(1) It constitutes the photoreceptors of the retina, i.e., the optic pigments.　　It is known that vitamin A deficiency mainly affects dark vision, and dark vision is related to the retinal rod cells contained in the visual purple (visual purple, also known as rhodopsin). Visual purple is produced by the binding of an aldehyde derivative of vitamin A (retinaldehyde) to a protein. The binding of retinaldehyde to retinal protein requires that the latter has a certain conformation, and in vivo only 11-cis retinaldehyde can bind to retinal protein, a binding reaction that requires energy and takes place only in darkness, because retinaldehyde breaks down readily in the presence of light. Retinal is very sensitive to low light, and even a single light quantum can induce a photochemical reaction that leads to its eventual breakdown into retinoids and all-trans retinoids.　　This process is also called "bleaching" because of the loss of color due to the breakdown of retinal pigments. Bleaching of retinal pigments is an exergonic reaction, in which energy is converted to nerve impulses through structures unique to the outer segments of the optic rod cells, causing vision. Due to the decomposition of the retinal plasma, the amount of retinal plasma remaining in the retina is very small, if not synthesized in time, the retina can no longer feel the stimulation of low light, and at this time in the dark of the weak light can not see the object. However, the all-trans retinaldehyde produced by the decomposition of retinal pigment can be converted to 11-cis retinol by reduction and isomerization, and further oxidized to 11-cis retinaldehyde. In this way, in the dark, 11-cis-retinal can bind to retinal to produce retinal again.　　People from the bright light into the dark, initially can not see the object, but stop for a while, due to the synthesis of retinaldehyde in the dark increased, the decomposition is reduced, the rod cell content of retinaldehyde gradually accumulated, the perception of low light is strengthened, and then can see the object, a process known as dark adaptation (dark adaptation). From the above figure, we can see that when vitamin A deficiency, 11-cis-retinal can not get enough supplementation, the synthesis of the rod cell retinoschisin is weakened, the ability of dark adaptation decreases, which can lead to night blindness (night blindness), the motherland medicine called this symptom "bird's eye".　　(2) Maintain the integrity and soundness of the epithelial structure Vitamin A is necessary to maintain the soundness of all epithelial tissues, the lack of epithelial dryness, hyperplasia and keratinization, including the eye, the respiratory tract, the digestive tract, the urinary tract and the reproductive system, etc., epithelial impact is most significant. In the eye, due to keratinization of the lacrimal epithelium, tear secretion is impeded, resulting in corneal, conjunctival dryness produces dry eye disease (xerophthalmia), so vitamin A is also known as anti-dry eye vitamin. Sebaceous glands and sweat glands keratinization, dry skin, perifollicular hyperkeratosis, follicular papules and hair loss. Due to the incomplete epithelial tissue, the body's ability to resist microbial invasion is reduced, and it is easy to get infected with diseases.　　(3) Promote growth and development When vitamin A is deficient, children may experience growth arrest, poor bone growth and stunted development. In vitamin A deficient female rats, ovulation is reduced, affecting reproduction.　　The mechanism of how vitamin A maintains the integrity of epithelial tissue and promotes growth and development in children and young animals has not been fully elucidated. Recent studies have shown that vitamin A (retinol) and its derivative retinoic acid can affect the differentiation process of epithelial cells. In vitamin A deficiency, epithelial cells in culture tend to differentiate into complex squamous epithelia, whereas the addition of vitamin A to the culture medium attenuates the expression of this phenotype and stimulates the formation of mucus-secreting epithelia. The molecular mechanism of vitamin A has been shown to have steroid hormone-like effects by binding to intracellular receptors, forming complexes that translocate to the nucleus, initiating the transcription of certain genes, and promoting the synthesis of certain proteins. This effect has been confirmed in keratin synthesis in keratinocytes and type IV collagen synthesis in embryonic cancer cells. Retinoic acid also promotes normal embryonic development and differentiation and acts against pro-cancer agents (promoters). However, it has been suggested that the anticancer effect of vitamin A does not lie in its modulation of gene expression, but is related to its action on the cell surface. Vitamin A is known to promote the synthesis of glycoproteins, especially glycoproteins and fibronectin, which are cell surface receptors. Cancerous cells lose their normal adhesion capacity on their surface due to the lack of fibronectin, a defect that can be reversed by vitamin A. Vitamin A also increases the number of EGF receptors (epithelial growth factor receptors) on the cell surface, which promotes growth by facilitating the binding of EGF to cells.