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Dietary Vitamins

Agussalim Bukhari
Department of Nutrition
Faculty of Medicine, Hasanuddin University
Objectives

 To introduce the concepts of structural compl

exity and functional diversity of vitamins

 To explain the biochemical actions of both wa

ter-soluble and fat-soluble vitamins and the

consequences on vitamin deficiency


What are vitamins
 Small organic molecules
 Required in the diet in only very small amounts
 Not produced in the body or at the rate required

 Specific, vital functions


 Do not directly produce energy
 Not used for structural purposes
 May be present as inactive precursors (provitami

ns)
 Many are enzyme cofactors
Vitamins
 Frank deficiencies are rare in developed count
ries
 Deficiencies-due to unvaried diets & malabso

rption
 Most cooperate with other vitamins,minerals

and fatty acids


 Deficiency of one vitamin can interfere with th

e function of other vitamins


 Excessive intake may lead to toxicity and/or

vitamin imbalance
Vitamins
 Water soluble (group B & C)  Fat soluble (A,D,E,K)
 Enter the body freely  Required fat to be absorbed
 Absorb directly into blood  Absorbed into lymph then bloo
 Not readily stored d
 Excess is excreted in urine  Readily stored
 Unlikely to reach toxic level  Excess not typically excreted
 Most function as coenzymes  A and D can be toxic
 Interconnected functions  Individual action
 Easily destroyed or lost  Relatively stable
Vitamin-vitamin interaction
 Requirement for optimum a  Vit B6/B12,folate/thiamine
bsorption
 Interference with absorption  Vit E/vit K, vit B6/Niacin, Th
or metabolism iamine/Riboflavin
 Requirement for metabolism
 Riboflavin/vit B6, Niacin/vit
B6
 Protection against excess ca
tabolism or urinary loss
 Vitamin C/vitamin B6
 Protection against oxidative  Vitamin E/vitamin A, vitami
destruction
n C/vitamin E
 Obstruction of diagnosis of  Folate/vitamin B12
deficiency
Relative stability in food during proce
ssing and storage

Stable Unstable Very Unstable

Niacin (B-3) Pyridoxine (B-6) Ascorbic acid

Vitamin K Riboflavin Thiamine

Vitamin D Vitamin A Folate

Biotin (B-7) Cobalamin (B-12)

Pantothenic acid (B-5) Vitamin E


B groups vitamins

 Often occur in the same foods

 Multiple deficiencies may occur

 Required in metabolism of fat, carbohydrate, and prot

ein

 Thus indirectly provide energy

 Pathways intercept
B group vitamin and coenzymes
 Vitamin  Coenzyme form
 Thiamin (B1)  Thiamin pyrophosphate
 Niacin (nicotinic acid)
 NAD+, NADP+
 FAD, FMN
 Riboflavin (B2)  Coenzyme A
 Pantothenic acid  Pyridoxal phosphate
 Pyridoxal, pyridoxine  5’deoxyadenosylcobalam
 Cobalamine in, methylcobalamin
 Biotin  Biotin lysine complex
 Folic acid  Tetrahydrofolate
B Vitamin deficiencies
 Any vitamin B deficiency will result in changes to a
number of pathways
 Therefore there may be similar symptoms
 Nausea, severe exhaustion, irritability, depression,
neurological disorders, loss of appetite and weigh
t, muscle pain, impairment of immune response,
anaemia, severe skin problems
 Deficiencies may be due to genetic abnormalities,
diseases conditions, metabolic stress, alcoholism
 Rarely see deficiency of a single B group vitamin
 Beriberi and pellagra
4D : Diarrhea, Dermatitis, Dementia, Death
Occurs in population where corn is the staple food
B group sources
Vitamin C (Ascorbic acid)
 2 forms : L-ascorbic acid (major form)
L-dehydroascorbic acid
 Source : fruits & vegetables. Very easily destroyed by
high temp.,air, alkali, prolonged storage, lost in water
 Important in : collagen formation, as an antioxidant,
brain and nerve function, iron absorption, folic acid
metabolism
 Deficiency : scurvy,
 Toxicity due to megadose therapy: oxalate stone for
mation in kidneys, blood clotting, B12 deficiency, enh
ances absorption of toxic metals
Folate (Vit B-9)
 Group of compounds. Active form is tetrahydrofolate
 Source : intestine: small amount produced by
bacteria
 Animal food: absorbed unaltered
 Plant food: conjugated with glutamic acid
 One of the most unstable vitamins
 Functions:
 Coenzymes in transport of carbon atoms in the synthesis of:
 - purine nucleotide, thymine involved in DNA synth
esis
 - convert B12 to coenzyme form
 - other enzymatic reaction
Sources of folate
Folate : deficiency/toxicity
 Deficiency : the most common vitamin deficiency in Au
stralia
 Causes: low dietary intake
 Destruction in food preparation
 Poor intestinal absorption
 Effects: shortage of nucleotide
 Impairment of DNA replication
 Immature RBC cannot divide and become megaloblasts
 Symptoms: megaloblastic (macrocytic) anemia
 At risk: pregnant women, elderly, alcoholics,
 (is linked with neural tube defect in foetus)
Vitamin B12 (cobalamin)
 Group of compounds that contain cobalt
 Source : synthezised only by microorganisms-
 Found in food of animal origin
 Not in plants
 Functions: coenzyme in only 2 reactions:
 Isomerisation of methylmalonyl CoA --- succin
yl CoA
 Methylation of homocysteine --- methionine
 Converts folate to active form
 Maintains sheath that surrounds nerve fibres
Vitamin B12-deficiency
 rare in developed countries except among stri
ct vegetarians
 Pernicious anemia: megaloblastic (macrocytic

