vitamin A Flashcards

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1
Q

what is the definition of vit A

A

Fat soluble

Includes all naturally occurring compounds with the biological activity of retinol and pro-vitamin A carotenoids:

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2
Q

what are the Preformed vitamin A retinoids (3 vitamers)

A

Retinol
Retinaldehyde
Retinoic acid

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3
Q

what are Pro-vitamin A carotenoids

A

Of >500 known natural carotenoids, only ~50 converted to vit A.

Cleaved to yield retinaldehyde, and hence retinol & retinoic acid.

Not all carotenoids can be converted to vitamin A

Carotenoids natural are associated with plant material and algae

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4
Q

name some Chemical structures that have genuine vit A biological activity:

A

retinol
retinaldehyde
all-trans-retinoic acid
11-cis-retinol
9-cis-retinoic acid

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5
Q

explain carotenoids

A

Photosynthetic Pigments widely found in nature – photosynthetic tissue.

Yellow, orange or red.

Yeast, bacteria, fungi, vegetables, fruit.

Animals cannot synthesise carotenoids but can deposit them in body tissues with or without alteration of the basic structure.

They participate in photosynthesis

Pink colour in flamingos is due to feeding on plankton in water with carotenoids which is a pink colour , Same situation for salmon

Most carotenoids in our diet are from plant material

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6
Q

name some Major pro-vitamin A carotenes structures

A

alpha carotene
beta carotene
gamma carotene
beta-cryptoxanthine (3hydroxy-beta-carotene)

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7
Q

what are the Major pro-vitamin A carotenes able to metabolise

A

Able to be metabolised into retinol or retinoic acid

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8
Q

what does it mean by - carotenoids without vit A activity

A

ones don’t confer vit A activity

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9
Q

what are some Carotenoids without vit A activity and explain them

A

Lycopene – is associated with tomatoes
Not essential nutrient, but
prominent phytochemical
Cooking tomatoes increases bioavailability of lycopene

Lutein
Luteus – yellow colour
Functions in the eye (reduce risk of macular degeneration and cataracts in eye)
Used as Food additive (E161b) – extracted from marigold petals

Zeathanthin
Xanthos – yellow colour
Found in Maize corn and leaves of green plants

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10
Q

what are some vit A retinol sources

A

Foods of animal origin and a small number of bacteria, mainly in the form of retinyl palmitate in animal tissues.

Liver
Fatty fish
Egg yolk – egg yolks yellow so indicates this
Milk
Butter
Enriched margarine

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11
Q

what are some carotenoids food sources

A

associated with (red, orange, yellow) plant material in diet

Carrots, peppers, tomatoes
Brocolli, kale, spinach, brussels sprouts, green beans
Peaches, apricots, mangoes, pink grapefruit, melon

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12
Q

explain absorption of retinol and of carotenoids

A

Retinol: ~70-90% is normally absorbed.

Carotenoids: ~5-60%, depending on carotenoid and cooking.

Absorption of carotenoids and retinol impaired if diet provides <10% E from fat. So bioavailability reduced

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13
Q

explain the bioavailability of beta carotene

A

The most biologically active carotenoid.

Pure β-carotene yields 50% the vitamin A activity of retinol:
conversion factor 2:1 pure β-carotene : retinol

Lower bioavailability from plant sources:
conversion factor 6:1 β-carotene : retinol

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14
Q

describe the bioavailability in terms of the conversion factor of other carotenoids excluding beta carotene

A

Conversion factor is 12:1

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15
Q

total vit A in foods is expressed as what

A

as μg retinol equivalents (REQ)

1 μg REQ = 1 μg preformed retinol
6 μg β-carotene
12 μg other carotenes with vit A activity

REQ = ∑preformed vit A + (β-carotene/ 6)+ (other pro-vit A carotenoids/ 12)

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16
Q

Vit A content of foods used is to be expressed in what units

A

in standardised international units: 1 IU = 0.3 μg retinol or 0.6 μg β-carotene

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17
Q

explain the formation of retinol from carotenes

A

Beta carotene absorbed and oxygen added and enzyme carotene dioxygenase, which forms 2 retinal aldehydes
That’s then converted to retinol by enzyme retinol dehydrogenase or retinoic acid by aldehyde oxidase

