Vitamin A is a group of biologically active molecules called retinoids. It has 4 different forms (i.e. retinol, retinoic acid, retinal phosphate, and retinal) which are mainly involved in vision. Humans cannot synthesize retinoids and instead they use external sources rich in β-carotene which is a precursor of retinol (e.g. yellow and orange fruits and vegetables Figure 1). Figure 2 shows that β-carotene, when oxidized, will be cleaved at the center and will produce 2 molecules of retinol which
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when oxidized again will produce 11-cis-retinal, which is also convertible to 11-trans-retinal via photoisomerization. These two , 11-cis-retinal and 11-trans-retinal, are essential molecules for the sense of vision and are necessary for sending neural signals from the retina of the eye, to the brain (Nelson & Cox, 2008).
In the absence of light the photoreceptor cells in the retina (Figure 3) contains metarhodopsin I which is composed of 11-cis-retina and opsin. In the presence of light, 11-cis-retinal will undergo geometrical changes and will become 11-trans-retinal. The photoisomerization will then be the reason for the conformational change of metarhodopsin I to metarhodopsin II. Metarhodopsin II will then activate the G-protein and produce a cascade of complex biochemical reactions resulting into the generation of nerve impulses to the
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occipital lobe, the visual center for proper interpretation. Metarhodopsin II is also unstable and will split yielding opsin and the 11-trans-retinal. The expelled 11-trans-retinal will then be combined with an opsin to regenerate 11-cis-retinal via isomerization.
Besides the retina, retinoids also exist on different cells (e.g. epithelial cells). Retinoic acid, from the oxidation of retinol, enters the nucleus with the help of the cellular retinol-binding proteins and the cellular retinoic acid binding proteins. In the nucleus, retinoic acid binds to its receptors forming an activated retinoic acid receptor complex which then binds to the hormone response elements (HRE) of the DNA, activating transcription of specific genes, resulting into the translation of specific proteins that mediate several physiologic and metabolic functions.
In vitamin A deficiency, there is a possible loss of sensitivity to green light, impairment to adapt to dim light and night blindness. Prolonged deficiency leads to xerophthalmia, the keratination of cornea and blindness. Mild deficiency will also lead to increased susceptibility to infectious diseases as it has an important role in the differentiation of immune system cells (Murray et al. 2009).
As there is a limited capacity in storing fat soluble vitamins, excessive intakes of vitamin A will lead to accumulation beyond the capacity of binding proteins where unbound vitamin A will cause tissue damage. Central nervous system will also be affected as there is an increase in cerebrospinal fluid. Liver, calcium homeostasis and the skin should also be observed (Murray et al. 2009).
In vitamin A deficiency, there is a possible loss of sensitivity to green light, impairment to adapt to dim light and night blindness. Prolonged deficiency leads to xerophthalmia, the keratination of cornea and blindness. Mild deficiency will also lead to increased susceptibility to infectious diseases as it has an important role in the differentiation of immune system cells (Murray et al. 2009).
As there is a limited capacity in storing fat soluble vitamins, excessive intakes of vitamin A will lead to accumulation beyond the capacity of binding proteins where unbound vitamin A will cause tissue damage. Central nervous system will also be affected as there is an increase in cerebrospinal fluid. Liver, calcium homeostasis and the skin should also be observed (Murray et al. 2009).