6 1 overview
Vitamins are a kind of small molecular organic compounds that cannot be synthesized by human body, but are necessary for normal physiological metabolism, and have different functions. They have the following characteristics: ① they exist in natural foods in the form of bulk or precursor compounds; ② It cannot be synthesized in vivo and must be supplied by food; ③ It does not provide energy in the body, and does not participate in the composition of body tissues, but it plays a very important role in regulating substance metabolism; ④ When the body lacks vitamins, the metabolism of substances is impaired, showing different symptoms of deficiency.
There are three naming systems for vitamins. First, according to the historical order of discovery, they are named by English letters, such as vitamin A, vitamin B, vitamin C and vitamin E. Second, it is named after its unique functions, such as anti-dry eye vitamin, anti-furuncle vitamin, anti-circulating blood acid and so on. The third is named after its chemical structure, such as retinol, thiamine and riboflavin. These three naming systems are common to each other.
There are many kinds of vitamins, and their chemical structures are quite different. Generally, it is divided into fat-soluble and water-soluble according to solubility. Fat-soluble vitamins include vitamin A, vitamin D, vitamin E and vitamin K, while water-soluble vitamins include B vitamins (vitamin B 1, vitamin B2, nicotinic acid, pantothenic acid, vitamin B6, folic acid, vitamin B 12, biotin and choline) and vitamin C. The absorption of fat-soluble vitamins in the body is often related to the absorption of fat by the body, and the excretion efficiency is not high. Excessive intake can accumulate in the body and even produce harmful effects, while water-soluble vitamins have high excretion rate, generally do not accumulate in the body and have low toxicity. However, when the equivalent exceeds the physiological needs, there may be adverse effects such as abnormal metabolism of vitamins and other nutrients.
There are also some compounds, such as bioflavonoids, taurine, carnitine, inositol, coenzyme Q and so on. Its activity is similar to that of vitamins, and it is called vitamins.
Many factors can cause vitamin deficiency or deficiency in human body. Vitamin deficiency in human body includes primary and secondary: the primary deficiency is mainly due to insufficient food supply, and the secondary deficiency is caused by factors such as vitamin absorption disorder, enhanced destruction and decomposition, and increased physiological demand. Vitamin deficiency is a gradual process in the body; The initial reserve decreased, followed by abnormal biochemical metabolism and physiological function changes, followed by histopathological changes and clinical symptoms and signs. Mild vitamin deficiency does not necessarily have clinical symptoms, but it can reduce labor efficiency and low resistance to diseases, which is called subclinical deficiency or deficiency. Because the symptoms of subclinical deficiency are not obvious and specific, they are often ignored and should be highly vigilant. The symptoms and signs of multivitamin mixed deficiency are very common in clinic.
6.2 Vitamin A (retinol, an anti-dry eye vitamin)
Physical and chemical properties of 6.2 1 vitamin a
Vitamin A, also known as retinol, exists only in animal foods. There are two forms in animals, namely retinol (A 1) and dehydroretinol (A2), and retinol palmitate is the main storage form. The biological activity of vitamin A exists in the form of alcohol, aldehyde and acid. In vivo, retinol can be oxidized to retinaldehyde, which can be further oxidized to retinoic acid. Retinal aldehyde is the main active form of vitamin A. Some carotenoids can be converted into vitamin A in the body, so they are called provitamin A. At present, about 50 natural carotenoids can be converted into vitamin A, among them, β-carotene, α-carotene, γ-carotene and so on. Both are important. β -carotene has the highest activity and often coexists with chlorophyll. Vitamin A converted from β -carotene accounts for about 2/3 of human vitamin A requirements.
Vitamin A and carotene are soluble in fat and most organic solvents, but insoluble in water. Vitamin A, which naturally exists in animal foods, is relatively stable, and it is not easy to be destroyed in general cooking and canning. However, retinol and its homologues are extremely unstable under the action of oxygen. Only weak oxidants can oxidize retinol, and ultraviolet rays can promote this oxidation process. Under anaerobic conditions, retinol is stable to alkali, but unstable to acid. In the process of rancidity, vitamin A contained in oil will be seriously destroyed, but antioxidant substances such as phospholipids and vitamin E contained in food can improve the stability of vitamin A.
