RETINAL ABNORMALITIES IN EXPERIMENTAL VITAMIN-E-DEFICIENCY

Physiological and biochemical studies have been carried out longitudin ally over a period of 12 months in vitamin E deficient and control rat s to gain an understanding of the mechanism whereby vitamin E conserve s normal retinal function. Electroretinographic studies indicated that the primary effect of vitamin E deficiency was on the photoreceptors. Ultrastructural studies, however, did not show any morphological chan ges to the photoreceptors which could explain receptor dysfunction. A 30-40% loss of vitamin A (retinol) was found to be associated with vit amin E deficiency. This could be corrected by repletion with vitamin E , but there was no associated improvement in visual function. An irrev ersible loss of the long-chain polyunsaturated fatty acids from the re tina, increased lipid peroxidation and alterations in membrane fluidit y were also detected during vitamin E deficiency. We suggest that a de ficiency of vitamin E leads to changes in the membrane microenvironmen t, which could affect photo transduction by either impairing the abili ty of rhodopsin to undergo conformational changes to the active form, or by disrupting the hyperpolarising and depolarising processes of the photoreceptors. (C) 1998 Elsevier Science Inc.