Time course of antioxidant enzyme activities in mice corneas after the exposure to urban air pollution

JANEZIC N ; EVELSON P; LLESUY S; TESONE AI,; TAU J.; FERREIRA SM; LASAGNI VITAR R ; MARCHINI T; BERRA A

Barcelona

Congreso; Congress of the European Society of Ophthalmology (SOE 2017); 2017

Sociedad Europea de Oftalmología

: Purpose: The exposure to air pollution leads to adverse health effects at levels that arecurrently experienced by urban populations, in which oxidative stress is suggested to play acentral role. The aim of the present study was to evaluate the antioxidant enzyme activities inmice corneas after the exposure to urban air pollution for 4 weeks.Method: 8-week-old Balb/c male mice were exposed to urban air or filtered air (control) in anexposure chamber located in a highly populated area of Buenos Aires city. Air particulatematter levels in this area range between 20-60 µg/m3. The animals were exposed for 8h/day, 5 days/week, for 1, 2, and 4 weeks during december 2016. The local committee foranimal care approved every experimental procedure. Superoxide dismutase (SOD), catalase(CAT), and glutathione peroxidase (GPx) activities were evaluated in corneal lysates.One-way ANOVA following Tukey´s post hoc test was used for statistical analysis.Results: The animals exposed to urban air pollution showed an increase in SOD (115%) andCAT (218%) activities after a 1-week exposure (p< 0.05 vs control), while GPx activityremained unchanged. After 2 weeks, exposed mice exhibited an increase in SOD activity(56%, p< 0.001), but this level diminished when compared to the 1-week result (p< 0.001).After 4 weeks, SOD and GPX activities were decreased compared to the control group (42%and 34 %, p< 0.05) and to earlier time points results (p< 0.05). CAT levels returned to controlvalues after 2 weeks of exposure.Conclusion: The corneas of exposed mice exhibit an increase in enzymatic antioxidantdefences after a short exposure, suggesting an early adaptive response to air pollutants.After longer exposures, this antioxidant response is shut-down and could leave the corneamore susceptible to oxidative damage. These results suggest that the corneal antioxidantdefences play a central role in the toxicological mechanisms triggered by the exposure tourban air pollutants.