According to the absorption rate and conversion efficiency, most countries use the conversion method that 1μg all-trans retinol is equivalent to 6 μ g β -carotene and 12μg other vitamin A protocarotenoids to calculate the retinol equivalent (RE) of food. That is, Re (μg) = retinol (μg)+0. 1.67× β carotene (μ g)) 0.084× other vitamin A protocarotene (μ g).
In the past, the amount of bioactive substances containing vitamin A was usually expressed in international units (IU).
1000IU vitamin a is equivalent to 300μg invisible flavanol.
1μ GRE = 3.33IU Vitamin A = 6 μ g β -carotene
6.2.2 absorption and metabolism of vitamin a
Vitamin A in food mostly exists in the form of retinyl ester. Retinoic acid ester and vitamin A carotenoid are released from food after being digested by protease in the stomach and polymerized with other lipids. In the small intestine, the ester of retinol and carotene is hydrolyzed by the interaction of bile salts and pancreatic lipase. Digestive products such as retinol, carotene alcohol and carotenoid are emulsified together and absorbed by intestinal mucosa. Bile in the small intestine is a necessary condition for emulsification. Adequate fat promotes the absorption of vitamin A, and antioxidants such as vitamin E and lecithin are also beneficial to the absorption of vitamin A. The use of mineral oil and the existence of intestinal parasites are not conducive to absorption. The absorption rate of vitamin A is significantly higher than that of carotene, which is negatively related to its intake and more obviously depends on the existence of bile salts.
In human body, the main way to convert all-trans β -carotene and other pre-vitamin A carotenoids into vitamin A is oxidative cleavage of the 15 and 15' double bonds in the middle position of carotene. 1β- carotene can form 2 molecules of vitamin A, while other provitamins can only form 1 molecule of vitamin A after decomposition. Most of vitamin A enters the liver from lymphatic vessels through thoracic duct, where it is esterified and stored in hepatic parenchymal cells and stellate cells. A well-nourished person's liver can store more than 90% of total vitamin A, and the storage capacity of kidney is about 1% of that of liver. Vitamin A in the ocular pigment epithelium is the reservoir of retina. The main factors affecting the storage of vitamin A are intake, dietary composition, physiological status of the body, storage and release efficiency of the body, etc.
The average half-life of vitamin A in the body is 128 ~ 154 d, and the daily consumption rate in the liver is about 0.5% of its content without vitamin A intake. Usually, vitamin A in the body will be hydroxylated, epoxidized, dehydrated and oxidized by carbon-carbon bonds, and lose its activity.
6.2.3 Physiological Functions of Vitamin A
(1) Maintaining normal vision The most common function of vitamin A is to maintain certain vision in dark light, which is related to the prevention of night blindness. There are two kinds of photoreceptors in human retina, namely, rod-shaped cells sensitive to dark light and cone-shaped cells sensitive to strong light. Rhodopseudomonas is a photosensitive pigment in retinal rod cells, which is condensed from retinal protein and retinal.
After focusing with red light, the spatial configuration of retinoic acid changes, and finally, qu 1 1- cis-homoretinoic acid is converted into all-trans retinoic acid, which is separated from retinin (that is, rhodopsin is bleached). This change triggered a nerve impulse, which became an image when it was introduced into the brain. This process is light adaptation. At this time, if you enter the darkness, you can't see anything because the rhodopsin sensitive to light disappears. However, if there is enough all-trans retinoic acid (rhodopsin bleaching product from liver and rhodopsin), it can be isomerized by retinol isomerase to form 1 1- cis retinoic acid, and then oxidized to 1 1- cis retinoic acid, and retinol can be synthesized again. The speed of dark adaptation depends on the nature of light (wavelength, intensity, irradiation time) and the nutritional level of vitamin A in the body before entering the dark. If the irradiation conditions are fixed, the speed of dark adaptation depends only on the nutritional level of vitamin A. If vitamin A is sufficient, rhodopsin can regenerate quickly and completely, and the dark adaptation time is short. If vitamin A is insufficient, dark adaptation takes a long time, which can cause night blindness (sparrow blindness) in severe cases. Patients often can't see clearly when they go into the darkness at dusk or in bright places.
