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Nutrition and Metabolism > Minerals > Flashcards

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
Q

Ligand donors of amino acids in metalloproteins

A

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
Q

Distribution of Fe in the body

A

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
Q

Fe uptake in intestinal cell

A

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
Q

Fe storage

A

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
Q

Iron uptake with receptor mediated endocytosis

A

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
Q

Genetic diseases and Fe metabolism

A

Primary iron overload disorder (haemochromatosis type 1)
Treated with phlebotomy

Juvenile/HFE2, HFE3, HFE4
Aceruloplasminemia, atransferrinemia

31
Q

Chelating agents for iron overload

A

Deferoxamine to treat secondary iron overload, removes excess Fe

32
Q

Differences between Fe and Zn

A

Red
>90% in haem
Redox active Fe2+/Fe3+
Clinical tests

Colourless
Diluted among many proteins
Redox inert Zn2+
No clinical test

33
Q

Uses of zinc in proteins

A

Carbonic anhydrase, alcohol dehydrogenase
Many proteins (Zn insulin complex, NT in brain)
All enzymes,e families
Recognition of DNA/RNA, lipids, gene expression

34
Q

Cellular Zn homeostasis

No of proteins that are associated with Zn and their function

A

ZIP, zinc import, 14 proteins
ZNT, zinc export, 10 proteins
MT, metallothiones (zinc transport, > 10 proteins)
MTF1-zinc sensor

35
Q

Zn total amount and requirements

A

Total amount 2-3g

Daily requirement 2-3mg

36
Q

Human zinc deficiency reasons

A

Lack of Zn in nutrition
Parasites
Fe deficient
Genetic

37
Q

Signs of Zn deficiency

A 
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
Q

Genetic basis for Zn deficiency

-2 pathologies

A

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
Q

Uses of copper (Cu) in proteins

A

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
Q

Genetic diseases, copper accumulation

Treatment for copper accumulation

A

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
Q

Genetic diseases, copper deficiency

Treatment for copper deficiency

A

Defective absorption of Cu in intestines
Hair depigmentation, steely, kinky
Deterioration of NS

No cure in infants

42
Q

Cellular Cu homeostasis

How is Cu taken up into the cell and processed

A

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

Nutrition and Metabolism (14 decks)

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