Agussalim Bukhari

Department of Nutrition
Faculty of Medicine, Hasanuddin
University
 To introduce the concepts of structural

complexity and functional diversity of vitamins

 To explain the biochemical actions of both

water-soluble and fat-soluble vitamins and the

consequences on vitamin deficiency

 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
(provitamins)
 Many are enzyme cofactors
 Frank deficiencies are rare in developed
countries
 Deficiencies-due to unvaried diets &
malabsorption
 Most cooperate with other vitamins,minerals
and fatty acids
 Deficiency of one vitamin can interfere with
the function of other vitamins
 Excessive intake may lead to toxicity and/or
vitamin imbalance
 Water soluble (group B & C)
 Enter the body freely
 Absorb directly into blood
 Not readily stored
 Excess is excreted in urine
 Unlikely to reach toxic level
 Most function as coenzymes
 Interconnected functions
 Easily destroyed or lost
 Fat soluble (A,D,E,K)
 Required fat to be absorbed
 Absorbed into lymph then
blood
 Readily stored
 Excess not typically excreted
 A and D can be toxic
 Individual action
 Relatively stable
 Requirement for optimum
absorption
 Interference with
absorption or metabolism
 Requirement for
metabolism
 Protection against excess
catabolism or urinary loss
 Protection against oxidative
destruction
 Obstruction of diagnosis of
deficiency
 Vit B6/B12,folate/thiamine
 Vit E/vit K, vit B6/Niacin,
Thiamine/Riboflavin
 Riboflavin/vit B6, Niacin/vit
B6
 Vitamin C/vitamin B6
 Vitamin E/vitamin A,
vitamin C/vitamin E
 Folate/vitamin B12
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

 Often occur in the same foods

 Multiple deficiencies may occur

 Required in metabolism of fat, carbohydrate, and

protein

 Thus indirectly provide energy

 Pathways intercept
 Vitamin
 Thiamin (B1)
 Niacin (nicotinic acid)
 Riboflavin (B2)
 Pantothenic acid
 Pyridoxal, pyridoxine
 Cobalamine
 Biotin
 Folic acid
 Coenzyme form
 Thiamin pyrophosphate
 NAD+, NADP+
 FAD, FMN
 Coenzyme A
 Pyridoxal phosphate
 5’deoxyadenosylcobala
min, methylcobalamin
 Biotin lysine complex
 Tetrahydrofolate
 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 weight, 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
 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
formation in kidneys, blood clotting, B12
deficiency, enhances absorption of toxic metals
 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
synthesis
 - convert B12 to coenzyme form
 - other enzymatic reaction
 Deficiency : the most common vitamin deficiency
in Australia
 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)
 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 --- succinyl
CoA
 Methylation of homocysteine --- methionine
 Converts folate to active form
 Maintains sheath that surrounds nerve fibres
 rare in developed countries except among
strict vegetarians
 Pernicious anemia: megaloblastic (macrocytic
anemia) and neurological disturbances
 Causes:
 Malabsorption
 Lack of intrinsic factor (in stomach)
 Inadequate intake (vegans, alcoholics)
 Main forms: preformed vitamin A
 Precursor, provitamin A (carotenes,
carotenoids)
 b carotene is the most abundant in food
 Carotenes are poorly absorbed
 Activity is measured as retinol equivalents
which accounts for absorption of carotene
and degree of conversion to vitamin A
 Functions: vision, cellular differentiation,
antioxidant
 Deficiency : nyctalopia (night blindess)
Risk of infection
Keratinitation of epithelial
surface
 Toxicity : rare, loss of appetite, blurred vision,
dry flaking skin, excess b carotene can cause
yellowing of the skin and supplemental b
carotene has been linked with lung cancer
 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
 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
bones
 Involves in the haematopoetic system
 Effects cell differentiation and proliferation
 Deficiency: rickets and osteomalacia
 Toxicity : loss of appetite, high serum calcium &
phosphorus levels, calcification of soft tissues
 7-dehidrocholesterol
In the skin UV light

Vitamin D (cholecalciferol)

Liver enzyme oxidises C-25

Kidney enzyme oxidises C-1

1,25 dihydroxycholecalciferol)
 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)

 Source:
 Vegetable oils (high polyunsaturated fatty
acids), 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
 Source: K-1 (green plant leaves)
 K-1 (produced by bacteria in human intestine)
 Function: clotting of blood, involved in formation
of prothrombin & 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
competitive inhibitor of prothrombin formation
(anticoagulant)
 Toxicity: relatively non-toxic unless given large
dose over a prolonged period of time.
 Compounds that protect others from
oxidation 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
 Free radical formation: during normal energy metabolisms,
hydrogens and electrons are added to oxygen in a series of
reactions called electron transport chain. This sequence
eventually 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)

 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
membrane, 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

polyunsaturated fatty acid) it generates a lipid radical and water. The
lipid radical can in turn, react with oxygen to form another lipid
radical which in turn, remove hydrogen atoms from other lipids,
producing new radicals, thereby initiating a chain reaction.
3.Antioxidant protection:
Antioxidants interact with free radicals and break the destructive
chain 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 the radicals from causing more damage and generating
more radicals. Vitamin E can be reactivated by accepting a hydrogen
atom from fellow antioxidant vitamin C