HYPERTHERMIA ACCELERATES RETINAL LIGHT DAMAGE IN RATS

Purpose. To study the time course of visual cell damage resulting from hyperthermic light exposure and the possible involvement of rod outer segment (ROS) lipids in the process. Methods. Rats were acclimated in darkness for 2 hours in a hyperthermic chamber to elevate core body t emperature and then exposed to intense green light for up to 4 hours d uring hyperthermia. After light exposure, the animals were either sacr ificed immediately for biochemical or morphologic analysis of retinal light damage or returned to darkness for up to 2 weeks at ambient temp erature before analysis. Rod outer segment lipid profiles were charact erized, and visual cell loss was determined by rhodopsin and visual ce ll DNA measurements. Morphology was performed at the light and electro n microscopic level. Results. Retinal damage resulting from hypertherm ic light exposure was found to be temperature, time, and light intensi ty dependent. At an elevated environmental temperature of 34.5 degrees , 50% visual cell loss was found after 1.5 hours of 1100 lux light exp osure; the same degree of visual cell loss occurred after only 1 hour when rats were maintained at 37 degrees C. At ambient temperatures, 4 hours of light exposure had no effect on visual cell lass. Irrespectiv e of environmental temperature, when rats were maintained in darkness no visual cell loss occurred. Whereas docosahexaenoic acid (22:6) was unchanged in the purest fraction of ROS isolated immediately after lig ht treatment, a 5 mol% loss of the polyunsaturated fatty acid was foun d in ROS isolated 2 or 24 hours after light exposure. Rod outer segmen t lipid composition was largely unaffected by hyperthermic light expos ure, but the density of some ROS increased. Morphologically, the ROS a ppeared to be nearly normal immediately after hyperthermic light expos ure and structurally more abnormal 2 and 24 hours later. The retinal p igment epithelium exhibited damage immediately after exposure, which a lso increased 2 and 24 hours later. Conclusions. Hyperthermia in rats dramatically accelerates retinal light damage compared with light expo sure under euthermic conditions. Overt loss of ROS 22:6 does not occur during hyperthermic light exposure, but it is apparent during the 24- hour period after light treatment. This suggests that the disappearanc e of 22:6 from ROS occurs in tandem with the process of visual cell de ath resulting from retinal light damage.