VITAMINS 2 BY DR. MARYJANE

WATER SOLUBLE VITAMINS

FOLIC ACID SOURCES: leafy vegetables, liver and kidney

Folic Acid Glu PABA pteridine Folic Acid Tetrahydrofolic Acid (THF) Amino Acid Synthesis Purine Synthesis Thymine Synthesis Dihydropteroate synthetase sulfonamide Plays a key role in one- carbon metabolism Tetrahydrofolate (THF) which is the active form of folic acid receives one- carbon fragment from donors such as ser, gly and his and transfers them to intermediates in the synthesis of amino acids, purines and thymine (which is important for DNA synthesis). methotrexate dihydrofolate reductase

Folic Acid Deficiency Causes: Poor absorption due to a pathology of the small intestine, alcoholism or treatment with drugs that are dihydrofolate reductase inhibitors 1.Megaloblastic anemia - diminished synthesis of purines and thymine which leads to the inability of the cells to divide secondary to decreased synthesis of DNA. 2. Open neural tube defect (ONTD) - abnormal development of the neural tube. 1. critical folate-dependent development occurs in the first week of fetal life 2. supplementation < 1 mg/day (14nmol/L) Example: spina bifida

Cobalamin (B 12 ) -important in the synthesis of methionine and isomerization of methylmalonylCoA Cobalamin is synthesized only by microorganisms. It is not present in plants. Cobalamin is present in appreciable amounts in liver, whole milk, eggs, oysters, fresh shrimp, pork and chicken.

Cobalamin absorption Significant amounts of vitamin B 12 are stored in the body (4 to 5 mg). It may take several years for deficiency to develop as a result of partial gastrectomy, Antibodies against intrinsic factor and gastric parietal cells, Diphyllobothriasis can also result in B12 def. Pernicious anemia is an autoimmune disorder (antibodies attack the parietal cells) where the intrinsic factor is deficient. Lack of intrinsic factor prevents the absorption of vit B12 Patients are usually anemic but later on show neuropsychiatric symptoms.

DEFICIENCY OF COBALAMIN Pernicious anemia Dementia Spinal degeneration Symptoms: megaloblastic anemia, neuropsychaitric illness

Ascorbic Acid 1.required in the hydroxylation of lysine and proline in collagen 2.facilitates in the absorption of dietary iron from the intestine 3.water-soluble antioxidant Deficiency in ascorbic acid leads to scurvy. Scurvy is characterized by sore, spongy gums, loose teeth, fragile blood vessels, swollen joints, increased bleeding time, normal prothrombin time and anemia. Collagen quality will be poor in Vitamin C deficiency.

Pyridoxine (B 6 ) plant source animal source Vitamin B 6 is involved in the following reactions: 1.Transamination 2.Deamination 3.Decarboxylation 4.Heme synthesis Isoniazid induces a B 6 deficiency by forming an inactive derivative with pyridoxal phosphate. B6 def can result in sideroblastic anemia Neurologic symptoms have been observed at intakes of greater than 2g/day.

Thiamine (B 1 ) Thiamine pyrophosphate (TPP) is the biologically active form.

Thiamine Deficiency 1)Polyneuropathy (Dry Beriberi) 2) Cardiovascular Syndrome (Wet Beriberi) 3)Wernicke-Korsakoff Syndrome Beriberi -severe thiamine deficiency where unenriched polished rice is part of the diet. Dry Beriberi -Symmetric Polyneuropathy, Non specific-motor, sensory, reflex -Usually start in the Leg, extend to arm -toe drop→ foot drop→ wrist drop; fatigue Wet Beriberi -Peripheral Vasodilation→ AV shunting→ High output Cardiac failure→ Peripheral Edema

Extreme thiamine deficiency may lead to neuronal degeneration and development of: Wernicke’s disease: is characterized by 1. occular disturbance 2. ataxia (loss of muscular coordination) Korsakoff’s syndrome: characterized by: 1. defective memory 2. impaired learning ability. Combination of both wernicke’s and korsakoff is known as wernicke korsakoff syndrome is mainly seen in alcoholics characterized by confabulation.

Niacin -Found in unrefined and enriched grains and cereal, milk and lean meats especially liver -Can also be obtained in limited quantity from tryptophan

Niacin deficiency Pellagra (4Ds) Dermatitis, Diarrhea and Dementia (Death if untreated) Treatment of hyperlipidemia (typeIIb hyperlipoproteinemia) Niacin (1.5 g/day) strongly inhibits lipolysis in adipose tissue. VLDL and LDL are lowered.

HARTNUP DISEASE is as a result of decreased reabsorption or uptake of tryptophan by the kidney leading to pellagra. Sources of tryptophan: corn I

Riboflavin (B 2 ) Riboflavin has a dimethylisoalloxazine ring bound to ribitol. Riboflavin is the precursor of FMN and FAD. Riboflavin is degraded to inactive products on exposure to visible light. Riboflavin is also required in dehydrogenase reactions Riboflavin deficiency shows cheilosis, angular chelitis glossitis, sore throat and dermatitis. Infants who are under phototherapy for hyperbilirubinemia may experience riboflavin deficiency.

Biotin Biotin is important in the activation of CO 2 in carboxylation reactions. A large percentage of biotin is supplied by the intestinal bacteria. Addition of raw egg white in the diet induces biotin deficiency (dermatitis, glossitis, loss of appetite, nausea) due to the presence of avidin, a glycoprotein which tightly binds with biotin.

Pantothenic Acid Pantothenic acid consists of pantoic acid and  - alanine. Required to produce CoA which is necessary to sustain life Eggs, liver and yeast are the most important sources of pantothenic acid.

Enzymes that require panthotenic acid The following enzymes require panthothenic acid for their action Fatty acid synthase Fatty acyl CoA synthase Pyruvate dehydrogenase Alpha ketoglutarate dehydrogenase Deficiency of panthothenic acid is rare

Fat soluble vitamins OTHER NAMES ACTIVE FORM FUNCTIONVITAMIN

Fat soluble vitamins DEFICIENCY SIGNS & SYMPTOMS TOXIC? NOTESVITAMIN

ACTIVE FORM FUNCTIONVITAMIN OTHER NAMES

DEFICIENCY SIGNS & SYMPTOMS TOXIC? NOTESVITAMIN