(2) Maintaining the structural integrity of epithelial cells. Epithelial tissues are distributed all over the body, such as epidermis, respiratory tract, digestive tract, urinary system and glandular tissues. Vitamin A plays an important role in maintaining the normal growth and differentiation of human skin cells. Vitamin A deficiency can cause epithelial tissue changes, such as decreased gland secretion, dry skin, hyperkeratosis and hyperplasia, desquamation and so on. And eventually lead to dysfunction of the corresponding tissues and organs. The possible mechanism is that vitamin A may participate in the function of glycosyltransferase system and play a role in the operation and activation of glycosyl. When vitamin A is insufficient, it will inhibit the biosynthesis of glycoprotein in mucosal cells, thus affecting the normal function of mucosa.
(3) Promoting growth and maintaining normal immune function Vitamin A can promote protein's biosynthesis and differentiation of bone cells, accelerate growth and enhance the body's low resistance. Alfred, an American epidemiologist and preventive ophthalmologist, believes that children with vitamin A deficiency are more likely to suffer from anemia, infectious diseases and death than normal children, and the incidence rate is directly related to the degree of vitamin A deficiency; If vitamin A is supplemented to a certain amount, the growth will be accelerated, and the disease mortality will be reduced by 30% ~ 40% compared with the same lack of vitamin A.
(4) Effect on Reproduction The relationship between vitamin A and reproduction is related to its effect on the epithelium of reproductive organs. Animal experiments show that female rats suffer from ovulation disorder due to poor development of oviduct epithelial cells caused by vitamin A deficiency. In male rats, the epithelium of vas deferens degenerated, the weight of testis decreased, and sperm and spermatogonia disappeared. In addition, some enzymes with reduced activity due to vitamin A deficiency are necessary for steroid synthesis.
(5) Anti-cancer effect Vitamin A can promote the normal differentiation of epithelial cells and inhibit canceration. Vitamin A can reduce the carcinogenesis of 3,4-phenylpropyl pyrene on liver and lung in rats, and also inhibit the carcinogenesis of nitrosamines on esophagus. Therefore, vitamin A analog 1, 3- cis retinoic acid has been used to prevent epithelial-related cancers, such as skin cancer, lung cancer, bladder cancer, breast cancer and so on. It is also used to treat acute myeloid leukemia.
6.2.4 Vitamin A deficiency and its toxicity
Vitamin a deficiency
In many underdeveloped areas, vitamin A deficiency is a major public health problem. The main reasons for vitamin A deficiency are insufficient vitamin A or provitamin in diet, obstacles in absorption, storage and utilization, and increased physiological requirements without increased intake.
Long-term lack of vitamin A first leads to the decline of dark adaptability and night blindness, and then a series of symptoms that affect the normal development of epithelial tissues, such as dry skin, scaly skin, prickly papules, abnormal roughness and desquamation, are always called hyperkeratosis of hair follicles. The mucosa of respiratory tract, digestive tract, genitourinary organs, cornea and conjunctiva can also be keratinized by epithelial cells, resulting in corresponding symptoms, such as decreased secretion of salivary glands, gastric glands and secretory glands. One of the most obvious is dry eye caused by corneal and conjunctival epithelial degeneration and reduced tear secretion. Patients often feel dry eyes, fear of light, tears, inflammation and pain. In severe cases, it can cause corneal softening and ulcer, corneal folds and Bito's spots (the most important clinical diagnosis sign of vitamin A deficiency in children), which can lead to blindness. It is estimated that about 500 thousand preschool children are blind every year because of lack of vitamin A, and most blind children cannot survive. In addition, due to keratinization and cilia loss of epithelial cells in the absorption tract, the low resistance of the respiratory tract can be reduced and it is easy to be infected, especially for children and the elderly.
