423
absorption efficiency is assessed as 80%. Retinol levels should exceed 300 μg/L of
blood plasma.
Vitamin A deficiency may manifest itself by decreased immunity to infections,
growth inhibition, and reproduction disorders. Typical pathological signs of vitamin
A avitaminosis include lesions of the mucous membranes of the gastrointestinal
tract, air passages, and urinary system. Skin keratosis can be seen, especially around
outlets of the hair sheaths (phrynoderma). Vitamin A can be toxic when ingested in
overly large doses. The most common sign of excessive vitamin A intake is the socalled dermal paralysis manifested by changes in skin pigmentation and dryness,
accompanied by nail brittleness and hair loss. Vitamin A excess may be the reason
for joint and bone pain as well as weight loss. Enlargement of the liver and spleen
usually occurs (hepatosplenomegaly). Teratogenic activity has also been suggested,
notably birth defects. Symptoms of acute toxicity include a headache, nausea and
vomiting, convulsions, and light intolerance.
Vitamin D
Vitamin D is considered a hormone-like compound. Ergosterol is a vitamin D 2 precursor, a phytosterol that occurs mainly in plants. Ergocalciferol results from UV
irradiation of ergosterol. 7-Dehydrocholesterol can be converted into the most
active form—vitamin D 3 (cholecalciferol). Ergosterol and 7-dehydrocholesterol are
clearly identified as provitamin D because, after irradiation of the skin with UV
light or exposure to sunlight, they can be converted into the active vitamin D 2 and
D 3 forms.
Vitamins synthesized in the skin (D 3 ) and those supplied with food undergo the
same transformations, finally leading to the generation of their active metabolites.
They are deposited in the liver, lungs, and kidneys as well as in fatty tissue. The
amount of vitamin D in the organism depends on exposure to sunshine and diet, and
it ranges from 65 to 165 IU/100 mL blood. All forms of this vitamin are being
absorbed in the small intestine with a bile salt, fatty acids, and acylglycerols present,
and then delivered to the liver bound to a specific vitamin D-binding protein. From
the liver, the vitamin is transported via chylomicrons to the bloodstream. Molecules
of vitamin D 2 and D 3 are activated in the liver by hydroxylation; the OH group
appears at carbon-25 to give 25-hydroxy-D 3 [25-(OH)]D. Further reaction occurs in
the kidneys, bone, cartilage, and/or in the placenta under the influence of the specific
D 3 –1-hydroxylase. The next two stages produce the most potent and physiologically
active molecule, 1,25-dihydroxy vitamin D 3 [1,25-(OH) 2 D 3 ]. According to the most
recent nomenclature, it is called calcitriol. 25-(OH)-D is activated under the influence of the specific D3–24-hydroxylase at carbon-24 [24,25-(OH)2D3]. Both circulate in the bloodstream, and their main function as active metabolites is maintaining
the homeostasis of calcium and phosphorus, which is vital for many body functions.
In human and animal organisms, vitamin D deficiency can result from its decreased
synthesis in the skin or disturbances in its metabolism related to malabsorption in the
Nutraceutical Properties of Lipids
absorption efficiency is assessed as 80%. Retinol levels should exceed 300 μg/L of
blood plasma.
Vitamin A deficiency may manifest itself by decreased immunity to infections,
growth inhibition, and reproduction disorders. Typical pathological signs of vitamin
A avitaminosis include lesions of the mucous membranes of the gastrointestinal
tract, air passages, and urinary system. Skin keratosis can be seen, especially around
outlets of the hair sheaths (phrynoderma). Vitamin A can be toxic when ingested in
overly large doses. The most common sign of excessive vitamin A intake is the socalled dermal paralysis manifested by changes in skin pigmentation and dryness,
accompanied by nail brittleness and hair loss. Vitamin A excess may be the reason
for joint and bone pain as well as weight loss. Enlargement of the liver and spleen
usually occurs (hepatosplenomegaly). Teratogenic activity has also been suggested,
notably birth defects. Symptoms of acute toxicity include a headache, nausea and
vomiting, convulsions, and light intolerance.
Vitamin D
Vitamin D is considered a hormone-like compound. Ergosterol is a vitamin D 2 precursor, a phytosterol that occurs mainly in plants. Ergocalciferol results from UV
irradiation of ergosterol. 7-Dehydrocholesterol can be converted into the most
active form—vitamin D 3 (cholecalciferol). Ergosterol and 7-dehydrocholesterol are
clearly identified as provitamin D because, after irradiation of the skin with UV
light or exposure to sunlight, they can be converted into the active vitamin D 2 and
D 3 forms.
Vitamins synthesized in the skin (D 3 ) and those supplied with food undergo the
same transformations, finally leading to the generation of their active metabolites.
They are deposited in the liver, lungs, and kidneys as well as in fatty tissue. The
amount of vitamin D in the organism depends on exposure to sunshine and diet, and
it ranges from 65 to 165 IU/100 mL blood. All forms of this vitamin are being
absorbed in the small intestine with a bile salt, fatty acids, and acylglycerols present,
and then delivered to the liver bound to a specific vitamin D-binding protein. From
the liver, the vitamin is transported via chylomicrons to the bloodstream. Molecules
of vitamin D 2 and D 3 are activated in the liver by hydroxylation; the OH group
appears at carbon-25 to give 25-hydroxy-D 3 [25-(OH)]D. Further reaction occurs in
the kidneys, bone, cartilage, and/or in the placenta under the influence of the specific
D 3 –1-hydroxylase. The next two stages produce the most potent and physiologically
active molecule, 1,25-dihydroxy vitamin D 3 [1,25-(OH) 2 D 3 ]. According to the most
recent nomenclature, it is called calcitriol. 25-(OH)-D is activated under the influence of the specific D3–24-hydroxylase at carbon-24 [24,25-(OH)2D3]. Both circulate in the bloodstream, and their main function as active metabolites is maintaining
the homeostasis of calcium and phosphorus, which is vital for many body functions.
In human and animal organisms, vitamin D deficiency can result from its decreased
synthesis in the skin or disturbances in its metabolism related to malabsorption in the
Nutraceutical Properties of Lipids