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Vitamin A Forms

Retinol (alcohol)

Retinal (aldehyde)

Retinoic Acid (carboxylic acid)

Provitamin- Beta-carotene

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Vitamin A Sources

Retinol in forms of retinyl esters from animal products (meat, liver, milk, dairy produce, eggs, fish liver oil)

Beta-carotene from plant products, carrots, dark green vegetables, yellow fruits (fresh green crops when grazing, dried grass, hay, maize)

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Vitamin A Molecule

Long hydrocarbon chain with some branching, OH group on the end and a hydrocarbon ring

Retinol will react with FA to form retinal esters

Vitamin A gets stored as retinal esters and they're also the form in which supplementation of diet with vitamin A takes place

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Can undergo enzymatic cleavage to produce 2 molecules of retinal

Very rarely cleaved in the middle and so often end up with one molecule with hydrocarbon chain longer than the vitamin A chain (can be shortened but shorter chain can't be lengthened)

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Vitamin A How its Measured

Retinol Equivalents (RE)

at- all trans (refers to arrangement of hydrogens around the double bond)

1 microgram retinol=12 micrograms b-carotene

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Metabolic Functions of Vitamin A


Maintenance of epithelial cells

Cell differentiation and development

If you want to ensure that reproduction carries on normally, need to provide vitamin A in form of retinol or something that can form vitamin A- if give retinoic acid, does't supplement sufficiently to allow normal reproduction as its unable to pass into tissues which require it- retinol goes into reproductive tissues and is then converted to retinoic acid (which can't be given directly to support reproduction)

Retinol is oxidised to retinal, which can be reduced back, however retinal to retinoic acid is only one way and is oxidation

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Vitamin A Role in Vision

Component of light sensitive pigment rhodopsin found in rod cells of the retina

Rods are responsible for vision in dim light

11-cis retinal binds to the protein opsin to give rhodopsin

When light hits the rod cell the retinal is converted to all-trans retinal initiating change of conformation of the protein (kink to straight)

Initiates a signal which is transmitted to the brain-sight

Retinal released from activated protein, converted back to 11-cis form and cycle starts again

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Vitamin A Nightblindness

Can see during the day but unable to see in dim light/night- don't have sufficient retinal going into eye to allow cycle to take place

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Vitamin A Function in Eye

If level of vitamin A in blood falls, level in eye fall as well

Rhodopsin changes shape in presence of light

Meta-rhodopsin II- formation results in nerve stimulation and leads to vision

RAL- retinal

ROH- retinol

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Vitamin A Function as a Steroid Hormone

Retinoic acid is the active form

Binds to retinoic acid binding protein in the cytosol (CRABP)

Transferred to retinoic acid receptor in the nucleus

RAR-RA complex binds to DNA at the appropriate response element (RARE)

Influences transcription of genes

Affects proteins in cell

Important for cell differentiation, maintenance of epithelial cell

Vitamin A is always found in cells linked to other proteins

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Vitamin A Systematic Function

RBP- retinol binding protein (needed to transport non-polar retinol in blood)

Retinol needs binding protein to help it travel in the cell as its fat soluble

Retinoic acid gets bound to albumin and then gets taken into cells- once in the nucleus it binds to RARE- once the two are complexed they're able to bind to the response element

If plenty of vitamin A in the body, converted to retinal ester and stored in the liver and when needed in the body broken down to retinol- then binds to retinol binding protein which takes it from the liver to areas where its needed

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Vitamin A Deficiency

Leading cause of preventable blindness in children and increases the risk of disease and death from infection

In pregnant women VAD causes nightblindness and increases the risk of maternal mortality

Public health problem in more than half of all countries, especially Africa and SE Asia, hitting hardest young children and pregnant women in low income countries

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Vitamin A Deficiency on Eyes


Xerophthalmia- medical condition in which the eye fails to produce tears- cells which usually prodice and secrete mucus secrete keratin instead 

In some stages for eyes giving vitamin A can stop conditions worsening- sight impaired but not gone

When it gets too later stage the conditions are irreversible

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Vitamin A Systematic Deficiency Symptoms

Impaired reproductive performance

Keratinisation of epithelial cells

Increased CSF (cerebral spinal fluid) pressure (bulging eye)- pressure builds and has to be released

