[Hearing, mental performance, psyche].
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Biomedical subjects
Publications and source records attributed to R Albrecht.
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The effects of vitamin A deficiency in the rat eye, as measured by the electroretinogram and changes in rhodopsin content, are critically dependent upon the levels of illumination to which the animals are exposed daily. Depleted animals kept in darkness maintained virtually normal electroretinogram function and rhodopsin content for 5 to 6 months while those kept in weak cyclic light lost rhodopsin continuously. A fraction of the retinol released from rhodopsin during illumination disappears presumably from the pigment epithelium into the blood and becomes unavailable for rhodopsin regeneration. A sequence of three first-order reactions was assumed to estimate the rate constant of this disappearance (0.03 per hour). Computer simulation supporting the experimental data illustrates the dependence of the retinal abnormalities on light.
Diffuse retinal irradiation by visible light produces in the rat the death of visual cells and pigment epithelium. Typically, cage illumination of 1500 lux from fluorescent light through a green filter leads to severe damage when continued for 40 hours. Vitamin A deficiency protects against this damage but experiments show that retinol released by light from rhodopsin is probably not the toxic agent. Protection against light damage depends on a long-range state of cell adaptation to light itself. The normal diurnal cycle of light and dark seems to be the essential factor in controlling visual cell viability and susceptibility.
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