of exposure to UA, and after 4 w in the case of the OB (26% and 60% respectively; p<0.05). NADPH oxidase and GPx activities were augmented in all the studied time points, while this increase was observed only after 4 w for SOD and GR activities, in CX of UA group (p<0.05). After 4 w, increased GFAP expression levels showed reactive astrocytes in OB, probably associated with the altered olfactory function observed by a behavioral test, in UA compared to FA mice (p<0.05). Also, UA mice showed impaired mitochondrial function due to reduction by 50 % in O2 consumption in active state (p<0.05), a 65% decrease in ATP production rate (p<0.01) and a 30% increase of H2O2 production (p<0.01). Moreover, respiratory complexes I-III and II-III activities were decreased in UA group (30% and 36% respectively vs. FA; p<0.05). UA exposed mice showed alterations in mice olfaction and mitochondrial function, increased oxidant production, along with an inflammatory process evidenced by astrocyte activation. These data indicate that oxidative stress and inflammation may play a key role in CNS damage mechanisms, triggered by air pollution.