Excessive and Toxicity of Vitamin A in 6.2.4.2
Because vitamin A can be stored in the body, excessive intake of vitamin A may cause toxic reactions, including acute, chronic and teratogenic toxicity. Acute toxicity refers to the continuous intake of large doses of vitamin A for one or more times, which often exceeds 100 times the recommended intake for adults or 20 times the recommended intake for children. Its early symptoms include nausea, vomiting, headache, dizziness, blurred vision, muscle disorder and infantile fontanelle. When the dose is particularly large, drowsiness, anorexia, itching and repeated vomiting may occur. Chronic toxicity is more common than acute toxicity, because vitamin A is taken repeatedly within several weeks to several years, and the dose exceeds 10 times of the recommended intake. Common poisoning manifestations include headache, alopecia, cleft lip, dry and itchy skin, pain around the end of long bones, hepatomegaly, muscle stiffness and so on. Embryo absorption, abortion, birth defects and permanent learning loss of offspring are the most serious teratogenic effects of vitamin A. If pregnant women take large doses of vitamin A every day during pregnancy, the relative risk of giving birth to deformed children is 25.6.
6.2.5 Reference Intake of Vitamin A and Food Sources
The results show that the minimum requirement for preventing vitamin A deficiency is not less than 300μ g/d, and the appropriate supply is 600 ~1000μ GRE/d. The RNI (μ GRE/d) of dietary vitamin A in China residents is 400(AI) for 0.5 ~ 3 years old, 500 for 4 ~ 6 years old, and 7 ~/kloc-0. The UL (μ GRE/d) of vitamin a is set as: 4 ~ 17 years old 2000, 18 years old 3000, and pregnant women 2400.
There are two main kinds of vitamin A obtained by human body from food: one is provitamin A, that is, various carotenoids, which mainly exist in dark green or red and yellow vegetables, fruits and other plant foods. Rich in content are spinach, alfalfa, pea seedlings, red sweet potatoes, carrots, green peppers and pumpkins. The other is vitamin A from animal food, which mostly exists in animal liver, milk and dairy products (non-defatted) and eggs in the form of esters.
6.3 vitamin d (calciferol, anti-rickets vitamin)
5.3. Physical and chemical properties of1vitamin D
Vitamin D is the sum of a group of molecules with the same ring structure of A, B, C and D, but different side chains. It is a compound with biological activity of cholecalciferol based on cyclopentadienyl phenanthrene ring. Vitamin D2 and vitamin D3 are the most common. Under the irradiation of sunlight or ultraviolet rays, the precursor of 7- dehydrocholesterol existing in the epidermis or skin tissue of most advanced animals can be converted into vitamin D 3； through photochemical reaction; Vitamin D2 is produced by ultraviolet irradiation of ergosterol in yeast or ergot. Although this vitamin also exists in nature, its stock is very small. There is no difference in the utilization of vitamin D3 and vitamin D2 in mammals.
Vitamin D is a fat-soluble vitamin, which is soluble in fat and fat solvents. Stable to heat under neutral and alkaline conditions. If heated at 130℃ for 90min, its activity can still be maintained, so it is generally not destroyed in daily cooking, but light and acid can promote its isomerization. The oil solution of vitamin D is stable after adding antioxidants. Excessive radiation exposure will form a small amount of toxic compounds.
6.3.2 absorption and metabolism of vitamin d
Vitamin D is always involved in regulating the balance of calcium and minerals in the body. It is now known that these important biological effects are caused by the metabolites of vitamin D. ..
There are two ways to obtain vitamin D needed by human beings, namely, it is formed in the skin and it is obtained from food by mouth. If the skin is exposed to the ultraviolet rays of the sun, many 7- dehydrocholesterol contained in the epidermis and dermis will have a photochemical reaction to form provitamin D3. Once provitamin D3 is formed in the skin, it will be slowly transformed into vitamin D3 at a certain temperature, which takes at least 3 days to complete. Then, the vitamin D binding protein transports vitamin D3 from the skin to the circulatory system. With the help of bile, oral vitamin D is absorbed by small intestine together with fat.