anemia) and neurological disturbances


 Causes:
 Malabsorption
 Lack of intrinsic factor (in stomach)
 Inadequate intake (vegans, alcoholics)
Vitamin A - Retinol
 Main forms: preformed vitamin A
 Precursor, provitamin A (carotenes, carotenoi

ds)
 b carotene is the most abundant in food
 Carotenes are poorly absorbed
 Activity is measured as retinol equivalents wh

ich accounts for absorption of carotene and d


egree of conversion to vitamin A
Vitamin A
 Functions: vision, cellular differentiation, anti
oxidant
 Deficiency : nyctalopia (night blindess)

Risk of infection
Keratinitation of epithelial
surface
 Toxicity : rare, loss of appetite, blurred visio

n, dry flaking skin, excess b carotene can cau


se yellowing of the skin and supplemental b c
arotene has been linked with lung cancer
Metabolism of vitamin A
 Plant foods (mainly b carotene ) &
 Animal foods (all-trans-retinol, mainly as fatty acid esters
Bile acid
Carotene oxigenease
(mucosal cell intestinal epithelium)
 All-trans-retinol

Liver storage

 Stored as all-trans-retinol (as fatty acid ester)


Plasma carrier protein

 tissues
Vitamin D
 Several forms (can be shyntesized in the body)
 Major sources : sunlight, fatty fish, fortified foods
 Function:
 Regulation of calcium level in the body
 Overall: increase Calcium and phophorus in the bo

nes
 Involves in the haematopoetic system
 Effects cell differentiation and proliferation
 Deficiency: rickets and osteomalacia
 Toxicity : loss of appetite, high serum calcium & ph

osphorus levels, calcification of soft tissues


Synthesis of vitamin D
7-dehidrocholesterol
In the skin UV light

Vitamin D (cholecalciferol)

Liver enzyme oxidises C-25


Kidney enzyme oxidises C-1

1,25 dihydroxycholecalciferol)
Vitamin E
 Closely related group of compounds-Tocopherols
 Alpha-tocopherol is the most abundant

FUNCTIONS

Antioxidant (ie prevents or inhibits oxidation)


 Inhibits oxidative modification of LDL
 Inhibits lipid oxidation in cell membranes
 Preserves the integrity of RBC`s (red blood cells)
 Protects against toxicants eg lead and mercury (heavy metals)
Vitamin E
 Source:
 Vegetable oils (high polyunsaturated fatty aci

ds), nuts, seeds


 Deficiency:
 Very rare
 Can be associated with fat malabsorption
 Premature babies with low levels are prone to

haemolytic anemia
 Toxicity : no clear data
Vitamin K (K-1 & K-2)
 Source: K-1 (green plant leaves)
 K-1 (produced by bacteria in human intestine)
 Function: clotting of blood, involved in formation of p
rothrombin & blood clotting factors (II,VII,IX,X)
 Deficiency: haemorrage
 May occur in new born (low at birth)
 Can be secondary to disease or drug treatment
 Warfarin: a synthetic analogue of vitamin K competitiv
e inhibitor of prothrombin formation (anticoagulant)
 Toxicity: relatively non-toxic unless given large dose
over a prolonged period of time.
Antioxidants
 Compounds that protect others from oxidatio
n by being oxidised themselves
 Donate electrons to other substances which

becomes reduced while antioxidant becomes


oxidised
 Includes :

Vitamin A
Vitamin C
Vitamin E
 May protect against : cancer, heart diseases
Actions of free radicals and antioxida
nts
 Free radical formation: during normal energy metabolisms, hy
drogens and electrons are added to oxygen in a series of reac
tions called electron transport chain. This sequence eventuall
y produce water, but some intermediate compounds created
during process are free radicals

 O2 superoxide hydrogen hydroxil+ water

radicals radicals radicals

( a radical is a molecule with an extra unpaired electron)


Actions of free radicals and antioxida
nts
 Free radical chain reaction & damage:
 Hydroxyl radicals are highly reactive, wanting to match the unpaired
electrons. Eg. they might take electrons from the lipid in a cell memb
rane, which causes damage that gives rise to degenerative diseases
 Lipid + OH+ lipid+ + water
 When a hydroxyl radical takes a hydrogen atom from lipid (such as p
olyunsaturated fatty acid) it generates a lipid radical and water. The l
ipid radical can in turn, react with oxygen to form another lipid radic
al which in turn, remove hydrogen atoms from other lipids, producin
g new radicals, thereby initiating a chain reaction.
Actions of free radicals and antioxida
nts
3.Antioxidant protection:
Antioxidants interact with free radicals and break the destructive chai
n reaction that damages tissues.

active vitamin E + lipid+ inactive vitamin E* + lipid

Inactive vitamin E + vitamin C (with H atoms) = active vitamin E (with


H atoms)+ vitamin c (without H atoms)

Vitamin E gives up one of its hydrogens to a lipid radical*.The results


is that vitamin E is no longer active but it has successfully stopped t
he radicals from causing more damage and generating more radical
s. Vitamin E can be reactivated by accepting a hydrogen atom from f
ellow antioxidant vitamin C

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