Vitamins PDF

Physiological Functions of Vitamins Prof. Dr. Özgür Kasımay What will we talk about? Daily Requirements Fat / Water Soluble Vitamins Storage of Vitamins Vitamin A Thiamine (Vitamin B1) Niacin Riboflavin (Vitamin B2) Vitamin B12 Folic Acid (Pteroylglutamic Ac...

Physiological Functions of Vitamins Prof. Dr. Özgür Kasımay What will we talk about? Daily Requirements Fat / Water Soluble Vitamins Storage of Vitamins Vitamin A Thiamine (Vitamin B1) Niacin Riboflavin (Vitamin B2) Vitamin B12 Folic Acid (Pteroylglutamic Acid) Pyridoxine (Vitamin B6) Pantothenic Acid Ascorbic Acid (Vitamin C) Vitamin D Vitamin E Vitamin K 2  Daily Requirements Essential nutrients needed for normal functioning, growth, and maintenance of body tissues Do not provide calories (energy) Needed in very small amounts mg = 1/1000 of a gram mcg = 1/1,000,000 of a gram Lack of vitamins in the diet can cause important metabolic deficits. These requirements differ, depending on body size, rate of growth, amount of exercise, and pregnancy. 3 4 5 6 Fat Soluble Vitamins A, D, E, K Absorbed with dietary fat Stored in liver and fat Toxicity more likely (especially A and D) 7 Water Soluble Vitamins C, the 8 B vitamins Little stored (except B12) Less toxic, excess is excreted More fragile, easily destroyed by –Cooking –Alkaline –Light 8 Storage of Vitamins Vitamins are stored to a slight extent in all cells. Some vitamins are stored to a major extent in the liver. The quantity of vitamin A stored in the liver may be sufficient to maintain a person for 5 to 10 months without any intake of vitamin A. vitamin D stores - 2 to 4 months The storage of most water-soluble vitamins is relatively slight. When a person’s diet is deficient in vitamin B compounds, clinical symptoms of the deficiency can sometimes be recognized within a few days (except vitamin B12). Absence of vitamin C, can cause symptoms within a few weeks and can cause death from scurvy in 20 to 30 weeks. 9 Vitamin A Fat soluble 3 active forms: retinol, retinal, retinoic acid Beta-carotene (and other carotenoids) are precursors or provitamins Beta-carotene yields two molecules of vitamin A 10 Vitamin A Vitamin A occurs in animal tissues as retinol. Vitamin A does not occur in vegetables. Provitamins have role in formation of vitamin A. They occur in many vegetable foods. yellow and red carotenoid pigments Y have similar chemical structures Y can be changed into vitamin A in the liver 11 Vitamin A Deficiency Vitamin A is used in the formation of the retinal pigments of the eye. Vitamin A is needed to form the visual pigments and prevent night blindness. Vitamin A is also necessary for normal growth of most cells of the body and especially epithelial cells. When vitamin A is lacking, the epithelial structures of the body tend to become stratified and keratinized. 12  Vitamin A deficiency manifests itself by 1) skin problems and sometimes acne; 2) failure of growth, cessation of skeletal growth; 3) failure of reproduction, atrophy of the germinal epithelium of the testes and interruption of the female sexual cycle; and 4) keratinization of the cornea, corneal opacity and blindness. 13 an “anti-infection” vitamin In vitamin A deficiency, the damaged epithelial structures often become infected, for example, the conjunctivae of the eyes, the linings of the urinary tract, and the respiratory passages. Vitamin A has been called an “anti-infection” vitamin. 14 Thiamine (Vitamin B1) Thiamine has a function in the body as thiamine pyrophosphate. It functions as a cocarboxylase, operating mainly in conjunction with a protein decarboxylase for decarboxylation of pyruvic acid and other a-keto acids. Thiamine is specifically needed for the final metabolism of carbohydrates and many amino acids. Thiamine deficiency (beriberi) causes decreased utilization of pyruvic acid and some amino acids by the tissues, but increased utilization of fats. 15 Thiamine Deficiency Causes Lesions of the Central and Peripheral Nervous Systems In thiamine deficiency, the utilization of glucose by nervous tissue may be decreased 50 to 60 per cent and is replaced by the utilization of ketone bodies derived from fat metabolism. The neuronal cells show chromatolysis and swelling during thiamine deficiency. Degeneration of myelin sheaths of nerve fibers in both the peripheral nerves and the central nervous system. Lesions in the peripheral nerves frequently cause them to become extremely irritable, resulting in “polyneuritis” Paralysis Muscles atrophy and severe weakness are also seen. 16 Thiamine Deficiency Weakens the Heart and Causes Peripheral Vasodilation A person with severe thiamine deficiency eventually develops cardiac failure because of weakened cardiac muscle. Thiamine deficiency causes peripheral vasodilation, as a result of decreased release of metabolic energy in the tissues, leading to local vascular dilation. Further, the venous return of blood to the heart may be increased to as much as two times normal. Peripheral edema, ascites also occur. 17  Thiamine Deficiency Causes Gastrointestinal Tract Disturbances Indigestion, severe constipation, anorexia, gastric atony, and hypochlorhydria All these effects presumably result from failure of the smooth muscle and glands of the gastrointestinal tract to derive sufficient energy from carbohydrate metabolism. The overall picture of thiamine deficiency, including polyneuritis, cardiovascular symptoms, and gastrointestinal disorders, is frequently referred to as beriberi. 