Effects of environmental lighting and dietary vitamin A on the vulnerability of the retina to light damage.

Abstract—The damaging effect of visible light on photoreceptors and pigment epithelium has been studied mainly in the albino rat with continuous or intermittent exposures to green light for up to several days. Similar damage as in the albino rat but with different doses of light and different times of exposures were observed in pigmented rats, hamster strains, mouse strains and in the nocturnal monkey. The damage is graded histologically mainly by the size of the area of the retina over which the photoreceptors have died. The damage is quantitatively assessed by the measurement of ERG and DNA content of the retina. The action spectrum for the irreversible damage agress with the absorption curve for rhodopsin. Threshold damage occurs with diffuse light that reduces acutely the rhodopsin of the whole retina by about 10%. Damage is a function of body and eye temperature during exposure. At a body temperature of 42°, 2–4 h of exposure produces the same damage as exposure for 30 h at normal temperature using 1500 lux. The damage is also very markedly dependent upon the light history of the animal prior to exposure. Cyclic environmental light of I to 10 ft-cd for several days or weeks reduces very significantly the damaging effect compared to animals reared simultaneously in continuous darkness. Cyclic light rearing is associated with a reduction in opsin and rhodopsin of the whole retina, an increase in the molar phospholipid/opsin ratio and a reduction in the length of the outer segment. Protection is also produced by Vitamin A deficiency but significantly only when rhodopsin content is decreased by maintenance in very weak cyclic light. Thus Vitamin A deficiency and environmental light seem to use the same mechanism. Results do not support the possibility that damage is caused by a cytotoxic effect of retinol.