14. Vitamins & Trace Elements

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Presentation transcript:

14. Vitamins & Trace Elements

What are Trace Elements? Trace elements are those elements that occur in human and animal tissues in mg/kg amounts or less. Essential when: deficient intake ►impairment of function restoration with physiological amounts of only that element prevents/alleviates impairment.

Trace Element Functions amplification- small amounts produce dramatic effects on the body e.g. Fe deficiency & anaemia specificity- cannot be effectively replaced by chemically similar constituents homeostasis- regulated mechanisms for absorption, storage and excretion - storage proteins such as ferritin & metallothioneins important in regulation of Fe, Zn, Cu interactions- overabundance of one trace element can interfere with metabolic use of another e.g. large dietary Zn affect Cu absorption.

Copper e.g. cytochrome oxidase, superoxide dismutase, tyrosinase, essential trace metal present in many intracellular enzymes e.g. cytochrome oxidase, superoxide dismutase, tyrosinase, - present in plasma in association with the copper-binding protein, ceruloplasmin. Laboratory Assessment: 1. serum copper : ~10-22 µmol/L, ~ 90% bound to ceruloplasmin 2. serum ceruloplasmin - normal adult levels 200-600 mg/L - levels useful in interpretation of serum copper levels. 3. urinary copper : ~ 0.1µmol/day

Copper balance

Vitamins Definition: Classification: unrelated organic catalysts that are necessary in trace amounts for normal metabolism Classification: Water soluble: B-Complex: B1 (thiamine), niacin, folate (9), riboflavin (B2), pyridoxine (B6), cyanocobalamin (B12), Others: ascorbate (C) Fat-soluble: A (retinol), D (cholecalciferol), K (phytomenadione), E (tocopherol)

Vitamin deficiency Causes: Inadequate intake with normal requirements Impaired absorption Impaired metabolism (e.g. vitamin D) Increased requirements e.g. pregnancy Increased losses Functions typically intracellular Plasma concentrations do not reflect intracellular levels or function – unreliable Tissue concentrations most reliable but not always easily available

Water-soluble Vitamins– folate (B9) & B12 not considered here sources function B1 thiamine Whole grain cereals, organ meats, flours, nuts, green vegs Cofactor in metabolism of pyruvate and 2-oxoglutarate and in pentose phosphate shunt (transketolase) B2 riboflavin Milk, organ meats, eggs, green vegs Oxidation-reduction enzymatic actions B6 pyridoxine Meat, poultry, fish, potatoes, vegetables Enzyme systems –amino acid transaminases, phosphorylases, decarboxylases niacin Whole grain, meat, fish, legumes, nuts, cereals, Coenzymes – NAD, NADP – in glycolysis and ox. phosphorylation C - ascorbate Citrus fruits, tomatoes, melons, cabbage, straw berries, green vegs Antioxidant, formation of connective tissue & catecholamines; cholesterol metabolism

Fat-soluble Vitamins Vitamin sources function A - retinol Animal – fish liver oils, butter, milk, liver, eggs Plants – green/yellow vegs, margarine, fruits Vision, growth of epithelia, immune responses, reproduction, anticancer agent; constituent of retinal pigment rhodopsin E – tocopherol Vegetable oils, wheat germ, rice germ, nuts, legumes, green vegs Antioxidant – membrane stability, cardiovascular disease prevention, RBC function; fertility K – Phytomenadione Green vegetables, spinach, cabbage, liver, synthesis in intestine Coagulation factors – prothrombin, VII, IX, X; osteocalcins – binding of calcium to proteins D – calciferol Fish liver oils, fortified milk, sun exposure, small amounts in butter, eggs, liver, salmon Calcification of bone and teeth

VITAMIN DEFICIENCIES

Complications of Thiamine (vitamin B1) Deficiency (Beri-beri)

Complications of Niacin Deficiency (Pellagra)

Complications of Riboflavin (vitamin B2) Deficiency

Complications of Ascorbate (Vitamin C) Deficiency

LESIONS IN SCURVY

Classification of Vitamins

Hypervitaminosis D: ▲intestinal absorption of Ca, PO4 Hypervitaminosis Classically seen with fat-soluble vitamins: A, D Seen with excessive vitamin nutritional supplements Hypervitaminosis A Acute toxicity: neurologic symptoms: headache, vomiting, stupor, papilloedema Chronic toxicity: neurologic, skeletal (loss of cortical bone), cutaneous (fissuring, ulcers), hepatomegaly with parenchymal damage. Symptoms subside with discontinuation of excess vit A intake Hypervitaminosis D: ▲intestinal absorption of Ca, PO4 ► hypercalcaemia, hyperphosphataemia, bone resorption ►renal calculi, osteoporosis, metastatic calcification