biochemistry entry 25 PUM 2nd year | Quizlet

general function of minerals

bone/teeth formation, fluid balance, nerve conduction, muscle conduction, signaling, catalysis

minerals required >100mg/day are

macrominerals (calcium, chloride, magnesium, phosphorus, potassium, sodium)

minerals required 1-100mg/day are

microminerals (chromium, copper, fluorine, iron, manganese, zinc)

minerals required <1mg/day are

ultra trace minerals (iodine, molybdenum, selenium)

calcium and phosphorus are considered together because they form

hydroxyapatite making up bone and teeth

most of Ca2+ os found in bones (98%) the rest is used for

signaling, muscle contraction, blood clotting

Ca2+ binds to and alters the activity of

calmodulin, phospholipase A, protein kinase C

Ca2+ is found in

dairy products, broccoli, fortified orange juice (not found in spinach!)

Upper limit of Ca2+

2,500 mg/day

hypercalcemia can result from

overproduction of PTH causing constipation and kidney stones

hypocalcemia can result from

deficiency of PTH or vitamin D causing bone demineralisation

age-related loss of bone mass is greatest in

postmenopausal caucasian women (Ca2+ and vitamin D supplementation decreases the risk)

most abundant intercellular anion

free phosphate (Pi)

85% of bodies phosphorus is in form of

inorganic hydroxyapatite (in phospholipids, nucleic acids, ATP, creatine phosphate)

phosphate is supplied as ATP for

kinases

phosphate is supplied as Pi for

phosphorylases

sources of phosphorus

widely distributed in foods especially milk

hypophosphodemia (causing muscle weakness) can be caused by

refeeding carbs to malnourished individuals, overuse of aluminium containing antacids, increased urinary loss caused by increased PTH

Hyperphosphodemia is primarily caused by

decreased PTH

in hyperphospodemia excess Pi combines with Ca2+ forming

crystals known as metatstatic calcification

Ca2+/Pi ratio in bone

2:1

control serum levels of Ca2+ and Pi

calcitriol and PTH (respond to Ca2+ decrease)

calcitriol causes increase of serum Ca2+ and Pi by

increase in bone/intestinal absorption, kidney reabsorption (and activation of renal 1-hydroxylase producing calcitriol from calcidiol)

Pi causes decrease in

Pi reabsorption (high serum Pi increases PTH and decreases calcitriol)

calcitonin responds to elevated Ca2+ by

increasing bone mineralization and renal Ca2+ excretion

while 60% of body Mg2+ is found in bone it only makes up

1% of bone mass

magnesium is required by

kinase and (phosphodiester bond formation) by DNA/RNA polymerase

Hypomagnesemia can result from

decreased absorption or increased secretion of it

symptoms of hypomagnesemia

hyerexcitability of skeletal muscle/nerves, cardiac arrhythmias (hypermagensemia causes hypotension)

used to treat preeclampsia (hypertensive pregnancy disorder)

magnesium sulfate

sodium chloride and potassium are considered together because they maintain

water balance, osmotic equilibrium, pH, membrane potential

Na+ and Cl- are primarily

extracellular electrolytes

Na+ is required for

intestinal/renal absorption/reabsorption of glucose and galactose, free amino acids by Na+ linked transporters

Cl- is required for

hydrochloric acid formation

Na+ is related to hypertension because

it stimulates thirst center in brain releasing antidiuretic hormone from pituitary lead-in to water retention

hypernatremia and hyponatremia can result in

severe brain damage

chronic hyponatremia causes

increase in Ca2+ excretion which can result in osteoporosis

potassium is primarily an

intracellular electrolyte

primary source of potassium

fruit and vegetables

range for potassium is very narrow even modest changes can cause

cardiac arrhythmias and skeletal muscle weakness

inappropriate use of laxatives to loose weight can result in

hypokalaemia

Cu is component of these enzymes

ferroxidases (like loplasmin and hephoxidase required for oxidation of iron from ferrous to ferric form)

dietary sources of Cu

meat, shellfish, nuts, whole grains

Upper limit of Cu

10mg/day

impaired in Menkes syndrome

efflux of cu out of enterocytes into circulation (by ATP7A)

systemic Cu deficiency in Menkes syndrome causes

low urinary and unbound Cu, ceruplasmin (carries 90%of Cu in circulation)

symptoms of Menkes syndrome

progressive neurological degeneration, connective tissue disorders, hair changes

treatment of Menkes syndrome

parenteral administration of Cu (carrying success)

mildest form of Menkes syndrome

occipital horn syndrome

impaired in Wilsons disease

Cu efflux from liver by ATP7B

in Wilsons disease Cu accumulates in liver

leaking into blood and deposited into brain, eyes, kidney, skin (urinary and serum Cu are high)