Bone malformations giving blindness and deafness- as skull develops, it doesn't do so properly and there are canals through which nerves have to get through to get to ears and eyes and without sufficient vitamin A canals narror and pinch nerves so theres a problem with blindness and deafness

Reduced immune response (particularly to viral infection)

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Vitamin A Toxicity

Excess intake exceeds capacity of binding proteins either in cell or blood

Build up of free vitamin A in tissues, damage cells

Increased CSF pressure, headache, nausea

Joint pains, thickening of bones, hypercalcaemia (high calcium concentration in blood)

Liver damage

Vitamin A terratogenity- excess vitamin A is terratogenic, causes birth defects

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Vitamin A Requirements

0-10 yo 350-500 ug RE/d

Males 600-700 ug RE/d

Females 600 ug RE/d

Pregnancy +100 ug RE/d (need to supply fetus)

Lactation +350 ug RE/d (need to supply vitamin A as nutrient to young)

Regular intakes should not exceed

-Males- 9,000ug RE/d

-Females- 7,500 ug RE/d

Need more as an adult as have more cells requiring vitamin A in order to function

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Antioxidant Micronutrients

Most cells need oxygen to survive

If don't have oxygen, can't generate energy through ETC and chemiosmotic process

Unwanted oxidation can cause damage

Reactive Oxygen Species (ROS) are compounds, often free radicals, which cause damage

Can damage nucleic acids, carbohydrates, proteins, redox state of cell

Antioxidant micronutrients minimise effect of ROS (either prevent reactive oxygen being formed or reduce damage)

Vitamins E and C, trace minerals Se (glutathione peroxidase), Cu, Zn, Mn (SOD), Fe (catalase)

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Free Radical

Molecule with unpaired electron- electrons like to be paired so its very reactive, cause damage to many essential macromolecues, damage redox state of cell and damage lipids in cell membranes

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Vitamin E Forms

α, β, γ, δ tocopherol

α, β, γ, δ tocotrienol

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Vitamin E Sources

Major source is vegetable oils

Low levels in meat, eggs, liver, milk

Green leafy plants, cereals

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Metabolic Functions of Vitamin E

Biological antioxidant- free radical scavenger (associated with Se, vitamin C and beta-carotene)

Components of membranes

Amphipathic- can go into membranes

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Vitamin E Molecule

Alcohol group is on the ring and not on the end of the chain as with vitamin A

For tocotrienol- 3 double bonds in the chain

Natural a-tocopherol is the most biologically active- acoutns for 90% vitamin E in the body and now considered to be one of the only biologically active

Synthetic a-tocopherol has potency of 0.45

Previously measured in a-tocopherol equivalents (TE)

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Vitamin E Structural Role

Tocopherol is incorportated into membranes

It forms part of the overall structure of a membrane

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Vitamin E Chemical Reactions as an Antioxidant

Protects PUFA from oxidation, particularly oxidation by free radicals

Breaks an oxidation chain reaction- membranes have to be fluid in order to carry out normal function of taking in nutirents, getting rid etc- PUFA keep it fluid but due to double bond very prone to oxidation- vitamin E breaks this chain

Acts as a free-radical scavenger

One of its functions is similar to that carried out by GSH-Px which requires Se as a cofactor

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Antioxidant Role of Vitamin E

Hydroperoxides are toxic to the cell and cause cell damage- vitamin E stops this- reactive with peroxy radical preventing it reacting with neighbouring HC chain and form vitamin E radical and hydroperoxide- hydroperoxide then reacts with other vitamin E and converts it to vitamin E quinone- not toxic but gets excreted and in doing so it converted to hydroperoxide to alcohol which isn't toxic

Prevents chain reactions, takes toxic compound and makes it non-toxic

Free radical pull H off hydrocarbon chain and reduces the reactive oxygen species so its no longer reactive- leaves C on chain with unpaired electron

Formed lipid radical- react readily with any molecular oxygen which is around and forms peroxy radcal

In membrane if no vitamin E, peroxy radical would go and interact with neighbouring HC chain, form other free radical on HC chain and peroxy radical converted to hydroperoxide

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Vitamin E Deficiency

Humans- Rare as food we eat is usually quite balanced (premature infants, fat malabsorption)

Neurological disorders (ataxia, weakness, sensory dsiturbances)

Animals- More common as not such a varied diet

Myopathy- nutritional muscular dystrophy, white muscle disease, stiff lamb disease- muscle weak, unable to move well- like muscular dystrophy but caused by nutritional source

