Vitamins and Minerals

Question 1

Which vitamins are fat/lipid soluble?

Answer 1

ADEK — A (retinol, B-carotenes), D (cholecalciferol), E (tocopherols), K (phylloquinones, K1; menaquinones, K2)

Question 2

Which vitamins are water soluble?

Answer 2

Vitamin B1
Vitamin B2
Vitamin B3
Vitamin B6
Vitamin B12
Vitamin C
Folate
Panthotenic acid
Biotin

Question 3

Where are fat soluble vitamins stored?

Answer 3

Fat soluble vitamins can be stored in the liver or adipose tissue, water soluble vitamins: B12 and B6 can be stored

Question 4

How are vitamins absorbed and transported?

Answer 4

Absorption is through the intestines, fat-soluble vitamins (absorption enhanced by lipids, packaged in chylomicrons —> lymphatics —> circulation)

Question 5

What are the three active compounds of vitamin A?

Answer 5

Retinol, retinal, and retinoic acid

Question 6

Where is vitamin A stored? As what?

Answer 6

Large amounts are stored in stellate cell of the liver (as retinylesters)

Question 7

What are the sources of vitamin A?

Answer 7

Preformed vitamin A (animal liver products), B-carotene (dark-green, leafy vegetables)

Question 8

What are the functions of vitamin A?

What’s another name for it?

Answer 8

Vision: retinal is part of rhodopsin in rod and cone cells
Cell signaling: retinoic acid binds to intranuclear receptors and modulates gene expression
Maintenance of epithelial integrity (protects from infections)
Spermatogenesis
Embryonic development

Another name for it is retinol

Question 9

What are the two forms of vitamin A deficiency? What are the differences between the two forms?

Answer 9

Mild form — night blindness

Severe form — complete blindness due to aberrant differentiation (keratinization) of epithelial cells in the eye

Question 10

What is the function of vitamin D?

What’s another name for it?

Answer 10

Increases calcium absorption from intestine, decreases renal calcium excretion, mobilizes calcium from bones

Cholecalciferol

Question 11

What happens in vitamin D deficiency? How are children and adults affected differently?

Answer 11

Soft, pliable bones (bowed leg), children: rickets, adults: osteomalacia

Question 12

What happens in vitamin D toxicity?

Answer 12

Loss of appetite, nausea, thirst, stupor, hypercalcinemia (calcium deposition in kidneys and arteries)

Question 13

What is the function of vitamin E?

What’s another name for it?

Answer 13

It is the main fat-soluble antioxidant of the human body. It protects membrane-lipids from free radical damage

Tocopherols

Question 14

What happens in vitamin E deficiency?

Answer 14

Hemolytic anemia in premature infants (tocopherol stores are not yet formed), nerve damage in older children and adults (myelin is damaged)

Question 15

What is the main function of Vitamin K? What inhibits its action?

Answer 15

It is important for blood coagulation. Coagulation factors (II, VII, IX, X, and prothrombin), osteocalcin (a Ca2+ binding protein involved in bone formation)

Coenzyme for the synthesis of γ-carboxyglutamate residues in proteins. γ-carboxyglutamate is essential for Ca2+ binding in these proteins.

It is inhibited by Warfarin (anti-coagulant)

Question 16

What are the main sources of vitamin K?

Answer 16

Intestinal bacteria, green leafy vegetables

Question 17

What happens in the deficiency of vitamin K?

Answer 17

Bleeding in newborns (intestinal bacterial flora has not yet formed), newborns receive vitamin K injection at birth. Bleeding may occur in adults if bacterial flora is killed by excessive antibiotics

Question 18

What is the active form of vitamin B1 (thiamine)?

Answer 18

Thiamine-pyrophosphate (coenzyme)

Question 19

Why is pyruvate and a-ketoglutarate dehydrogenases especially important for the nervous system?

Answer 19

Glucose is the main energy source of the brain) — its deficiency will lead to a variety of neurological symptoms

Question 20

What is beriberi? What are its two different forms? What are the differences?

Answer 20

Beriberi — severe thiamine deficiency

Infantile form — tachycardia, vomiting, convulsion

Adult form — dry skin, irritability, disorderly thinking, progressive paralysis

Question 21

What is Wernicke-Korsakoff syndrome?

Describe its mechanism including some of its symptoms

Answer 21

It is a form if vitamin B1 deficiency due to chronic alcoholism

Alcohol impairs thiamine absorption from the intestines, symptoms include apathy, loss of memory, confusion, inability to move eyes

Question 22

What is the function of vitamin B12 (riboflavin)?

Answer 22

Coenzyme in the forms of flavin mononucleotide (FMN) and flavin adenine dinucleotide (FAD), it is used in oxidation-reduction reactions

Question 23

What happens in the event of vitamin B12 deficiency?

Answer 23

Cracked lips at the corner of the mouth (cheliosis), dermatitis, purple smooth tongue (glossitis)

Question 24

What is the function of vitamin B3?

What’s another name for it?

Answer 24

Precursor for NAD and NADP (oxidation-reduction reactions), tryptophan can substitute for it

Question 25

What occurs in the event of vitamin B3 deficiency?

Answer 25

Pellagra (4Ds — Dermatitis, Diarrhea, Dementia, Death)

Question 26

How is vitamin B3 used pharmacologically?

