13_Biochem Block 4.10 Micronutrients Ii

Front 1

Vitamin C (AKA ?) is found in:

Back 1

Ascorbate is found in all fruits and vegetable but is highest in citrus fruits, green peppers, strawberries, tomatoes, broccoli, green leafy vegetables and potatoes.

Front 2

What is the major beneficial effect of VitC? How does it do that?

Back 2

Reduces active oxygen species. Does so by keeping iron in the +2 state.

Front 3

VitC is key to hydroxylation of two aa found in proteins:
What protein is this especially important for?

Back 3

Proline and Lysine. Collagen

Front 4

Iron transitions between Fe3+ and Fe2+ in the body. Which form can pass through the intestinal membrane?

Back 4

Fe2+

Front 5

What vitamin does VitC reduce?

Back 5

VitE

Front 6

What disease is caused by deficiency of VitC? What is the symptoms of this disease and why does it happen?

Back 6

Scurvy. Bleeding and corkscrew hairs due to lack of uncontrolled cross linking of disulfide bonds.

Front 7

Describe the structure of VitE (p485) What is it similar to?

Back 7

It has a ring and a chain. Vit K

Front 8

Where is Vit E found at highest level (3)

Back 8

Oils, meets and eggs

Front 9

Where is VitE found in the body? What does it do there?

Back 9

In the lipid bilayer. It reacts and neutralizes free radicals.

Front 10

When VitE reacts with a free radical, is it oxidized or reduced? What is used to metabolize this altered form so that it can be recycled? (p485)

Back 10

It is oxidized. Vitamin C is used to convert it back to its reduced form.

Front 11

Who experiences VitE deficiencies?

Back 11

Premature infants. Adults with malabsorption syndroms or bowel resection.

Front 12

What is a major known symptom of VitE deficiency? Is there a toxicity in VitE overdose?

Back 12

Fragility of RBCs. No toxicity.

Front 13

Vitamin A exists in three different forms. What are they and what are they used for?

Back 13

1. Carotenoid form = Antioxidant
2. Aldehyde form = Vision
3. Acid form = Gene expression control

Front 14

Where is B-caretene typically found?

Back 14

Found in intensely colored vegetables such as carrots, sweet potatoes, and red peppers.

Front 15

The structure of VitaminA as an antioxidant is simply:
(discuss the methyl group frequency and the point of the conjugated double bonds)

Back 15

Two retinol molecules put together with a methyl group attached on the phytyl chain at every fourth carbon. The conjugated double bonds are necessary for absorbing free electrons.

Front 16

What is the name of VitA used to help vision? How much is needed/d. It is found in the same foods as B-carotene, however, this form is found in eggs, meat, and dairy products:

Back 16

Retinal - 800 ug/d. Retinyl Esters

Front 17

Since VitA is a fat soluble vitamin, how does it enter the system? (Starting with b-carotene)

Back 17

B-carotene undergoes cleavage by monooxygenase and converted first to retinaldehyde and then reduced to retinol. The retinol is then esterified and incorportated into chylomicrons for distribution.

Front 18

Retinol is essentially beta-carotene that has been cleaved. How is it loaded into chylomicrons?

Back 18

It is esterified with palmitic or stearic acid with LRAT - lecithin:retino acyl transferase and then loaded into a chylomicron.

Front 19

Where and in what form is retinol stored in the body?>

Back 19

Liver, retinyl ester

Front 20

When needed, how is retinol released from the liver?

Back 20

Retinyl esters are hydrolyzed by a retinyl hydrolase to free all-trans-retinol and released from the liver bound to retinol binding protein, RBP, in complex with thyroid hormone receptor transthyretinin (TRR), a thyroid protein

Front 21

Why is it necessary for retinol to bind to TRR

Back 21

Otherwise it'll be lost to the urine.

Front 22

What is the target cell receptor for retinol? Where is this receptor found?

Back 22

Megalin - found on pigment epithelial cells.

Front 23

What is the active form of retinol for vision?

Back 23

11-cis-Retinal

Front 24

Before Retinol (vitA) can be used in the eye, it must be converted to:
How is this done?

Back 24

11-cis-Retinal.
1. LRAT converts all trans to 11-cis form
2. Dehydrogenase converts alcohol to aldehyde

Front 25

What is 11-cis-retinal added to in rod and cones?

Back 25

11-cis-retinal forms a schiff base with opsin to become Rhodopsin - this form can absorb light at different wavelengths.

Front 26

How can the pigments absorb different wavelengths?

Back 26

Bc of different amino acids in the binding pockets of the four proteins.

Front 27

What is the conformational change that occurs when light hits 11-cis-retinal? What happens that ultimately leads to a visual signal?

