We designed an experiment to study the role of light history and polyunsaturated fatty acids (PUFA) on the susceptibility of the albino rat retina to light damage. Albino rats were born to dams that had been kept in either 1 lx or 250 lx cyclic light for 0-4 days prior to delivery and fed one of three diets containing either 10% (by weight) hydrogenated coconut oil (COC, no n-3 nor n-6 fatty acids), safflower oil (SAF, high n-6, < 0.1% n-3 fatty acids), or linseed oil (LIN, high n-3, low n-6 fatty acids). After weaning, the rats were maintained in the same light environment and fed the same diets for 9 weeks, at which time some were killed and their retinas processed for morphometric analysis. Animals raised in bright cyclic light had shorter ROS lengths and thinner outer nuclear layers (ONL) than rats raised in dim cyclic light. The LIN animals had a thinner ONL than animals of the SAF or COC groups. Rats from each diet and light rearing groups were exposed to constant illumination of 2000 lx for 24 hr, after which they and non-exposed controls were placed in 1 lx cyclic light for 10 days and analysed for changes in ONL thickness. In the 250 lx (bright; B) groups, there was no effect of acute light stress on ONL thickness, although both control and stressed LIN animals had a thinner ONL than the corresponding COC and SAF groups. However, in the rats raised in 1 lx cyclic light, acute stress resulted in significant retinal damage (i.e. decrease in ONL thickness) in the three diet groups combined. The superior region was damaged the most and the severity was dependent on diet, as evidenced by the LIN group having a greater reduction in ONL thickness than the SAF group after light stress. From these results we conclude that rats on diets high in n-3 fatty acids are more susceptible to photoreceptor cell loss than animals fed n-6 or no polyunsaturated fatty acids when raised in dim cyclic light. These results show that both diet and light history play a role in the susceptibility of the retina to acute and chronic effects of light and suggest a role for lipid peroxidation in retinal light damage.