RETINAL LIGHT DAMAGE IN RATS WITH ALTERED LEVELS OF ROD OUTER SEGMENTDOCOSAHEXAENOATE

Purpose. To compare retinal light damage in rats with either normal or reduced levels of rod outer segment (ROS) docosahexaenoic acid. Metho ds. Weanling male albino rats were maintained in a weak cyclic light e nvironment and fed either a nonpurified control diet or a purified die t deficient in the linolenic acid precursor of docosahexaenoic acid (D HA). Half the rats on the deficient diet were given linseed oil, conta ining more than 50 mol% linolenic acid, once a week to maintain ROS DH A at near normal levels. Diets and linseed oil supplementation were co ntinued for 7 to 12 weeks. To replenish DHA in their ROS, some 10 week -old rats on the deficient diet were given linseed oil three times a w eek for up to 3 additional weeks. Groups of animals were killed at var ious times for ROS fatty acid determinations or were exposed to intens e green light using intermittent or hyperthermic light treatments. The extent of retinal light damage was determined biochemically by rhodop sin or photoreceptor cell DNA measurements 2 weeks after exposure and morphologically by light and electron microscopy at various times afte r light treatment. Results. Rats maintained for 7 to 12 weeks on the l inolenic acid-deficient diet had Significantly lower levels of DHA and significantly higher levels of n-6 docosapentaenoic acid (22:5n-6) in their ROS than deficient-diet animals supplemented once a week with l inseed oil or those fed the nonpurified control diet. As determined by rhodopsin levels and photoreceptor cell DNA measurements, deficient-d iet rats exhibited protection against retinal damage from either inter mittent or hyperthermic light exposure. However, the unsaturated fatty acid content of ROS from all three dietary groups was the same and gr eater than 60 mol%. In 10 week-old deficient-diet rats given linseed o il three times a week, ROS DHA was unchanged for the first 10 days, wh ereas 22:5n-6 levels declined by 50%. After 3 weeks of treatment with linseed oil, ROS DHA and 22:5n-6 were nearly the same as in rats suppl emented with linseed oil from weaning. The time course of susceptibili ty to retinal light damage, however, was different. Hyperthermic light damage in rats given linseed oil for only 2 days was the same as for rats always fed the deficient diet. Six days after the start of linsee d oil treatment, retinal light damage was the same as in rats given th e linseed oil supplement from weaning. Morphologic alterations in ROS of linseed oil-supplemented rats immediately after intermittent light exposure were more extensive than in either the deficient-diet animals or those fed the control diet. The deficient-diet rats also exhibited better preservation of photoreceptor cell nuclei and structure 2 week s after exposure. Conclusions. Rats fed a diet deficient in the linole nic acid precursor of DHA are protected against experimental retinal l ight damage. The relationship between retinal light damage and ROS lip ids does not depend on the total unsaturated fatty acid content of ROS ; the damage appears to be related to the relative levels of DHA and 2 2:5n-6.