Micronutrients
- Created by: Poppy Greacen
- Created on: 03-05-16 15:00
Vitamin A Forms
Retinol (alcohol)
Retinal (aldehyde)
Retinoic Acid (carboxylic acid)
Provitamin- Beta-carotene
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)
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
B-Carotene
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)
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
Metabolic Functions of Vitamin A
Vision
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
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
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
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
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
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
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
Vitamin A Deficiency on Eyes
Nightnblindness
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
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)
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
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
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)
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
Vitamin E Forms
α, β, γ, δ tocopherol
α, β, γ, δ tocotrienol
Vitamin E Sources
Major source is vegetable oils
Low levels in meat, eggs, liver, milk
Green leafy plants, cereals
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
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)
Vitamin E Structural Role
Tocopherol is incorportated into membranes
It forms part of the overall structure of a membrane
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
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
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)
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
Selenium Forms
Selenium
Selenite
Selenite
Selenocysteine
Selenomethionine
Selenium Sources
Cereals
Vegetables
Herbage
Meat
Fish
Amount in plant material dependent on amount in soil
Selenium Metabolic Functions
Essential cofactors for some enzymes- glutathione peroxidase (PSH-Px)
Antioxidant
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
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
Selenium Deficiency
Humans
-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)
Animals
-nutritional muscular dystrophy, myopathy, ill-thrift (general unwellness)
Difficult to distinguish deficiency symptoms between selenium and vitamin E
Selenium Toxicity
Alkali disease
Blind staggers
Stiff joints
Looks of hair
Death from respiratory failure
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
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)
Vitamin C forms
Ascorbic acid
Dehydroascorbic acid
Vitamin C Sources
Humans
-green vegetables, cirrus fruits, potatoes, berries
Animals
-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
Ascorbic Acid and Dehydroascorbic Acid +2H
Forms a redox couple
Can accept 2H Dehydroascorbic
Can lose 2H Ascorbic
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
Requirements
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
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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