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18
Q

explain absorption transport and storage of vit A

A

Bile will act as emulsifier breaking liquid up inro smaller units allowing enzymes to digest the fat
Bile forms a micelle which the fats are incorporated into and is where the digestion happens
Everything lipid soluble is digested into micelle structure to absorb it.
Cant absorb anything lipid soluble without bile secretion, which you need enough fat in the diet to get this bile secretion so is why we need aft in diet for vit A absorption.
We form lipoproteins which he protein emulsifies the fat in this structure which salifies it.
Chylomicron enters lymphatic circulation
When in blood circulation it travels through tissues which remove some of the trigylcerol for their own purposes

19
Q

whys liver good vit A source

A

There are significant stores of vit A in liver so is why it’s a good source of vit A

20
Q

explain the stages involved in absorption transport and storage of vit A

A

Absorbed from small intestine dissolved in lipid

Retinyl esters formed in the intestinal mucosa enter lymphatic circulation in chylomicrons with dietary lipid & carotenoids

then either:
Tissues can take up retinol esters from chylomicrons
or
Most remains in chylomicron remnants that are
taken up by liver where the esters are hydrolysed

after Most remains in chylomicron remnants that are taken up by liver where the esters are hydrolysed

theyre either:
Retinol Stored as esters in stellate cells in liver
or
Vitamin secreted from liver bound to retinol-binding protein (RBP)
RBP delivers the vitamin to target tissues

21
Q

functions of vit A

A

Vision - forms light sensitive complex rhodopsin(as this is produces from retinol) in retina – night vision

Gene expression & cell differentiation – such as of blood cells, and during embryonic development

Morphogenesis – (making our morphology) & embryogenesis- (making embryo)

Growth

Integrity of the immune system

beta-carotene is an antioxidant. (Retinol isn’t a antioxidant though)
- High intakes associated with low incidence of Cardio Vascular Disease & some cancers, but not as supplements!

22
Q

explain vit A and vision

A

Vit A - essential to vision at low light intensity.

In the retinal pigment epithelium of the eye, all-trans-retinol is isomerised to 11-cis-retinol and oxidised to 11-cis-retinal.

11-cis-retinal binds to the amino group of lysine on the light sensitive protein opsin to produce rhodopsin.

Rhodopsin is a light absorbing complex in the rods.

Rhodopsin is used in low light intensities

Exposure to light activates 11-cis-retinal/rhodopsin complex.

This generates Electrical signals which are transmitted to the optic nerve, enabling the eye to adapt to low light intensity and darkness.

23
Q

explain vit A importance in gene expression and cell differentiation

A

Control of cell differentiation & turnover.

All-trans-retinoic acid & 9-cis-retinoic acid are involved in regulation of growth, development & tissue differentiation, with different actions in different tissues.

Retinoic acid binds to nuclear receptors that bind to control regions of DNA, thereby regulating gene transcription.

There are two families of nuclear retinoid receptors:
RAR (retinoic acid receptors)
RXR (retinoid X receptors)

24
Q

explain vit A in terms of Morphogenesis + embryogenesis

A

Biological effects of retinoic acid are mediated by changes in gene expression caused by the RARs & RXRs.

Change in expression of RARs influences neural tube closure.

Switch in expression from RAR-γ (gamma) (open neural tube) to RAR-β (closed neural tube) is essential for proper posterior neural tube closure. – its though that folate is important in signalling molecule in change between beta and gamma receptor

Exposure to excess retinoic acid may result in congenital neural tube defects. Due to it affecting the ‘switching’ process

Retinoic acid has been implicated in expression of many genes which determine sequential development of various parts of an organism.

So is why recommended pregnant females don’t eat liver or too much vit A

25
Q

what country is largely deficient in vit A

A

majority of Africa

26
Q

what are the WHO Stages of xerophthalmia

A

Night blindness -> Bitot’s spots -> keratomalacia

Xerophthalmia = full vit A deficiency

Keratomalacia interferes with all vision so become completely blind

27
Q

what is night blindness

A

Impaired colour vision: loss of sensitivity to green light.

