PubMed · 5294942
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H Viallefont. 1965. [Dyschromatopsia and work problems].. https://pubmed.ncbi.nlm.nih.gov/5294942/
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Normal colour vision is trichromatic and is mediated by the blue, green and red visual pigments present in the corresponding blue, green, and red cone cells of the retina. The red and green pigment genes have evolved from an ancestral pigment gene and reside in a head-to-tail tandem array on the long arm of the X chromosome. This arrangement and a high degree of homology predispose to illegitimate recombination between the red and green pigment genes explaining the various forms and the high frequency of red-green colour vision defects.
Color vision standards for various occupations and schools have been greatly eased recently. However, if the trend is unaccompanied with proper advice for color defective persons, there is a risk of accidents such as occurred in the past when color vision standards had not been introduced, because the color vision defect is unchanged. In this context, the history of color vision standards and the color confusion by color defective persons in their daily life were reviewed. The collected data together with pathophysiological characteristics of defective color vision suggest that at least the following measures are necessary from a practical point of view: (1) By education and awareness, color defective persons can avoid errors in color in most cases. Therefore, ophthalmologists should inform them of their defects in childhood and give instructions on how to compensate for their disadvantages. (2) In public and occupational situations, all the information conveyed by color should include lettering or other forms of redundancy for the convenience of color defective persons.
Mutations of the gene encoding rhodopsin are responsible for 30% of the cases autosomal dominant retinitis pigmentosa. Rhodopsin molecules are key G-coupled transmembrane proteins initiating the visual transduction cascade in rods. These cells are specialized retinal cells allowing the detection of low intensity lights. Mutations in the rhodopsin gene lead to the progressive destruction of rods, clinically translated by night blindness, a progressive bilateral loss of the peripheral visual field, and predominant alterations of the rod component of the electroretinograms. Inherited colour vision deficiencies are mainly caused by alterations of the genes encoding coloured opsins. These proteins are G-coupled receptors specialized in visual transduction in the cones. These sensorial cells are localized in the center of the neural retina where they allow the detection of refined details and chromatic lights. Rearrangements of the genes encoding the green and the red color pigments are responsible for daltonism.