Vitamin D3 obtained from diet and skin binds to plasma α-globulin, of which 60% ~ 80% is accepted by the liver, where it is catalyzed by vitamin D3-25 hydroxylase. 25-(OH) 2-D3 was first hydroxylated at 25 carbon, and then transported to the kidney to be converted into 1a, 25-(OH) 2. A large number of biological effects of vitamin D occur through its metabolite 1a, 25-(OH) 2-D3.
Vitamin D is mainly stored in adipose tissue, followed by liver, and a small amount exists in brain, lung, spleen, bone and skin. Vitamin D is mainly metabolized in the liver, and it is easier to decompose by oral administration than vitamin D obtained from the skin. The main way of vitamin D excretion is through bile, excreted by feces, and a small amount (2% ~ 4%) is excreted by urine.
6.3.3 Physiological Functions of Vitamin D
Vitamin D is mainly related to the metabolism of calcium and phosphorus, which affects the absorption and deposition of these minerals in bone tissue. Vitamin D is converted into active form in liver and kidney, and is passively sent to intestine, bone and kidney, and works with parathyroid hormone to maintain blood calcium level. When the blood calcium level is low, it can promote the synthesis of calcium-binding protein in small intestine, thus increasing the absorption of calcium and phosphorus, and can also promote the reabsorption of calcium by renal tubules and mobilize calcium and phosphorus from bones; When the blood calcium is too high, it will promote the parathyroid gland to produce calcitonin, prevent calcium from mobilizing from bone, and increase the excretion of calcium and phosphorus in urine. Vitamin D promotes the mineralization of bones, cartilage and teeth, and is constantly updated to maintain their normal growth. In addition, vitamin D plays an important role in preventing the loss of amino acids when passing through the kidney, and also has the function of immune regulation, which can change the body's response to infection.
6.3.4 Vitamin D deficiency and its toxicity
Vitamin d deficiency
Lack of vitamin D leads to decreased absorption of calcium and phosphorus in intestine and decreased reabsorption of calcium and phosphorus in renal tubules, which leads to abnormal mineralization of bone marrow and teeth, and then leads to skeletal deformity. The main shortcomings are:
(1) Vitamin D deficiency in rickets leads to abnormal calcification, softening, bending and deformity of bone marrow, which affects the functions of nerves, muscles, hematopoiesis and immune organs. More common in infants.
(2) Osteomalacia is common in adults, especially pregnant women, lactating women and the elderly. The main manifestations are osteomalacia and easy to fracture. At the beginning, the pain in the back and legs was not located, and the activities were often aggravated; In severe cases, it will cause decalcification of bones, osteoporosis, spontaneous and multiple fractures.
Excessive and Toxicity of Vitamin D in 6.3.4.2
The tolerance of human body to vitamin D varies from person to person. Generally, the daily intake should not exceed 400IU( 10μG). Some scholars believe that long-term and short-term intake of 200IU(50μG) of vitamin D will lead to poisoning. Symptoms of vitamin D poisoning include hypercalcemia, hypercalcemia, anorexia, nausea, vomiting, thirst, polyuria, itchy skin, muscle weakness and joint pain. Calcium can be deposited in soft tissues (such as heart, blood vessels, renal tubules, etc. ), which often leads to calcification of heart, kidney and aorta, normal cardiovascular system and renal failure, is the main cause of death. Excessive intake of vitamin D during pregnancy and early infancy can lead to low birth weight, and in severe cases, it can lead to mental retardation and sclerosis.
But usually the source of vitamin D in the diet will not cause excessive consumption.
6.3.5 Reference Intake of Vitamin D and Food Sources (DRIS)
The minimum requirement of vitamin D is still difficult to determine, because the amount of vitamin D3 formed by skin varies greatly. The demand for vitamin D is also related to the intake of calcium and phosphorus. The RNI (μ g/d) of residents' vitamin D is determined as follows: infants ~ 10 years old,1~ 49 years old, 5 years old, pregnant women and lactating mothers over 50 years old, middle and late stage 10, and pregnancy 5.
