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Morphological changes in the photoreceptor cells and retinal epithelium of the albino wistar rat in vitamin A deficiency Yang, Wan Ching


Structural changes in the outer retinas of rats kept on a vitamin. A free diet supplemented with, vitamin A acid were studied by light and electron microscopic techniques. Retinas were sampled at frequent intervals over a period of 11 months of vitamin A deficiency and their morphology compared with that of retinas from rats of the same age, fed a normal diet. Other studies done in conjunction with the above included, (1) measurements of weight gain and plasma vitamin A content in control and vitamin A deficient rats (2) localization of acid phosphatase activity in the retinal epithelium in vitamin A deficiency (3) radioautographic study of H³-methionine incorporation into retinas of control and vitamin A deficient rats. The results showed that vitamin A deficient animals gained weight more slowly than the controls and suffered a rapid decline in plasma vitamin A content after 3 weeks on the special diet. Light microscopic study revealed that the first portions of the photoreceptor cell to suffer degeneration in vitamin A deficiency were the outer segments followed successively by the inner segments, synaptic processes and photoreceptor nuclei. Electron microscopic study revealed that after 3-4 weeks on the special diet, corresponding to the fall in plasma vitamin A levels, the lamellar discs of the photoreceptor outer segments began to break down into vesicles and tubules. After 2.5 months of vitamin A deficiency, the photoreceptor inner segments began to swell and shorten and display loss of mitochonria [sic] and ribosomes in their cytoplasm. After 4-5 months, many outer segments had completely disappeared and further shortening of the inner segments was evident. After 6 months, very few of the "remaining outer segments were intact although it was still possible to identify small number of polysomes and mitochondria within the proximal inner segment cytoplasm next to the photoreceptor nuclei. At this stage, the photoreceptor synaptic processes were also severely affected. The number of synaptic vesicles in each process was greatly reduced and large gaps appeared in the plasma membranes. The synaptic processes were considerably shortened and synaptic sites reduced in number. After 9 months, the outer segments had completely disappeared except for a few remaining clusters of disordered saccules. Both the inner segments and the synaptic processes had retracted markedly towards the photoreceptor nuclei. For the first time, the photoreceptor nuclear envelope began to break down although the nuclear chromatin appeared unchanged. After 10-11 months, only a single irregular row of photoreceptor nuclei remained and each nucleus was surrounded by a narrow rim of cytoplasm containing only a few recognizable organelles. Each photoreceptor cell was surrounded by several layers of membranes probably from glial cell processes. The cell junctions normally forming the outer limiting membrane were now absent in many places. Due to the loss of the photoreceptors the inner neural retina lay very close to the pigment epithelium and the outer processes of the Miller cells were deflected laterally, contributing to the cell membranes surrounding the photoreceptor remnants. Progressive changes were also noted in the structure of the retinal epithelium of the vitamin A deficient animals which were not present in control animals of the same age. By 4-5 months of vitamin A deficiency, large numbers of lysosomes had accumulated in the retinal epithelial cytoplasm close to its inner border. This increase in lysosomes persisted throughout the study as the degeneration of the photoreceptors continued. The lysosomes and the Golgi complexes of the retinal epithelium were found to contain the enzyme, acid phosphatase. The inner or apical processes of the retinal epithelium also proliferated markedly and became very proniinent after 11 months of vitamin A deficiency. Radioautographic studies showed that H³-methionine was incorporated into photoreceptors of both, control and vitamin A deficient animals, thus indicating that protein synthesis continued in photoreceptors in vitamin A deficiency.

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