symptoms of Wilsons disease

hepatic disfunction, neurological/psychatric symptoms, Kaiser-Fleischer rings

treatment of Wilsons disease

Cu-chelating agents like penicillamine (life-long)

excess Zn decreases

Cu absorption (Cu is needed for Fe absorption)

amount of Fe found in adult body

3-4g

Fe can exist linked to

sulfur; part of heme prosthetic group (aprox 70% of all Fe)

dietary sources of Fe

meat, poultry, shellfish, fortified cereal/grains, lentils, green leafy vegetables

amount of ingested Fe that is absorbed

10% or 1-2mg/day

intestinal uptake of heme

by heme carrier protein to enterocyte where oxygenate releases Fe2+

intestinal uptake of non heme Fe

via apical membrane proteins divalent metal ion transporter-1 (DMT-1) (vitamin C enhances absorption)

fate of absorbed Fe2+

oxidised to to Fe3+ and stored by ferritin; moved out of enterocyte by ferroportin and oxidzed by hephaestin

cells that are not enterocytes don't use hephaestin they use

ceruloplasmin

hepcidin is the central molecule in Fe homeostasis because

it regulate ferroportin action

free heme from damaged/phogocytosed cells is

sent out of cells by ferroportin and oxidized by ceroplasmin (about 90% of daily need)

transferrin bound Fe3+ is taken up by

receptor mediated endocytosis

Fe deficiency can result in

microcytic, hypochromic anemia (treatment is Fe administration)

Fe poisoning is the most common poisoning in

children <6 years (UL for children: 40mg/day; UL for adults: 45mg/day) it is treated with Fe chelator

Fe overload can occur in genetic defects like

hereditary hemochrombtosis

symptoms of hereditary hemochromatosis

hyperpigmentation with hyperglycaemia (bronze diabetes); damage to liver, pancreas, heart; increased serum Fe and Tf

treatment of hereditary hemochromatosis

phlebotomy of Fe Chelators

enzymes requiring manganese

Arginase-I, glycosyl transferase, pyruvate carboxylase, superoxide dismutase

sources of Manganese

whole grains, legumes (beans/peas), nuts, tea (especially green tea)

toxicity of manganese is rare the upper limit is

11mg/day (for adults)

zinc play a structural role in body as

zinc fingers are supersecondary structures in protein

hundreds of enzymes require zinc important examples are

alcohol dehydrogenase, carbonic anhydrase, ALA dehydratase, superoxide dismutase

dietary sources of zinc

meat, fish, eggs, dairy products

phosphate storage molecules found in plants that irreversible bind Zin inhibiting absorption in intestine

Phytates (may also bind Ca2+ and nonheme Fe)

can cause zinc deficiency

several drugs like penicillanine, chelate metals

disease in which zinc deficiency is seen

acrodermatitis enteropathica (defect of intestinal zinc transporters)

symptoms of acrodermatitis enteropathica

rashes around orifices and limbs, slowed growth/development, diarrhoea, immune deficiency (vision problems can also occur because zinc in needed for vitamin A metabolism)

eukaryotic cell infected with bacteria can reduce availability of Fe, Mn, Zn to pathogen

decreasing its survival rate aka nutritional immunity

function of chromium

potentiate action of insulin

sources of chromium

fruit, vegetables, dairy products, meat

function of fluorine in fluoride (F-) form

replace hydroxyl group of hydroxylapatite forming fluoroapatite

function of Iodine

needed for T3 and T4 synthesis

Iodide is converted to Iodine in follicular lumen of thyroid by

thyroperoxidase

inderingestion of Iodine can result in

goiter ot hypothyroidism when more severe

hypothyroidism is characterised by

fatigue, weight gain, decreased thermogenesis/metabolic rate

when hypothyroidism occurs durning fetal and infant development

intellectual disability, hearing loss, spasticity, short statue can result

source of Iodine

seafood, meat, dairy products, iodised salt

Hyperthyroidism can be caused by

Iodide over ingestion (UL=1,1g/day) but is incommon

in human selenium can be found in

selenoproteins (there are 25) constitutes of selenocysteine

important selenoproteins are

glutathione peroxidase, thioredoxin reductase, ribonucleotide reductase, deiodiniase

sources of selenium

meat, dairy products, grains

cardiomyopathy caused by eating plants grown on Se-deficient soil

Keshan disease

toxicity (selenosis) of selenium supplement over ingestion (UL: 400µg) causes

brittle nails/hair, cutaneous/neurologic effects

Molybdenum is cofactor of these oxidases

aldehyde, sulfite and Xanthine oxidase

Upper limit of Molybdenum

2mg/day (for adults)

ultra trace mineral that is component of vitamin B12

cobalt