Abstract
Purpose: :
Oxidative stress plays a role in the pathophysiology of retinal degenerative diseases. Retinal neurons are especially sensitive to pro-oxidants due to their high lipid content and elevated oxygen consumption. Ambient ozone (O3) is a strong oxidant that upon inhalation reaches the retina. The goals of this study are 1) to investigate the effects of in vivo O3 exposure in mediating the apoptotic TNF-α extrinsic pathway and 2) to examine the role of cytokines in the retinas of O3-exposed Long Evans rats.
Methods: :
Age and sex-matched rats were randomly separated into four groups (n=4); one control (clean air) and three O3-exposed groups (0.4 ppm for 4 hours; 1 day, 7 days, and 28 days). Upon completion of the exposures, the O3-exposed and age and sex-matched controls were sacrificed and neural retinal tissue collected for biochemical analysis. The content of the cytokines IL -1β, IL - 10 and TNF-α were measured by enzyme-linked immunosorbent assays (ELISAs) in retinal homogenates.
Results: :
The TNF-α content significantly increased (p< 0.001) in the retinas of the 1-day and 7-day ozone-exposed groups as compared to controls, and the IL - 1β levels significantly decreased (p < 0.05) in the 7-day exposed group and 28-day group. Although the levels of IL - 10 increased in the 1-day exposed group, the increase was not statistically significant.
Conclusions: :
This data provides evidence that in vivo exposure to O3 causes oxidative stress in the mammalian retina, which is manifested by a specific increase in the levels of TNF-α with a concomitant decrease in the pro-inflammatory cytokine IL - 1β and a slight increase in the levels of the anti-inflammatory cytokine, IL -10. This environmental air pollution relevant work provides useful data regarding the effects of ozone air pollution on the retina, especially for the clinically sensitive populations suffering from retinal degenerative diseases.
Keywords: retinal degenerations: cell biology • cytokines/chemokines • oxidation/oxidative or free radical damage