Mulberry heart disease- breakdown of tissue and rupturing

Dietary hepatic neurosis- dead cells in liver

Exudative diathesis- walls of capillaries detereorate so blood and fluid escapes and gets under skin and then haemoglobin breaks down and you get green fluid under tissues

Nutritional encephalomalacia- what happens if green fluid goes to brain (crazy chick disease)

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Vitamin E Requirments

No DRVs specified for humans

Dependent on level of PUFA consumed so single values would be meaningless

Association of vitamin E with PUFA in biological systems results in increased vitamin E intake with increased PUFA intake

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Selenium Forms


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Selenium Sources

Amount in plant material dependent on amount in soil

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Selenium Metabolic Functions

Essential cofactors for some enzymes- glutathione peroxidase (PSH-Px)

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Selenium can make Selenomethionine and selenocyste

Selenomethionine- selenium gets incorporated into methionine by random, doesn't matter which it incorporates
Selenocysteine- very different, only some proteins contain it- it's synthesised whilst protein is being translated- under certain conditions stop codon for DNA codes for celenocysteine

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Antioxidant role of Selenium

Oxidised- oxygen pulled out of peroxide, binds to 2H to give water, end up with GSSG and alcohol
Alternative for converting peroxide to alcohol is to use vitamin E, another is for glutathione peroxidase to catalyse oxidation of glutathione- 2 different reactions achieve same result- don't happen together, either/or
Glutathione peroxidase is the selenium containing enzyme and one of the best known functions of selenium in the body

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Selenium Deficiency

-Muscle pain and weakness
-Keshan disease (insufficiency of cardiac function, cardiac enlargement, abnormal rhythm- often fatal- heart becomes enlarged because muscle becomes less effective and so increase amount of muscle to try and counteract- abnormal rhythm)
-Kaschin Beck Disease (osteoarthropathy, enlarged joints, shortened fingers/toes, dwarphism)
-nutritional muscular dystrophy, myopathy, ill-thrift (general unwellness)
Difficult to distinguish deficiency symptoms between selenium and vitamin E

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Selenium Toxicity

Alkali disease
Blind staggers
Stiff joints
Looks of hair
Death from respiratory failure

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Selenium Requirements

RNI 1ug/kg (tiny amount but if don't eat it start to be ill- 6x amount can become toxic)
70-75ug/d men
60ug/d women
No extra requirement in pregnancy but extra 15ug/d in lactation
Infant values based on intake from milk- 10-15ug/d increases to 45ug/d
Recommended max intake for adults 450ug/d

Balanced diet, adequate micronutrients almost without trying- when don't have balanced diet that's when problems start

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Link between oxidative damage and Atherosclerosis

Failure to prevent atherosclerosis can result in a number of diseases e,g cancer, cataracts, atherosclerosis
High intakes of PUFA increase requirement for antioxidant micronutrients
Vitamin E and Se can substitute for each other to some extent (Se involved in enzymes other than GSH-Px)

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Vitamin C forms

Ascorbic acid
Dehydroascorbic acid

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Vitamin C Sources

-green vegetables, cirrus fruits, potatoes, berries
-no dietary requirements for animals except higher apes, Guinea pigs, red vented bul-bul bird, Indian fruit bat
-most animals can synthesise vitamin C from sugars- animals requiring vitamin C all tend to be consuming lots of fruits and berries

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Ascorbic Acid and Dehydroascorbic Acid +2H

Forms a redox couple
Can accept 2H Dehydroascorbic
Can lose 2H Ascorbic

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Vitamin C Deficiency

Scurvy- swelling/bleeding gums, haemorrgages, oedema, poor wound healing, extreme weakness, aching bones, reduced immunity to infection
Fresh fruit can prevent symptoms

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RNI 40mg/d for men and women
Additional 10mg/d during late pregnancy and 70mg/d during lactation
Infants receive 25mg/d from breast milk so is set as RNI for infants

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Hydroxylation is essential to make collagen

Presence of vitamin C
-ribosome synthesises collagen molecule and as doing this lysine and some proline get OH added to them
-3 molecules come together, twist around each other and form tropocollagen- the building block from which we make collagen
Absence of vitamin C
-ribosome producing collagen but no hydroxylation of lysine or proline so although 3 molecules come together they don't twist and don't get active collagen

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