Presentation is loading. Please wait.

Presentation is loading. Please wait.

Water – soluble Vitamins

Similar presentations

Presentation on theme: "Water – soluble Vitamins"— Presentation transcript:

1 Water – soluble Vitamins
folic acid Thiamine niacin cobalamin Riboflavin biotin ascorbic acid pantothenic acid pyridoxine

2 Water – soluble Vitamins

3 water-soluble Vitamins;
Vitamins : are chemically unrelated organic compounds cannot be synthesized by humans must be supplied by the diet. water-soluble Vitamins; folic acid cobalamin (B12) ascorbic acid (C) pyridoxine (B6) Thiamine (B1) niacin (B3) Riboflavin (B2) biotin pantothenic acid Many of the water-soluble vitamins are precursors of coenzymes for the enzymes of intermediary metabolism.

4 FOLIC ACID (Folate) Function of Folic acid
Plays a key role in one-carbon metabolism. Essential for the biosynthesis of AA, purines, thymine...etc. Folic acid deficiency is the most common vitamin deficiency in the United States, particularly among pregnant women and alcoholics. Function of Folic acid Serine, glycine, and histidine  one-carbon fragments to Tetrahydrofolate  transfers them to intermediates in the synthesis of amino acids, purines, and thymine - a pyrimidine found in DNA.

5 Nutritional anemias Low blood [Hb]  O2 transport Anemia
Nutritional anemias : classified according to RBC size or MCV. Microcytic anemia (MCV<80 m3): caused by lack of iron the most common form of nutritional anemia. b) Macrocytic anemias (MCV>100 m3): due to folic acid or vit B12 def. called megaloblastic because folic acid or vit B12 def. accumulation of large, immature red cell precursors (megaloblasts) in the bone marrow.


7 Folate and anemia: poor absorption: pathology of gut Causes of  serum
increased demand: Pregnancy Lactation poor absorption: pathology of gut Alcoholism ttt with : Methotrexate (DHF reductase inhibitor) Causes of  serum folate levels folate-free diet Results of folic acid deficiency megaloblastic anemia due to  synthesis of purines and thymidine   DNA synthesis and cell division. The causes of the megaloblastic anemia should be evaluated prior to instituting therapy because vitamin B12 deficiency  indirectly causes this disorder.


9 Folate and neural tube defects in the fetus:
Spina bifida and anencephaly, the most common neural tube defects. affect ~ 4000 pregnancies in USA / year. Folic acid supplementation before conception and during the first trimester ( 0.4 mg/day)   the risk of neural tube defects in the fetus. The U.S. FDA has authorized the addition of folic acid to enriched grain products, ( about 0.1 mg day). This supplementation will allow ~ 50% of all reproductive-aged women to receive 0.4 mg of folate from all sources. Folic acid intake should not exceed ~ 1 mg/day to avoid misdiagnosis of vit B12 deficiency.

10 COBALAMIN (VITAMIN B12) Required in humans for 2 essential enzymatic reactions: A) Methionine synthesis B) isomerization of methylmalonyl CoA (produced during the degradation of some AA, and fatty acids with odd numbers of carbon atoms) Deficiency of B12  accumulation of abnormal fatty acids  incorporated into cell membranes, including nervous system  neurologic manifestations .

11 A. Structure of cobalamin and its coenzyme forms
Coordination bonds cyanide is replaced by CH3 group cyanide is replaced with 5-deoxyadenosine differs from the porphyrins in that two of the pyrrole rings are linked directly rather than through a CH3 bridge Cobalt is held in the center of the corrin ring by four coordination bonds from the nitrogens of the pyrrole groups

12 Distribution of vit B12 : Vitamin B12 is synthesized only by microorganisms. It is not present in plants. Animals obtain the vitamin preformed from: their natural bacterial flora. by eating foods derived from other animals. liver whole milk eggs oysters fresh shrimp chicken B12 is present in:

13 Folate trap hypothesis :
B12 deficiency affects: need both N5-N10-methylene & N10- formyl forms of THF for nucleotides synthesis required for DNA replication. the erythropoietic tissue of bone marrow the mucosal cells of the intestine In B12 deficiency, the N3-methyl form of tetrahydrofolate is not efficiently used. Methylated form of THF cannot be converted directly to other forms  accumulation of he N5-methyl form &  of other forms. B12 deficiency is hypothesized to  deficiency of the THF forms needed in purine and thymine synthesis,  megaloblastic anemia.

14 Clinical indications for vitamin B12
Unlike other water-sol Vitamins, significant amounts of vitamin B12 (4 - 5 mg) are stored in the body. SO, Development of clinical symptoms of B12 deficiency take several years in individuals with partial or total gastrectomy (intrinsic factor-deficient with loss of B12 absorption).