Answer 26

It is used as a drug for high cholesterol treatment. Reduces lipolysis in adipose tissue. It reduces triclyceride, VLDL and LDL levels in blood

Question 27

What is the function of vitamin B6? What's another name for it?

Answer 27

The active form, pyridoxal phosphate, is a coenzyme. It is used for transamination reactions, certain deamination reactions, certain decarboxylation reactions (dopamine, histamine, serotonin, GABA synthesis), and heme synthesis Pyridoxine

Question 28

Explain vitamin B6 deficiency and toxicity

Answer 28

Deficiency — hyperirritability, neuritis, convulsions Toxicity — excess supplements, rare; nerve damage

Question 29

How is vitamin B6 used pharmacologically?

Answer 29

Pharmacology — isoniazid, an anti-tuberculosis drug, depletes pyridoxal-phosphate

Question 30

What is the function of vitamin C?

Answer 30

``` Collagen synthesis (proline and lysine hydroxylaton is necessary for collagen crosslinking that is dependent on vitamin C) Neurotransmitter synthesis (dopamine to norepinephrine), tyrosine degradation (4-hydroxy-phenyl pyruvate to homogentisate) Antioxidant — scavenges free radicals, ascorbic acid keeps iron in a Fe2+ state ```

Question 31

Explain vitamin C deficiency and toxicity

Answer 31

Deficiency — bleeding, bruising, delayed wound healing, loose teeth, and in extreme cases, scurvy Toxicity — intestinal problems (diarrhea)

Question 32

What is the function of panthotenic acid?

Answer 32

Precursor of CoA Energy production from carbohydrates Fatty acids, amino acids, sphingolipid synthesis (palmitoyl-CoA), fatty acid and cholesterol synthesis (acetyl-CoA, malonyl-CoA), heme synthesis (succinyl-CoA) Neurotransmitter synthesis (i.e., ACh, melatonin—acetyl-CoA)

Question 33

What is the function of biotin? Explain its bioavailability

Answer 33

Coenzymes in carboxylation reactions, fatty acid synthesis (acetyl-CoA carboxylase), gluconeogenesis (pyruvate carboxylase), leucine degradation, propionyl CoA degradation (propionyl CoA carboxylase) Bioavailability varies — biotin in corn and soy is readily bioavailable, only a little biotin in wheat is bioavailable

Question 34

What happens to iron when it is not bound to proteins? How is iron found in the body?

Answer 34

Iron is toxic, it has to be bound to proteins. Part of heme and non-heme proteins (60-80% is in hemoglobin) Heme proteins — iron is chelated to porphyrin ring (e.g., hemoglobin) Non-heme proteins — iron-sulphur clusters (e.g., ferredoxins) and others

Question 35

Explain copper transport

Answer 35

Copper is transported in the circulation by ceruloplasmin (90%) and albumin (10%), it is necessary for the stability of ceruloplasmin. Both ATP7A and ATP7B deficiencies lead to low blood levels of ceruloplasmim

Question 36

In Menke’s disease, what is the deficient molecule? What is defective in relation to copper? What is the treatment?

Answer 36

Deficient molecule is ATP7A, experiences deficient intestinal uptake of copper, neurological effects, growth retardation, hypopigmentation, laxity of skin Treatment is copper-histidine

Question 37

In Wilson disease, what is the deficient molecule? What is defective in relation to copper? What is the treatment?

Answer 37

Deficient molecule is ATP7B, experiences deficient excretion of copper, cirrhosis, liver failure, neurological defects, psychiatric symptoms Treatment is copper-restricted diet, copper chelators, oral zinc tablets

Question 38

What is the function of zine?

Answer 38

Essential for the function of a wide variety of enzymes/proteins. Oxidative phosphorylation (cytochrome c oxidase), protection against oxidative stress (Cu/Zn superoxide dismutase), acid-base balance (carbonic anhydrase), protein degradation (metalloproteases), transcription (zinc finger domain used for DNA binding)

Question 39

What is the physiological role of zinc?

Answer 39

Wound healing, skin integrity, spermatogenesis, pancreatic function

Question 40

How is zinc stored?

Answer 40

They are stored in metallothioneine (also binds copper with even higher affinity), high Zn levels induce metallothioneine production

Question 41

What happens in the deficiency of zinc?

Answer 41

Acrodematitis enteropathica (deficient Zn transporter), red and inflamed patches of dry scaly skin that progress to blistered lesions, hair loss, diarrhea

Question 42

What is the importance of iodine?

Answer 42

Thyroid hormone synthesis

Question 43

What occurs in the deficiency of iodine? How are children affected?

Answer 43

Goiter: lack of iodine in diet (enlarged thyroid gland) Cretinism in children: mother had limited iodine intake during pregnancy (mental and growth retardation

Question 44

What is the function of selenium?

Answer 44

Presents mainly as selenocysteine and selenomethionine in the human body. Selenocysteine is the 21st proteinogenic amino acid (indirectly coded by the genetic code) Enzymes containing selenium include glutathione peroxidase (antioxidant), thioredoxin reductase (antioxidant), thyroid hormone deiodinase (conversion of T4 and T3)

Question 45

Explain selenium deficiency and toxicity

Answer 45

Deficiency — Keshan disease (China): cardiomyopathy Toxicity — brittles nails and hair, intestinal problems, garlic-like body odor, neurological problems