Due to the potential toxicity of excessive intake of vitamin D, it is generally believed that the intake of vitamin D should not exceed 25 micrograms per day, and the UL of vitamin D for adults and children in China is set at 20 micrograms per day.
Regular sun exposure is the best source of sufficient and effective vitamin D3 for human body, especially for infants and special underground workers. Cod liver oil is a rich source of vitamin D, and its content is as high as 8500 IU/ 100 g. Its preparation can be used as vitamin D supplement for infants, which is of great significance for preventing and treating rickets. Animal food is the main source of natural vitamin D. There are many fatty marine fish and fish eggs, animal liver, egg yolk and cream. Lean meat and milk are less, so many countries strengthen vitamin D in fresh milk and infant formula.
6.4 vitamin e
Physical and chemical properties of 6.4 1 vitamin e
Vitamin e is also tocopherol. At present, there are eight species in nature, including α, β, γ and δ tocopherols, α, β, γ and δ triene tocopherols, all of which have activities, among which α tocopherol has the greatest biological activity.
Vitamin E is a yellowish oily liquid, which is soluble in alcohol, fat and fat solvents, but insoluble in water. Stable to acid and heat, unstable to alkali, easy to oxidize. The rancidity of oil will accelerate the destruction of vitamin E.
6.4.2 Absorption and storage of vitamin E
Vitamin e in the diet is mainly composed of α-tocopherol and γ-tocopherol, and the absorption rate is 20% ~ 25% under normal circumstances. Because of the hydrophobicity of vitamin E, its absorption is similar to dietary fat, and the factors affecting fat absorption also affect its absorption. Vitamin E refers to the hydrolysis of pancreatic esterase and intestinal mucosal esterase before absorption. The absorption mode is mainly passive diffusion, and it can also penetrate into intestinal mucosal cells through intact micelles for absorption. disconnected
Once α -tocopherol and γ -tocopherol enter intestinal cells, they are mixed with other products of dietary lipid digestion and apolipoprotein produced by intestinal cells to form chylomicrons, which enter the systemic circulation through lymph. The liver has the storage function of quickly updating vitamin E, so the liver does not store much vitamin E. Adipose tissue is a long-term storage place for vitamin E, but the accumulation and release of vitamin E in adipose tissue are slow. Muscle is an important place to store tocopherol in the body. Vitamin E exists almost exclusively in fat droplets of fat cells, all cell membranes and lipoproteins in blood circulation.
6.4.3 Physiological Functions of Vitamins
(1) Antioxidant Effect Vitamin E is a strong antioxidant, which can protect cells from free radical damage in the body. Vitamin E is located on the cell membrane, and together with superoxide dismutase (SOD) and glutathione peroxidase (GSH- Peroxidase), it forms an antioxidant system in vivo, which protects polyunsaturated fatty acids, hydrophobic protein components, cytoskeleton and nucleic acids in cell membranes (including organelle membranes) from free radical attacks. Vitamin e can prevent the oxidation of vitamin a, vitamin c and ATP and ensure their normal functions in the body; It can also protect nervous system, skeletal muscle and retina from oxidative damage.
(2) Improving sports ability and anti-aging Vitamin E can protect blood vessels, improve blood flow, enhance mental vitality and improve sports ability; Vitamin E can prolong the life of red blood cells and inhibit catabolic enzymes. Vitamin E can reduce the formation of brown lipids (deposits after decomposition of some components in cells) and protect T lymphocytes, thus protecting human immune function.
(3) Regulating the synthesis of some substances in the body Vitamin E participates in DNA biosynthesis through pyrimidine bases and is related to the synthesis of coenzyme Q. ..
(4) Other vitamin E inhibits the oxidation of selenoprotein and non-hemoglobin ferritin. Protect hydrophobic groups in dehydrogenase from oxidation or chemical reaction with heavy metal ions to lose their functions; Vitamin E can quickly destroy nitrite ions in acidic environment, and it is more effective than vitamin C to block the generation of nitrosamines in the stomach.
