Vitamins Flashcards
Vitamins - why do we need them
Essential for normal body function Deficiency may cause disease Needed in small amounts (μg or mg/day) Do not provide energy Have to be supplied in diet Some can be synthesised (D - sun, B and K-gut bacteria)
Vitamins structure
Chemically disparate Organic compounds (trace elements and minerals: inorganic)
Vitamins functions
Co-enzymes Hormones Cell signalling Antioxidants Regulators of growth and differentiation
How were vitamins found
Casimir Funk (1884-1967) Milk contains 'accessory growth factor' Thought to be an amine Vita + amine = vitamine More than one factor in milk -A (lipid soluble in cream) -B (water soluble in whey)
Biological availability and adsorption
< adsorption can lead to deficiency
Properties of food e.g. low in fat could lead to not having fat soluble vitamins
Pre-existing disease
-e.g. celiac (impaired fat absorbtion)
-gastritis (low acid - B12)
Drugs may compete for absorbtion, kill bacteria
Recommended daily allowance
RDA: ‘an intake that is adequate to ensure the requirements of all healthy people are met’
Supplements and toxicity if too much is taken
Requirements may vary: children, pregnancy (folate: crucial role in development of embryos especially spinal cord) - for differentiation, growth etc.
Fat soluble vitamins
A, D, E, K
In general fat soluble can be stored, water soluble not
Water soluble vitamins
B vitamins, C
In general fat soluble can be stored, water soluble not
Vitamin A
Retinoids (active form) Carotenoid pigments (e.g. β carotene) in plants cleaved to yield retinoids
Vitamin A functions
Binds to proteins (opsin) in cells of retina to form visual pigments
Nuclear modulator of gene expression (signalling molecule)
-cell proliferation
-differentiation (especially epithelia)
-development
Lipid soluble, dissolves through cell membrane, binding to RA receptor, goes into nucleus, attaches to DNA, affects transcription
Vitamin A deficiency
Major cause of blindness in children under 5 in developing countries
Impaired resistance to infection
-differentiation and function of lymphocytes and neutrophils
Mild deficiency - night blindness
More prolonged/ severe
-metaplasia and keratinisation of the conjunctiva epithelial cells
-thickening of the cornea (xerophthalmia)
Vitamin D
Hormone precursor -vitamin D3 calciol/ cholecalciferol -vitamin D2 ercalciol/ ergocalciferol Endogenous synthesis more important than dietary sources -D3 - photolysis of 7-dehydrocholesterol
Vitamin D functions
Maintenance of plasma calcium conc. (along with parathyroid hormone and calcitonin)
Steroid hormone activating nuclear receptors and influencing >50 genes
Bone metabolism
Vit D stimulation of intestinal Ca2+ and PO43- absorption and renal Ca reabsorption
Mineralisation controlled by availability of Ca and PO4 (maintained by vit D)
Osteoblasts have receptors for calcitriol (active metabolite of vit D)
Osteoclast activity/ number (paradoxically) increased
Promotes formation and mineralisation of bone
Vitamin D deficiency
Rickets and osteomalacia
Failure of bone mineralisation
Eradication by supplementation in 1950s in ‘developed’ world
1 in 5 people in UK deficient (2016)
Racial genetic predisposition (defect in calcitriol hydrolase: no calcitriol)
Vit D deficient mice have impaired immune function (lymphocytes and monocytes)
Vitamin E and function
Lipid soluble antioxidant
Very active free radical trapping
Other effects on cell signalling (inactivates protein kinase C)
Deficiency not normally a problem
Vitamin K and function
Co-enzyme in postranslational carboxylation of glutamate to γ carboxy glutamate (gla)
Permits binding of proteins to membrane phospholipids
Vitamin K: klotting
Vit K dependent proteins involved in bood coagulation (thrombin, factors VII, IX and X, protein C, S and Z0
Clotting occurs on phospholipid surfaces
Deficiency leads to haemorrhagic disease (newborns particularly at risk)
Some anticoagulants are vitamin K antagonists (disrupting) e.g. warfarin
B vitamins examples
Thiamin (B1) Ribofavin (B2) Niacin (B3) B6 Folic acid (B9) B12 Panthothenic acid (B5)
B vitamins functions
All co-enzymes (co-factors)
-‘helper molecules’
-non-proteins but bind to protein (enzymes)
Required for protein’s biological activity
Thiamin
Vitamin B1
Co-enzyme in central energy yielding pathways (pyruvate and keto-glutarate dehydrogenase)
These produce ATP (lack of ATP = cell death)
Neurotransmitters, myelin
Pentose phosphate pathway
Co-enzyme in catabolism of leu, isoleu and val
Regulates nerve chloride channels
Thiamin pentose phosphate pathway
Co-enzyme
Transketolase: NADPH for biosynthesis and ribose for nucleotides
Thiamin deficiency
Berberi-peripheral neuritis: weakness, stiffness
Riboflavin
Vitamin B2
E- carriers in variety of oxidation and reduction reactions central to metabolism (mitochondrial e- transport chain)
Remain bound to enzyme
FAD, FMN oxidising coenzymes which accept two H atoms
FAD
flavin adenine dinucleotide
FMN
flavin mononucleotide
Riboflavin deficiency
Common but rarely a problem: bacterial synthesis, conservation and re-utilisation
Niacin
Vitamin B3
Precursor of co-enzymes NAD and NADP
E- carriers in metabolic redox reactions
Niacin synthesis
Synthesised from dietary tryptophan
Niacin deficiency
Rare, Pellegra
Vitamin B6
Pyridoxal phosphate
Amino acid metabolism (transamination)
Deficiency virtually unknown
Vitamin B12 and Folate (B9)
Coenzymes - one carbon carriers
DNA and myelin synthesis
Deficiency - anaemia and neurological damage
Folate supplementation in pregnancy
Vitamin C
Ascorbic acid (a reducing sugar) and anti-oxidant
Specific role in two enzyme classes
-dopamine β-hydroxylase: synthesis or adrenaline and noradrenaline (Cu + dependent)
-lysine and proline hydrolases: maturation of CT (collagen)
Iron uptake: keeps iron as Fe2+, chelates it which > absorption
Vitamin C deficiency
Scurvy
-malaise, < wound healing, loose teeth
Treated with limes, oranges, lemons
Vitamins and dentistry
You may be first to spot deficiency
Rapid turnover of epithelium makes it sensitive to nutritional deficiencies
Vitamins involved with: wound healing, bleeding, resistance to infection, bone/ tooth Ca2+
Oral manifestations of vit deficiencies in face
Malar pigmentation (Niacin, B vitamins) Nasolabial seborrhea (niacin, riboflavin, B6) Lack of colour (iron, malnutrition)
Oral manifestations of vit deficiencies on lips
Cheilosis (niacin, B6, riboflavin) Angular fissures (niacin, B6, riboflavin, iron)
Oral manifestations of vit deficiencies in gingiva
Spongy, bleeding, abnormal redness (vitamin C)
Oral manifestations of vit deficiencies in tongue
Glossitis - red, raw, fissured (folate, niacin, iron, B6, B12)
Pale, atrophic, smooth/ slick - filiform papillary atrophy (iron, folate)
Magenta colour (riboflavin)