Impaired ability to adapt to dim light.

Inability to see at all in dim light (night blindness).

28
Q

what are bitots spots

A

White marks on the eye

Its areas of the eye that are becoming keratinized

There are other pathological reasons why bitots spots may form

They have a foamy and cheesy state

29
Q

what is keratomalacia

A

Where cornea is affected so all vision is lost

Enzyme dissolves the cornea

This process sis irreversible

30
Q

how does vit A deficiency impair immune response

A

Mild deficiency → ↑ susceptibility to infectious diseases.

↓ RBP synthesis in liver in response to infection → ↓ circulating vit A conc and further impairment of immune responses.

31
Q

how does vitamin A deficiency occur secondary to protein - energy malnutrition (PEM)

A

Theres Impaired RBP synthesis (delivers vitamin to target tissues) – so inadequate vit A delivery to tissues.

32
Q

who is at risk of vit A deficiency

A

Those with diets low in animal fats & vegetables

Low protein diets

Fat malabsorption + low dietary fat

Children in developing countries from birth to 5y (peak 2-3y)

33
Q

name and explain methods for prevention and treatment of vit A deficiency

A
  • Supplementation
    Deficiency rare in UK.
    India – large doses of vit A in oil given every 4-6 months effective in children. Incidence of toxicity low.
    Vit a supliments Often done at same time as immunization activities or deworming of children. Every twice a year
  • Nutrition education
    30g fresh green leaves or some fruit could prevent deficiency.
    Often fails due to insufficient emphasis on maintaining altering behaviour.
  • Fortification
    Margarine + oil
    Dried skimmed milk (vits A + D)
    Sugar (Guatemala, mid 1970’s)
  • Golden rice
    GM to contain β-carotene.
    GR2 – super golden rice, more
    beta carotene
    Places where staple food was rice, vit A deficiency was common so GM rice so it has beta carotene this gave it a yellow colour
34
Q

where do excessive high intake of vit A accumulate

A

liver

35
Q

vit A toxicity occurs from more than how many mg/d of vit D in adults

A

> 7mg/d

36
Q

what are some symptoms of vit A toxicity

A

Central nervous system: headache, nausea, ataxia & anorexia

Liver: hepatomegaly with histological changes in liver (liver enlarges), increased collagen formation (scarring)& hyperlipidaemia.

Bones: joint pains, thickening of long bones, hypercalcaemia &
calcification of soft tissues.

Skin: excessive dryness, scaling & cracking of skin (so vulrneable to infection) & alopecia

37
Q

explain vit As Toxic effects in pregnancy

A

Retinol is teratogenic in first trimester, causing:
- Spontaneous abortion
- Birth defects
- Permanent learning disabilities

Advised against retinoid therapy, liver or supplements

38
Q

explain carotene - animal sources of vit A, and its toxic affects

A

Not known to have any adverse effects except giving orange-yellow colour to skin (hypercarotenosis) – unusual but not unheard of

However intervention trials in 1990s found ↑ lung cancer mortality in supplemented group.

39
Q

how can we use liver stores to asses vit A status

A

Most accurate – direct assessment of status.

Can’t be readily determined in living subjects.

40
Q

how can we asses vit A status by Looking at Plasma (or serum) retinol – via blood sample

A

Insensitive indicator of status (levels maintained constant over wide range of intakes). Its not precise
< 10 μg/100ml (0.3 μmol/l) – clinical deficiency state
< 20 μg/100ml (0.7 μmol/l) - marginal deficiency

41
Q

how can we asses vit A status by looking at breast milk conc

A

May be used to indicate status in lactating women.

42
Q

vit A requirements are Based on intakes needed to maintain what and why

A

liver conc of 70μmol/kg

This is adequate to maintain normal plasma concs.

Individuals with this level of liver reserves can exist on vit A-free diet for months before developing signs of deficiency.

43
Q

what are the RNIs for vit A during different stages of life

A

11-14y 600 (M) 600 (F)
15-50+y 700 (M) 600 (F)
Pregnancy - +100 (F)
Lactation - +350 (F)