18 Niacin (Vitamin B3) Nicotinic acid, nicotinamide adenine dinucleotide (NAD) and nicotinamide adenine dinucleotide phosphate (NADP) These coenzymes are hydrogen acceptors. Niacin can be made from the amino acid tryptophan. When a deficiency of niacin exists, oxidative delivery of energy from the foodstuffs to the functioning elements of all cells cannot occur at normal rates. 19 Niacin deficiency Muscle weakness and poor glandular secretion may occur. Niacin deficiency causes inflammation of the mucous membranes of the gastrointestinal tract, resulting in many digestive abnormalities. It is possible that this results from failure of appropriate epithelial repair. Tissue death, dementia or many types of psychoses, the skin problems can be seen. The clinical entity called pellagra is caused mainly by niacin deficiency. Pellagra ( Diarrhea, Dermatitis, Dementia, Death) Pellagra is greatly exacerbated in people on a corn diet, because corn is deficient in the amino acid tryptophan. 20 Riboflavin (Vitamin B2) Riboflavin combines in the tissues with phosphoric acid to form two coenzymes, flavin mononucleotide (FMN) and flavin adenine dinucleotide (FAD). They operate as hydrogen carriers in important oxidative systems of the mitochondria. Severe riboflavin deficiency can cause many of the same effects as a lack of niacin in the diet; because of depressed oxidative processes within the cells. Mild riboflavin deficiency causes digestive disturbances, burning sensations of the skin and eyes, cracking at the corners of the mouth, headaches, mental depression, forgetfulness. 21 Vitamin B12 Several cobalamin compounds that possess the common prosthetic group shown next exhibit so-called vitamin B12 activity. This prosthetic group contains cobalt, which has bonds similar to those of iron in the hemoglobin molecule. Roles: –Coenzyme in cell synthesis –Works with folate in RBC synthesis –Maintenance of nerve cells –Preventing nerve damage 22 Vitamin B12 Deficiency It acts as a coenzyme for reducing ribonucleotides to deoxyribonucleotides in the gene replication. Pernicious anemia is caused by failure of red blood cell maturation when vitamin B12 is deficient. Vitamin B12 deficiency causes demyelination of the large nerve fibers of the spinal cord. The usual cause of vitamin B12 deficiency is not lack of this vitamin in the food but deficiency of formation of intrinsic factor. Intrinsic factor is secreted by the parietal cells of the gastric glands and is essential for absorption of vitamin B12 by the ileal mucosa. 23 Folic Acid (Pteroylglutamic Acid) Several pteroylglutamic acids exhibit the “folic acid effect.” Folic acid (vitamin B9) functions as a carrier of hydroxymethyl and formyl groups. It is important in the synthesis of purines and thymine, which are required for formation of DNA. Therefore, folic acid, like vitamin B12, is required for replication of the cellular genes. It promotes growth. It is important for the maturation of red blood cells. One of the significant effects of folic acid deficiency is the development of macrocytic anemia. 24 Pyridoxine (Vitamin B6) Pyridoxine exists in the form of pyridoxal phosphate in the cells. Roles: - Coenzyme in the transamination process for the synthesis of amino acids. - Act in the transport of some amino acids across cell membranes. Pyridoxine deficiency cause seizures, dermatitis, and gastrointestinal disturbances such as nausea and vomiting. 25 Pantothenic Acid (Vitamin B5) Pantothenic acid mainly is incorporated in the body into coenzyme A (CoA), which has many metabolic roles in the cells. Roles; 1) conversion of pyruvic acid into acetyl-CoA before its entry into the citric acid cycle, and 2) degradation of fatty acid molecules into acetyl-CoA. Lack of pantothenic acid can lead to depressed metabolism of both carbohydrates and fats. In the human being, no definite deficiency syndrome has been proved, because of the wide occurrence of this vitamin in almost all foods. 26 Ascorbic Acid (Vitamin C) Ascorbic acid is essential for activating the enzyme prolyl hydroxylase, which promotes the hydroxylation step in the formation of hydroxyproline, an integral constituent of collagen. Without ascorbic acid, the collagen fibers are defective and weak. It is essential for the growth and strength of the fibers in subcutaneous tissue, cartilage, bone, and teeth. Ascorbic acid deficiency weakens collagen fibers throughout the body. Ascorbic Acid Deficiency Causes Scurvy Deficiency of ascorbic acid for 20 to 30 weeks causes scurvy. Failure of wounds to heal Lack of ascorbic acid also causes cessation of bone growth. The blood vessel walls become extremely fragile The capillaries are especially likely to rupture, many small petechial hemorrhages occur throughout the body. 27 Vitamin D Vitamin D increases calcium absorption from the gastrointestinal tract and helps control calcium deposition in the bone. Increases the formation of a calcium binding protein in the intestinal epithelial cells. Promotes phosphate absorption by the intestine. Decreases renal calcium and phosphate excretion. 28 29 Rickets—Vitamin D Deficiency Rickets occurs mainly in children. Calcium or phosphate deficiency in the extracellular fluid, usually caused by lack of vitamin D. If the child is adequately exposed to sunlight, the 7- dehydrocholesterol in the skin becomes activated by the ultraviolet rays and forms vitamin D3, which prevents rickets by promoting calcium and phosphate absorption from the intestines. Rickets weakens the bones (O bone or X bone) Tetany in Rickets (calcium