Minerals Flashcards

1
Q

Definition of mineral

A

Naturally occurring inorganic substance

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2
Q

Definition of manganism

A

A form of Parkinsonism caused by Mn overload. Reversible in early stages, irreversible in later stages due to ZnT10 transporter mutation.

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3
Q

Definition of reticuloendothelial macrophages

A

Have ability to phagocytose bacteria, viruses, foreign substances and worn out cells

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4
Q

Definition of primary haemochromatosis

A

Caused by genetic defect, that controls how much iron you absorb

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5
Q

Definition of secondary hemochromatosis

A

Result of another disease or condition that causes iron overload

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6
Q

Chelating agents

A

Chemical compounds that react with metal ions to form stable, water soluble complex

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7
Q

Nutritionally essential chemical elements

A
Na
K
Mg
Ca
Mo
Mn
Fe
Co
Cu
Zn
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8
Q

Describe the shape of the dose/response curve: essential substance

A

Low dose, deficient
Adequate dose, adequate
Overdose, overload, toxic

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9
Q

Elements in biological tissues

10-3mg/g

A

K
Ca
Na
Mg

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10
Q

Elements in biological tissues

10-6 ug/g

A
Zn
Fe
Cu
Sr*
Se
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11
Q

Elements in biological tissues

10-9 ng/g

A
Rb*
Mn
As*
Ba*
Ni*
Co
Hg*
Mo
Cs*
Cd*
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12
Q

Elements in biological tissue

10-12 pg/g

A

Cr
U*
Pb*

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13
Q

What are the 4 essential minerals

A

Na
Mg
K
Ca

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14
Q

Concs of Na, K inside and outside the cell and requirements and function

A
Na, inside cells (mM)
12
Na, outside cell (mM)
140
Requirement (g/d)
2.3
K, inside cells (mM)
140
K, outside cell (mM)
5
Requirement (g/d)
4.7

Major function nerve conduction

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15
Q

Mg2+ function

A
Cofactor complex (ATP)
Enzyme complexes
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16
Q

Ca2+ function

A

Signalling in cells

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17
Q

Essential trace metals

A
Mn
Fe
Mo
Co
Cu
Zn
18
Q

Amounts of each trace element

  • Mn
  • Fe
  • Cu
  • Zn
A

Mn 12-20mg
Fe 3.7g
Cu 100mg
Zn 2.3g

19
Q

Uses of cobalt (Co)

A

In cobalamin (B12)
2 enzymes only in humans
Total 1mg, 2ug/d for adults

20
Q

Uses of molybdenum (Mo)

A
Molybdenum cofactor
4 enzymes only
-sulfite
-xanthine
-aldehyde oxidases
-mitochondrial amidoxime reducing component (mARC)
21
Q

Uses of manganese

A

Used in many many enzymes such as

  • mitochondrial superoxidase dismutase
  • Arginase
  • glutamine synthase
  • pyruvate carboxylase
22
Q

Toxicity of manganese

A

Mn2+ relatively toxic

Overload leads to manganese (form of Parkinsonism)

23
Q

Daily values of Fe, Cu, Zn

A

Fe 18mg
Cu 2mg
Zn 15mg

24
Q

3 functions of metals in proteins

A

Catalysis
Structure
Regulation

25
Ligand donors of amino acids in metalloproteins
Only some proteins can bind to metal ions If they have N (his) If they have O (glu, asp, tyr) If they have S (cys, met)
26
Distribution of Fe in the body
Dietary Fe absorbed in the duodenum (makes up 10% of all absorbed Fe) Plasma transferin => myoglobin and bone marrow for formation of RBC and liver for storage Reticuloendothelial macrophages degrade RBCs, reload transferin Loss in sloughed mucosal cells, desquamation, blood loss. Hepcidin controls iron metabolism
27
Fe uptake in intestinal cell
Fe III reduced to Fe II by duodenal cytochrome b Divalent metal transporter I transports Fe II into intestinal cell. Fe II can either be stored in ferritin or it can be transported out of the cell with ferroportin Hephaestin reduces Fe II on the basal side of the cell to FeIII Fe III can bind to transferin and be carried in the blood
28
Fe storage
Feroxidase core 4 Fe2+ + 4 H+ + O2 = 4 Fe3+ + 2H2O When it needs to be stored, oxidized to Fe III When it needs to be released, reduced to Fe II
29
Iron uptake with receptor mediated endocytosis
Fe II, transferin binds to transferin receptor in clathrin coated pit Forms an endosome with divalent metal transporter Proton pump acidifies endosome, Fe dissociates from transferrin and exits via divalent metal transporters Apo-Tf and transferin receptor return to cell surface, endosome breaks down Fe either stored as ferritin or enters mitochondria If in ferritin, can form hemosiderin or the formation of nonerythroid cells
30
Genetic diseases and Fe metabolism
Primary iron overload disorder (haemochromatosis type 1) Treated with phlebotomy Juvenile/HFE2, HFE3, HFE4 Aceruloplasminemia, atransferrinemia
31
Chelating agents for iron overload
Deferoxamine to treat secondary iron overload, removes excess Fe
32
Differences between Fe and Zn
Red >90% in haem Redox active Fe2+/Fe3+ Clinical tests Colourless Diluted among many proteins Redox inert Zn2+ No clinical test
33
Uses of zinc in proteins
Carbonic anhydrase, alcohol dehydrogenase Many proteins (Zn insulin complex, NT in brain) All enzymes,e families Recognition of DNA/RNA, lipids, gene expression
34
Cellular Zn homeostasis | No of proteins that are associated with Zn and their function
ZIP, zinc import, 14 proteins ZNT, zinc export, 10 proteins MT, metallothiones (zinc transport, > 10 proteins) MTF1-zinc sensor
35
Zn total amount and requirements
Total amount 2-3g | Daily requirement 2-3mg
36
Human zinc deficiency reasons
Lack of Zn in nutrition Parasites Fe deficient Genetic
37
Signs of Zn deficiency
``` Suppressed cell mediated immunity Dermatitis Poor wound healing Alopecia Growth retardation Delayed sexual maturation Impaired CNS, PNS Taste, vision, smell affected Appetite loss Dwarfism ```
38
Genetic basis for Zn deficiency | -2 pathologies
Aerodermatitis enteropathica - severe skin lesions, death from infections - completely curable with Zn - Mutation in ZIP4, uptake low Transient neonatal zinc deficiency - affects child, does not obtain enough Zn from mother - curable when Zn given to child - Mutation in Zn T2
39
Uses of copper (Cu) in proteins
Ceruloplasmin, ferroxidase Superoxide dismutase , 2O2 + 2H+ => H2O2 + O2 Cytochrome C oxidase, terminal electron acceptor for O2 Lysol oxidase, collagen crosslinking Tyrosinase, melanin production Dopamine B hydroxyls, catecholamine synthesis Basically involved in hormone and energy metabolism
40
Genetic diseases, copper accumulation Treatment for copper accumulation
Wilson's disease In liver, toxicity, hepatolenticular degeneration Overflow of Cu => brain (mental deterioration) Kayser Fleischer rings Chelation therapy w D-penicillamine, treat Cu overload
41
Genetic diseases, copper deficiency Treatment for copper deficiency
Defective absorption of Cu in intestines Hair depigmentation, steely, kinky Deterioration of NS No cure in infants
42
Cellular Cu homeostasis | How is Cu taken up into the cell and processed
Cu II reduced to Cu I and taken up by Cu transporter I Specific chaperones will transport Cu I to where it is needed in the cell (mitochondria) ATPases export Cu