6.4.4 Vitamin E deficiency and its toxicity
Vitamin E widely exists in food, and it is less likely to be deficient due to insufficient intake of vitamin E. However, if the absorption of dietary fat in the intestine changes, it can lead to poor absorption of vitamin E, which in turn leads to deficiency. Excessive intake of polyunsaturated fatty acids can also lead to vitamin E deficiency. It is characterized by the decrease of vitamin E in blood and tissues, the increase of erythrocyte fragility and the increase of creatine excretion in urine. When vitamin E is applied, the above symptoms can be obviously alleviated. In addition, epidemiological studies show that the low intake of vitamin E and other antioxidants and the low level of vitamin E in plasma may increase the risk of some cancers, atherosclerosis, cataracts and other degenerative diseases in the elderly.
Due to the low transport rate of vitamin E in placenta, the plasma vitamin E level of newborns, especially premature infants, is low, and polyunsaturated fatty acids on cell membranes are often prone to oxidation and peroxidation, which leads to hemolytic anemia in newborns. Vitamin E supplementation can reduce anemia and restore the normal level of hemoglobin.
Compared with other fat-soluble vitamins, vitamin E is less toxic, but taking large doses of vitamin E will cause short-term gastrointestinal discomfort. A large number of oral vitamin E preparations for premature infants can often significantly increase the incidence of necrotizing enterocolitis. Intake of a large amount of vitamin E may dry up the absorption of vitamin A and vitamin K. When the daily intake is more than > 1200mg tocopherol equivalent, it may also dry up the metabolism of vitamins, thus enhancing the anticoagulant effect of some drugs (such as coumarin).
6 4 5
The AI (mg α-Te/d, α-Te is α-tocopherol equivalent) of dietary vitamin E in Chinese residents are 0 ~ 1 year-old 3, 1 ~ 4 years old 4, 4 ~ 7 years old 5, 7 ~1year-old 7, respectively. When the intake of polyunsaturated fatty acids is high, the intake of vitamin E should also increase accordingly. Generally, 0.4mg of vitamin E should be taken for every intake of 1g polyunsaturated fatty acids. Ul (mg α-te/d,) of vitamin e is determined as follows: infant 3, 1 ~ 4 years old is 4,4 ~ 11year old is 5,7 ~1year old is 7,71year old.
The total tocopherol content of edible vegetable oil is the highest, which can reach 72.37 mg/ 100 g, and the vitamin E content of cereal food is also higher, which is 0.96 mg/ 100 g. Therefore, grain and oil are the main food sources of vitamin E, and other foods such as wheat germ, nuts, beans and eggs are also rich, while meat, fish and fruits are also abundant.
6.5 vitamin B 1 (thiamine, anti-beriberi, anti-neuritis factor)
Physical and chemical properties of 6.5 1 vitamin B 1
Vitamin B 1, also known as thiamine, is the first vitamin obtained in pure form. Thiamine molecule contains a pyrimidine ring and a thiazole ring, which are connected by methylene bridge. Thiamine is white crystal, soluble in water and slightly soluble in ethanol, and smells like yeast. The commercial forms of thiamine are its hydrochloride and nitrate, which are extremely stable in dry conditions and acidic media, difficult to be oxidized and relatively heat-resistant, but easy to be oxidized and lose its activity in neutral, especially alkaline environment. Thiamine is particularly sensitive to sulfite, which can easily break its molecules and make it inactive. In some natural foods, there are anti-thiamine factors, such as sashimi and viscera of mollusks, which contain thiamine enzyme, which will cause the decomposition and destruction of thiamine. It has been reported that animals who eat sashimi for a long time will have vitamin B 1 deficiency. In addition, some vegetables and fruits, such as red cabbage, blackcurrant, and polyhydroxyphenols contained in tea and coffee, can inactivate thiamine through redox reaction.