15 Pernicious anemia: Vitamin B12 deficiency is rarely due to dietary insufficiency. Deficiencies are more common in patients with intestinal malabsorption of the vitamin  pernicious anemia. Autoimmune destruction of the gastric parietal cells   synthesis of the intrinsic factor (Glycoprotein). Normally, dietary vitamin B12 binds to intrinsic factor in the intestine  cobalamin - intrinsic factor complex  travels through the gut  binds to specific receptors on the surface of mucosal cells of the ileum  transported into the mucosal cell  general circulation  carried by B12-binding proteins.

16 Neuropsychiatric symptoms develops later .
Lack of intrinsic factor  prevents vitamin B12 absorption  pernicious anemia. Neuropsychiatric symptoms develops later . CNS symptoms may occur in the absence of anemia. The CNS effects are irreversible. Treatment by giving high-dose B12 orally, or cyanocobalamin IM. Therapy must be continued throughout the lives of patients with pernicious anemia. Folic acid administration alone reverses the hematologic abnormality  masks the B12 deficiency  severe neurologic dysfunction and pathology; therefore, megaloblastic anemia should be treated with a combination of folate and vitamin B12

The active form of vitamin C is ascorbic acid. The main function is as a reducing agent in several different reactions. Vitamin C has an essential role as a coenzyme in hydroxylation reactions, e.g, hydroxylation of prolyl- and lysyl-residues of collagen . Vitamin C is required for: maintenance of normal connective tissue wound healing facilitates the absorption of dietary iron from the intestine.

18 Deficiency of ascorbic acid:
Deficiency of ascorbic acid  deficiency in the hydroxylation of collagen  defective connective tissue  scurvy. sore spongy gums loose teeth fragile blood vessels swollen joints anemia Scurvy

19 Prevention of chronic disease:
Vitamin C , vitamin E and -carotene are known as antioxidants. Consumption of food or supplements rich in these compounds   Coronary heart disease and certain cancers. Supplementation with the isolated antioxidants have low beneficial effects.

pyridoxal pyridoxamine, Derivatives of pyridine. They differ only in the nature of the functional group attached to the ring in animal foods All three compounds can serve as precursors of the biologically active coenzyme, pyridoxal phosphate. Pyridoxal phosphate functions as a coenzyme  catalyze reactions involving amino acids primarily in plants

21 Example Reaction type Oxaloacetate + glutamate  aspartate + α-ketoglutarate Transamination Serine  pyruvate + NH3 Deamination Histidine  histamine + CO2 Decarboxylation Glycine + succinyl CoA δ-aminolevulinic acid Condensation

22 Clinical indications for pyridoxine:
Isoniazid (isonicotinic acid hydrazide), [a drug frequently used to treat TB]  B6 deficiency by forming an inactive derivative with pyridoxal phosphate. Dietary supplementation with B6 is important with isoniazide treatment. Dietary deficiencies in pyridoxine are rare but observed in: newborn infants fed formulas low in vitamin B6 women taking oral contraceptives alcoholics. intakes of greater than 2 g/day  Neurologic symptoms Toxicity of pyridoxine: Substantial improvement, but not complete recovery, occurs when the vitamin is discontinued

23 THIAMINE (VITAMIN B1) Thiamine pyrophosphate (TPP) is:
the biologically active form of the vitamin, formed by the transfer of a pyrophosphate group from ATP to thiamine PP from ATP

24 Clinical indications for thiamine:
Thiamine pyrophosphate (TPP) serves as a coenzyme in : the formation or degradation of α-ketols by transketolase the oxidative decarboxylation of pyruvate and α -keto acids Important for CNS Thiamine deficiency:   activity of dehydrogenase reactions   ATP  impaired cellular function. Thiamine deficiency is diagnosed by:  erythrocyte transketolase activity observed on addition of TPP.

25 Beri beri: Severe thiamine-deficiency syndrome.
Found in areas where polished rice is the major component of the diet. Rapid onset in nursing infants whose mothers are deficient in thiamine. infantile beriberi Adult beriberi tachycardia vomiting convulsions death (if untreated) dry skin irritability disorderly thinking progressive paralysis

26 Wernicke-Korsakoff syndrome:
In the United States, thiamine deficiency, which is seen primarily with chronic alcoholism, is due to: dietary insufficiency. impaired intestinal absorption of the vitamin. Some alcoholics Wernicke - Korsakoff syndrome - apathy, - loss of memory - rhythmical to-and-fro motion of the eyeballs

27 Niacin, or nicotinic acid, is a substituted pyridine derivative
The biologically active coenzyme forms are: nicotinamide adenine dinucleotide (NAD) and its phosphorylated derivative, nicotinamide adenine dinucleotide phosphate (NADP) Nicotinamide, a derivative of nicotinic acid that contains an amide instead of a carboxyl group, deaminated in the body So it is nutritionally equivalent to nicotinic acid.

