Abstract
Purpose :
The impact of the gaseous air pollutant ozone (O3), a strong oxidant, on the mammalian retina is unknown. This study aims to compare the electroretinogram (ERG) and Naka-Rushton parameters between control and O3-exposed rats to better understand the effect of O3 on retinal function.
Methods :
Dark-adapted luminance-response functions were obtained from groups of age- and sex-matched Long Evans rats (n=16 rats); eight control (clean air) and eight O3-exposed (0.4 ppm for 4 hours/day for 7 days). Full-field ERGs were recorded simultaneously from both eyes in each rat. The scotopic ERG was measured and compared between the two groups. Recordings were performed under general anesthesia (ketamine 70 mg/kg, xylazine 2.5 mg/kg, IP). Pupils were dilated with 2.5% phenylephrine and 1% tropicamide eye drops. Naka-Rushton curves were fitted to the dark-adapted ERGs and the Vmax, Km and n parameters compared between the two groups. A repeated measures ANOVA with luminance as the repeated factor was performed.
Results :
Experimental data indicates in the scotopic ERG, an acute exposure to O3 decreased Vmax from 1170mV in the control group to 1077mV after a 1-day (4hr) O3 exposure. A 7- day O3 exposure further decreased Vmax to 811 (p < 0.05). Amplitudes of the a-wave decreased significantly (p < 0.05) from 221 mV in the control group to 145 mV in the 7-day O3-exposed group. The Km increased in the 7-day exposed group from 0.0056 to 0.0065 in the control group. The n parameter decreased as a function of O3 exposure time from 0.49 in the control group, 0.45 in the 1-day exposed group to 0.39 in the 7-day O3-exposed group. No statistically significant differences in a-wave (F=0.527, p=0.609) and b-wave (F=2.271, p=0.166) implicit time were detected.
Conclusions :
This work demonstrates O3 is a retinal neurotoxin and environmental exposure leads to decreases in retinal responsiveness, changes in retinal sensitivity and homogeneity as indicated by the Naka-Rushton parameters. Results suggest O3 -exposure contributes to rod system deficits demonstrated by the ERG changes. The current work offers evidence that in sensitive populations living in air-polluted environments, retinal neuron dysfunction may result from O3–induced oxidative stress.
This is an abstract that was submitted for the 2018 ARVO Annual Meeting, held in Honolulu, Hawaii, April 29 - May 3, 2018.