6.5.2 Physiological Function of Vitamin B 1
The absorption of thiamine is mainly in jejunum, and the absorption modes are active transport and passive diffusion. Thiamine is phosphorylated into phosphate after entering cells. Phosphate forms of thiamine include thiamine monophosphate (TMP), thiamine pyrophosphate (TPP) and thiamine triphosphate (TTP). Free thiamine and its phosphorylated forms exist in different amounts in animal tissues. TPP is the most abundant, accounting for about 80% of the total thiamine, TTP accounts for 5% ~ 10%, and the rest are TMP and thiamine. In animals, these four forms can be transformed into each other. There are 25 ~ 30 mg of thiamine in adults, which are widely distributed in various tissues, especially in liver, kidney and heart.
(1) coenzyme function TPP is the main coenzyme form of thiamine, which participates in two important reactions in vivo, namely, the oxidative decarboxylation of α -keto acid and the trans-keto-alcohol reaction through pentose phosphate pathway. The former is the key link in the process of biological oxidation in mitochondria. TPP, as a coenzyme of pyruvate dehydrogenase and α -ketoglutarate dehydrogenase, participates in the oxidative decarboxylation of pyruvate and α -ketoglutarate. Pyruvate and α -ketoglutaric acid derived from glucose, fatty acids and branched-chain amino acids need oxidative decarboxylation to produce acetyl-CoA and succinyl-CoA, which can enter the bottom of the citric acid cycle of pickled mustard tuber and produce energy necessary for maintaining life. This is one of the most complicated and important reactions in energy metabolism. Therefore, the lack of thiamine will cause extensive damage to the body. Besides TPP, the following auxiliary factors are needed: coenzyme A containing pantothenic acid, nicotinamide adenine dinucleotide (NAD) containing nicotinic acid, magnesium ion and lipoic acid.
TPP is also related to trans-ketoalcoholization, which is an important reaction in pentose phosphate pathway. Through the catalytic reaction of cytoplasmic enzyme trans-ketoalcoholization, 2 or 3 carbons are partially transferred, and 3, 4, 5, 6, 7- carbons are reversibly crossed. Transketoalcoholization is not a direct pathway of glycolysis cycle in carbohydrate metabolism, but it is an important source of NADPH in pentose and fatty acid synthesis in nucleic acid synthesis. Because the activity of transketolase will decrease early when thiamine is deficient, measuring the activity of transketolase in red blood cells can be used as a reliable method to evaluate the nutritional status of thiamine.
(2) Thiamine, a non-coenzyme function, plays an obvious role in maintaining normal functions of nerves, muscles, especially myocardium, maintaining normal appetite, gastrointestinal peristalsis and secretion of digestive juice. This function belongs to non-coenzyme function, and TPP may be used to directly activate chloride channels in nerve cells, and the start of nerve conduction can be controlled by controlling the number of functional channels.
6.5.3 vitamin B 1 deficiency
Insufficient intake of vitamin B 1 and alcoholism are the most common causes of thiamine deficiency. Berberi is the final result of insufficient intake of thiamine by humans and many animals. Patients may have symptoms of gastrointestinal tract such as fatigue, fatigue, irritability, headache, anorexia, etc. at the initial stage of onset, and symptoms of cardiovascular system and nervous system may occur when they continue to lack it. The manifestations of cardiovascular system include cardiac hypertrophy and dilatation (especially right ventricle), tachycardia, respiratory distress and leg edema; Symptoms of nervous system include hyperreflexia, polyneuritis, muscle weakness and pain, and convulsions. "Burning foot syndrome" mostly occurs in the early stage of polyneuritis. When thiamine deficiency is serious, nervous system and cardiovascular symptoms may occur at the same time and may be fatal. Thiamine subclinical deficiency is common in developed countries, and the symptoms are not obvious, mainly manifested as fatigue, headache, decreased labor ability and so on.
In human central nervous system, thiamine deficiency may cause Wernicke encephalopathy and korsakov psychosis, which are typical symptoms of alcoholics. Wernicke encephalopathy is characterized by insanity, ataxia, ophthalmoplegia, psychosis and coma. Kosakov psychosis is a kind of amnesia psychosis.