Acute and Sub-acute Ozone Exposure Mediates a Cytokine Specific Retinal Inflammatory Response

Friday, October 28, 2011
Hall 1-2 (San Jose Convention Center)
Rolando Barrientes , Biological & Health science department, Texas A&M university-kingsville, kingsville, TX
Carlos Garcia, Phd , biological & health science, texas a&m university blvd., kingsville, TX
Shannon Ugarte , biological & health science, texas a&m university- kingsville, kingsville, TX
Neurons are sensitive to oxidative stress due to  high lipid content and elevated oxygen consumption.  Ambient ozone (O3) is a strong oxidant that upon inhalation reaches the retina.  Goals of this study are  1) investigate  effects of O3 exposure in mediating  apoptotic TNF-α pathway  2) examine the role of cytokines in retinas of O3–exposed rats. Age and sex-matched rats were separated into groups (n=4); one control and three O3-exposed groups (0.4 ppm for 4 hours; 1 day, 7 days, and 28 days).  Upon completion of exposures, rats were sacrificed and retinas collected for biochemical analysis. Content of  cytokines IL -1β, IL – 10 and TNF-α were measured by enzyme-linked immunosorbent assays in retinal homogenates. Results of this study include, i) TNF-α significantly increased (p< 0.001) in  retinas of  1-day and 7-day ozone-exposed groups, ii) IL – 1β levels significantly decreased (p < 0.05) in  7-day exposed group and 28-day group, and iii)  levels of IL – 10 increased in  1-day exposed group, the increase was not statistically significant. This data provides evidence that O3 exposure causes oxidative stress in mammalian retina, manifested by an increase in TNF-α with a concomitant decrease in IL – 1β and slight increase in levels of  anti-inflammatory cytokine, IL -10. This air pollution relevant work provides data regarding the effects of air pollution on the retina, especially for clinically sensitive populations suffering from retinal degenerative diseases.