Vitamin A is one of the earliest discovered vitamins. The effects of its deficiency were already known in ancient Egypt, Greece and Rome and were called the name of night blindness or blindness. The disease was treated by giving a boiled or raw liver. It was only at the turn of the 19th and 20th century that the relationship between improper nutrition and the development of chicken blindness was established. Vitamin A was discovered in 1913 by American researchers Elmer McCollum and Marguerite Davis, and the name “vitamin A” was given to it in the 1920s. Initially, the presence of vitamin A in the course of taking together with vitamin D caused problems in determining the actual properties of each of these vitamins.
In animal nutrition, the basic form in which vitamin A is present is an ester – retinol palmitate, which in the small intestine undergoes de-esterification into alcohol – retinol. Other important derivatives associated with vitamin A activity are retinal (aldehyde) and retinoic acid (tretinoin).
The content of vitamin A in food or dietary supplements is usually given in the so-called International Units (IU – International Units). On the other hand, scientists developing standards of recommended daily intake usually use another unit: micrograms of retinol equivalent (μg RAE – Retinol Activity Equivalents). Converting one unit to another is not straightforward (a varied diet containing 900 μg of retinol equivalent may contain 3-36 thousand IU of vitamin A):
1 IU retinol = 0.3 μg RAE
1 IU beta-carotene in the dietary supplement = 0.15 μg RAE
1 IU beta-carotene in food = 0.05 μg RAE
1 IU alpha-carotene or cryptoxanthin = 0.025 μg RAE
Recommended daily intake
The given values expressed in micrograms of retinol equivalent (μg RAE) are presented in the RDA (Recommended Dietary Allowance): average daily intake level sufficient to meet the nutritional requirements of almost every (97 – 98% of the total) healthy person.
* Exceptions are values for the age up to 12 months: they represent the so-called sufficient intake (AI – Adequate Intake)
Food sources of vitamin A
The richest natural sources of vitamin A for humans are: fish oil (30 mg RAE [a] / 100 g), liver and offal (2-28 mg RAE / 100 g), sweet potatoes (1 mg RAE / 100 g), carrots (835-850 μg RAE / 100 g), kale (500-700 μg RAE / 100 g), spinach (about 500 μg RAE / 100 g), pumpkin (300-400 μg RAE / 100 g).
The main source of active forms of vitamin A in the body is consumed with plant-derived food provitamin A (mainly β-carotene).
In the human body, the enzyme responsible for the conversion of β-carotene into retinal is β-carotene dioxygenase.
The physiological importance of vitamin A
Vitamin A performs many important physiological functions.
Functions of retinol (only it shows full biological activity) and retinal:
– plays an important role in receiving visual stimuli in the retina of the eye. The derivative of vitamin A, 11-cis retinal in rods, combines with the opsin protein to form rhodopsin (visual purple). Even a single photon raises the photoisomerization of 11-cis-retinal to trans-retinal, which leads to stimulation .
– responsible for the integrity of cell membranes
– is responsible for the proper functioning of epithelial tissue cells, both covering secretory and sensory
– regulates the growth of epithelial tissue and other body cells
– maintains the proper condition of the skin, hair and nails
– provides normal growth of bones and teeth by regulating the activity of bone tissue cells
– protects the epithelium of the respiratory system against germs
– is responsible for the proper production of type IV collagen and alkaline phosphatase
– differentiates cells: osteoblasts, keratinocytes, fibroblasts, spermatocytes and stem cells
– antitumor activity: in acute myelogenous leukemia, it inhibits cell proliferation, increases TNF alpha secretion and activates lymphocytes
Carotenoids are antioxidants and are generally moderately anticancer, however, in smokers, large doses of synthetic β-carotene both increase the incidence of lung cancer and higher mortality. A similar relationship was found in laboratory animals exposed to tobacco smoke.
When the body’s cells need retinol, it is released from the liver to the general circulation. Retinol in the blood is transported by the RBP protein (retinol binding protein), this complex is also combined with transthyretin (a protein that prevents the kidneys from expelling this complex). The retinoic acid in the blood is transported with albumin. In the cell, retinol combines with the cellular retinol binding protein (cRBP) and retinoic acid with cRABP. Bound retinoid molecules have specific RAR and RXR nuclear receptors containing DNA binding sites, also called RARE retinoic acid response sites.
The daily requirement of the human body for vitamin A is determined to be about 1 mg.
Vitamin A deficiency causes keratinization of epithelia:
– the digestive tract
The effects of scarcity:
– xerophthalmia – drying of the conjunctiva and cornea
– fragile, slowly growing nails
– dry skin, sometimes manifesting in areas of irritation
– lack of appetite
– twilight blindness (so-called “blindness blindness”)
– worsening of sight
– inhibition of growth
– disappearance of epithelia
– hand and foot horn
– alopecia areata
– tendency to diarrhea
– bad mood
In countries where the main component of the diet is rice, there are frequent deficiencies of vitamin A. In order to allow increased intake of vitamin A, genetic engineering has been produced so-called. golden rice, containing maize genes encoding provitamin A.
The livers of some animals, especially polar ones, often contain vitamin A in amounts toxic to humans.
A single dose of 2-5 million IU (0.6 to 1.5 g retinol) can cause symptoms of acute intoxication in an adult human. This corresponds approximately to the intake of 100 to 300 g of polar bear liver.
Symptoms of acute poisoning are probably caused by an increase in intracranial pressure:
– muscle coordination disorders
Other symptoms include:
– bad mood
– flaking of the epithelial skin
The first death (Xavier Mertz, a Swiss scientist) commonly attributed to hypervitaminosis A occurred in January 1913 during an expedition to Antarctica. Mertz, after losing his food supplies, was forced to eat draft dogs. However, this cause of the death of Xavier Mertz is questionable in the light of modern medical knowledge.
– congenital malformations in children of mothers with hypervitaminosis during pregnancy
– liver disorders
– reduced bone calcification that may lead to osteoporosis
– joint pain and swelling
– nausea and vomiting
– lack of appetite
– hemorrhagic diathesis
– subperiostatic bone thickening
Breeding of surgical eyes without water in the water containing vitamin A increases the probability of additional eye growth by 70%