minerals mineral resources

MINERALS AND TRACE ELEMENTS Jana Novotná Major components of body molecules C, H, O, N, S (obtained through intake of water fat, carbohydrates, proteins) Nutritionally important minerals Ca, P, Mg, Na K, Cl ( 7.44) causes hypokalemia → transient shifting of K+ into cells, presumably by stimulation of the Na-K-ATPase • Acidosis (pH < 7,36) causes hyperkalemia → transient shifting of K+ from cells at the expense of H+ • Hyperkalemia produces characteristic electrocardiographic changes (life-threatening effect of K+ excess on the heart) Calcium • Total content of calcium in the body is more than 1200 mg • 99% of total content is deposit in bones and teeth, • 1% in blood and body fluids • Intracellular calcium: - cytosol - mitochondria - other microsomes - regulated by "pumps" The serum level of calcium is closely regulated with a normal total calcium of -2.75 mmol/L (9-10.5 mg/dL) and a normal ionized calcium of 1.1-1.4 mmol/L (4.5-5.6 mg/dL) Calcium metabolism Multiple biological functions of calcium Cell signaling Neural transmission Muscle function Blood coagulation Enzymatic co-factor Membrane and cytoskeletal functions Secretion Biomineralization Magnesium metabolism • • • • Effect on central nervous system: Certain effects of Mg2+ are similar to Ca2+ Increased concentration of Mg2+ cause depression of CNS Decreased concentration of Mg2+ cause irritability of CNS Effect on neuromuscular system: Direct depressant effect on skeletal muscles – excess of Mg2+ cause decrease in acetylcholine release by motor nerve impulse • The action of increased Mg2+ on neuromuscular function are antagonized by Ca2+ • Abnormaly low concentration of Mg2+ in extracellular fluid result in increased acetylcholine release and increased muscle excitability (tetany) Excess of Mg2+ cause vasodilatation Magnesium metabolism Hypomagnesemia cause: • • • • changes in skeletal and cardiac muscle changes in neuromuscular function, hyperirritability, psychotic behaviour tetany Hypermagnesemia cause: • • • • muscle weakness hypotension ECG changes sedation and confusion Hypermagnesemia is usual due to renal insuficiency Copper • Cu is an essential nutrient • Rapid growth increases Cu demands in infancy • The adult body contains approximately 100 mg of copper – the highest concentrations are in liver, kidney, and hearth • The absorption in gastrointestinal tract requires a specific mechanism - metal binding protein metallothionein (Cu2+ ions are highly insoluble) • Ceruloplasmin (CP) is a glycoprotein, copper-dependent ferroxidase (95% of the total copper in human plasma), oxidizes Fe2+ to Fe3+ in gastrointestinal iron absorption mechanism Copper metabolism Model of Cu uptake and metabolism in hepatocytes: Cu cross the plasma membrane through Ctrl1 (copper transporter1) or DMT1 (divalent metal transporter1) to the trans Golgi network (TGN) by chaperone Hah1 Chaperone protein Ccs delivers Cu to cytosolic Cu/Zn SOD Cox17 delivers Cu to mitochondria for cytochrome c oxidase Carrol et all, 2004) Copper metabolism • Cu is an essential cofactor in a number of critical enzymes in metabolism: superoxide dismutase (Cu/Zn-SOD) cytochrome c oxidase (COX) tyrosinase monoamino oxidase lysyloxidase • Cu metabolism is altered in inflammation, infection, an cancer • In infection, Cu is essential for production of Ile-2 by activated lymphocytes • In cancer, plasma CP is positively correlated with disease stage Iron Major function of Fe – oxygen transport by hemoglobin Fe2+ and Fe3+ are highly insoluble – special transporter systems are required Food Fe is predominantly in Fe3+, tightly bound to organic molecules Apoferritin assimilates up to 300 Fe molecules to form Fe storage protein – ferritin In the retikuloendothelial system ferritin provides an available storage form for iron Apotransferrin (apoTf) – protein, that can bind atoms of Fe to form transferrin, Fe carrier in plasma Food iron is predominantly in the ferric state In the stomach, where the pH is less than 4, Fe3+ can dissociate and react with low-molecular weight compounds such fructose, ascorbic acid, citric acid, amino acids to form ferric complexes soluble in neutral pH of intestine fluid A protein DMT1 (divalent metal transporter 1), which transports all kinds of divalent metals, then transports the iron across the cell membrane of intestinal cells These intestinal lining cells can then store the iron as ferritin The transfer of iron from the storage ferritin (as Fe3+ ) involves reduction to ferrous state – Fe2+ in order for it to be released from ferritine The Fe2+ is subsequently again oxidized by ferroxidase ceruloplasmin and transported bound to plasma transferrin to storage sites in the bone marrow, liver muscle, other tissues Molybdenum Metal required for the function of the metalloenzymes: xantine oxydase aldehyde oxidase sulfite oxidase Some evidence that Mo can interfere with Co metabolism by the diminishing the efficiency of copper utilization (the foot content of Mo is highly dependent upon the soil type in which the foodstuff are grown) Selenium • an integral component of glutathion peroxidase (intracellular antioxidant), • a scavenger of peroxides, • an essential element for immune function (selenoproteins) • Selenoproteins catalyse oxido-reduction reactions, protective function from oxidative stress (macrophageor neutrophil-generated free-radical species, UV in sunlight The foot content of Se is highly dependent upon the soil type in which the foodstuff are grown Manganese • • High concentration of Mn2+ is present in mitochondria Functions as a necessary factor for activation of glycosyltransferases (enzymes responsible for the synthesis of oligosaccharides, glycoproteins, proteoglycans • Required for superoxid dismutase activity, for activity of metalloenzymes: hydrolases kinases decarboxylases transferases Deficiency of Mn extensively reduce glycoprotein and proteoglycan formation Zinc Component of zinc metalloenzymes : carbonic anhydrase lactate dehydrogenase glutamate dehydrogenase alkaline phosphatase thimidine kinase matrix metalloproteinases Gustin – protein in saliva – major role in taste Zinc Deficiency of Zn has serious consequence : • failure metabolism of nucleic acids (cell division, growth and differentiation) • multisystem disfunction as growth retardation, hypogonadism, ophtalmologic, gastrointestinal, neuropsychiatric symptoms Zink deficiency in children are marked by poor growth and impairment of sexual development Chromium Regulation of glucose metabolism as a component of glucose tolerance factor (GTF) GTF increases effect of insulin (by facilitating its binding to cell receptor site) Chromium regulates plasma lipoprotein concentration Reduces serum cholesterol and serum triglycerides Iodine Iodine is incorporated into thyroid hormones Iodine is absorbed in the form of inorganic iodine Thyreoperoxidase oxidizes inorganic iodine and oxidized I is transported to phenyl group of tyrosin of thyroglobulin Fluorine Inorganic matrix of bone and teeth Deficiency – osteoporosis and teeth caries Boron Influences of metabolism and use of Ca, Cu, Mn, N, glucose, triglycerides Control of membranes function and their stabilization Negative influence on many metabolic processes – inhibition of some key enzymes (inhibition of energetic metabolism), immune system (respiratory burst) Vanadium Control of sodium pump, inhibition of ATPase Tin Interaction with riboflavin Lithium Control of sodium pump, interference with the lipid metabolism Silicon Structural role in connective tissue, in metabolism of osteogenic cells Nickel Component of enzyme urease