28 NAD+ and NADP+ serve as coenzymes in oxidation-reduction reactions in which the coenzyme undergoes reduction of the pyridine ring by accepting a hydride ion (hydrogen atom plus one electron) The reduced forms: NAD+  NADH NADP+  NADPH

29 A. Distribution of niacin
Sources unrefined and enriched grains and cereals milk lean meats especially liver. Limited quantities of niacin can also be obtained from metabolism of tryptophan. 60 mg tryptophan  1 mg nicotinic acid tryptophan is metabolized to niacin only when there is a relative abundance of the amino acid

30 B. Clinical indications for niacin :
Deficiency of niacin Pellagra if untreated Dermatitis Diarrhea Dementia Death

31 Treatment of hyperlipidemia:
Niacin (at doses of 1.5 g /day or 100 times the RDA) inhibits lipolysis in adipose tissue ( the primary producer of circulating free fatty acids).  triacylglycerol synthesis in liver  VLDL and LDL Niacin is particularly useful in the treatment of type lIb hyperlipoproteinemia (in which  VLDL & LDL ).

(FMN) (FAD) FMN & FAD are: the 2 biologically active forms. formed by transfer of AMP from ATP  FMN. capable of reversibly accepting 2 H atoms  FMNH2 or FADH2 bound tightly - sometimes covalently - to flavoenzymes that catalyze the oxidation or reduction of a substrate. dermatitis cheilosis (fissuring at the corners of the mouth), glossitis (the tongue appearing smooth & purplish). Deficiency

33 BIOTIN A coenzyme in carboxylation reactions, ( serves as a carrier of activated CO2 ). Covalently bound to the -amino groups of lysine residues of biotin-dependent enzymes. Required by all organisms. Can only be synthesized by: bacteria, yeasts, molds, algae, and some plant species.

34 Each Carboxylase catalyzes an essential metabolic reaction:
Acetyl-CoA carboxylase: catalyzes the binding of HCO3- to acetyl-CoA to form malonyl-CoA required for the synthesis of fatty acids. Pyruvate carboxylase: in gluconeogenesis  formation of glucose from amino acids and fats. Each Carboxylase catalyzes an essential metabolic reaction: Methylorotonyl-CoA carboxylase: in the metabolism of leucine, an essential amino acid. Propionyl-CoA carboxylase: in the metabolism of amino acids, cholesterol, and odd chain fatty acids (fatty acids with an odd number of carbon molecules)

35 Biotin deficiency very rare. does not occur naturally.
the vitamin is widely distributed in food. in humans, big percentage is supplied by intestinal bacteria. Biotin deficiency prolonged IV feeding without biotin supplementation. consumption of raw egg white for a prolonged period . Human requirement for dietary biotin in:

36 symptoms of biotin deficiency
dermatitis glossitis loss of appetite loss of hair nausea scaly red rash around the eyes, nose, mouth, and genital area. Addition of raw egg-white to the diet as a source of protein symptoms of biotin deficiency depression lethargy hallucination numbness tingling of extremities. Neurologic symptoms in adults Raw egg white contains a glycoprotein, avidin  tightly binds biotin  prevents its absorption from the intestine. Cooking egg white  denatures avidin renders it digestable  unable to prevent the absorption of dietary biotin.

37 With a normal diet, 20 raw eggs / day would be required to induce a deficiency syndrome.
The Adequate Intake (AI): average intakes of biotin (35 mcg to 60 mcg/day) are meeting the dietary requirement. Uses: In larger doses, biotin is used to treat inborn errors of metabolism such as biotinidase deficiency. Biotin is incorporated into almost all nutritionally complete dietary supplements and infant formulas.

38 Pantothenic acid is also a component of fatty acid synthase .
A component of coenzyme A, which functions in the transfer of acyl groups Coenzyme A contains a thiol group that carries acyl compounds as activated thiol esters. such structures are succinyl CoA, fatty acyl C0A, and acetyl CoA. Sources: Eggs Liver Yeast Deficiency Is not well characterized in humans, No RDA is established. Pantothenic acid is also a component of fatty acid synthase .



Download ppt "Water – soluble Vitamins"

Similar presentations

Ads by Google