Back 27

It's converted to all-trans-retinal. This causes rhodopsin to become metarhodopsin II which has a binding site for transducin which, when bound, becomes activated via GTP to GDP exchange. This causes transducin to dissociate into its component subunits where the alpha subuint activates phosphodiesterase. This enzyme converts cyclic GMP to GMP and closes the cGMP gated sodium-calcium channel and sends a visual signal to the brain.

Front 28

A deficiency of VitA causes a problem in vision - what and how?

Back 28

Night blindlness due to an inability to recycle 11-cis-retinal fast enough.

Front 29

What form of VitA is used in controlling gene expression?

Back 29

Retinoic acid

Front 30

Retinol is toxic to the cell, it must first bind to:

Back 30

CRBP - cellular retinol binding protein.

Front 31

What are the steps to making retinoic acid? Which steps are reversible/irriversible?

Back 31

All-trans retinol (VitA) to all-trans retinaldehyde (reversible) to all-trans retinoic acid (irreversible)

Front 32

Retinoic acid binds to what two proteins in the nucleus?

Back 32

RXR and RAR

Front 33

There are two forms of retinoic acid that bind to RXR and RAR. What are they and how are they converted?

Back 33

1. All-trans retinoic acid
2. 9-cis-retinoic acid
Retinoic Acid isomerase converts them

Front 34

What do the Retinoic Acid/RXR/RAR complexes bind to? What does this cause?

Back 34

RARE - E=elements
Causes genes to be turned on or off.

Front 35

What is the form of retinoic acid that is used in acne creme? Pill?

Back 35

Creme: all-trans-retinoic acid (tretinoin)
Pill: 13-cis-retinoic acid (isotretinoin)

Front 36

What can deficiency in VitA cause?

Back 36

1. Bitot's spots on sclera
2. Xerophthalmia bc skin does not slough
3. Follicular hyperkeratosis
4. Keratomalacia

Front 37

What can VitA deficiency cause in regard to Viral infections?

Back 37

Severity is much greater

Front 38

What can VitA toxicity cause?

Back 38

Blurred vision, abdominal discomfort due to pealing of skin, loss of hair, headach, liver enlargement, bone deformities

Front 39

What are good sources of VitD? How much is required?

Back 39

Cheese, butter, margarine, fortified milk, fish, and fortified cereals. 20 ng/d

Front 40

What are the two forms of VitD from the diet?

Back 40

Plants = Ergocalciferol (VitD2)
Animals = Cholecalciferol (VitD3)

Front 41

VitD3 can be obtained from animal products. How else can it be formed?

Back 41

Synthesized by the body. First body forms 7-dehydrocholesterol that is then converted to VitD3 via light

Front 42

Before VitD3 is activated, it must be converted to ? in this organ:

Back 42

The kidney converts 25-(OH)D (vit D3) to 1,25-(OH)2D

Front 43

Conversion of VitD3 to 1,25-(OH)2 in the kidney is controlled by two factors:

Back 43

1. Low phosphate (PO4)3-
2. Parathyroid hormone

Front 44

How does 1,25-(OH)2 regulate gene expression?

Back 44

1. Binds to VDR that binds to retinoic acid receptor (RXR) to form an initiation complex for gene transcription.

Front 45

See p494 for some of the functions of 1,25-(OH)2 (she really just wants us to know that retinoic acid receptor and VDR combine to control gene expression)

Back 45

See p494 for some of the functions of 1,25-(OH)2 (she really just wants us to know that retinoic acid receptor and VDR combine to control gene expression)

Front 46

What affect does Hypocalcemia have on the body? What about hypercalcemia

Back 46

1. Low calcium increase PTH secretion
2. PTH stimulates:
a) kidney to retain Ca b) stimilates 1,25(OH)2D3 form which brings in more Ca into the intestine, thereby increasing Ca2+ c) pulls Ca2+ out of the bones.
3. Hypercalcemia is reversed
3.

Front 47

What affect does hypophosphatemia have on the body?

Back 47

1. Decreases PTH levels
2. Low P stimulates kidney to retain phosphate
3. Stimulates conversion to 1,25(OH)2D3

Front 48

How does VitD affect Ca2+ and Phosphate levels?

Back 48

It regulates the synthesis of calcium and phosphate proteins involved in absorption of both molecules in the intestine and retention in the bones.

Front 49

What has greater control of 1,25-(OH)2D3 formation in the kidney: PTH levels or low Phosphate levels?

Back 49

low phosphate levels.

Front 50

If Phosphate levels are high, what do you expect with respect to PTH levels and VitD3 levels?

Back 50

PTH is high to excrete excess phosphate but 1,25-dihydroxy-vitD is low.

Front 51

Deficiency of VitD causes:

Back 51

Rickets

Front 52

Excess VitD can be toxic and cause:

Back 52

Diarrhea, dermatitis, headache, nausea, anorexia, calcification of soft tissue, decalcification of bones and kidney stones.