differ chemically…….. Generally deficiencies due to water soluble vitamins are multiple rather than individual with overlapping symptoms. Cooking….as well as milling losses…..so the grains/cereal products are deliberately enriched with vitamins [ B-1,2,3…FA…Iron ] energy generation or hematopoises
Coenzyme: Small organic molecule that associates closely with enzyme functions.
First named aneurin for the detrimental neurological effects if not present in the diet..............Animals must obtain it from their diet critical role in the energy metabolism…………………….. helps orchestrate nerve impulses and movement in muscles as a result.
Most exceed RDA in diet Surplus is rapidly lost in urine; non toxic
(TPP) is formed when the OH group of thiamine reacts with two phosphates (pyrophosphates) donated by ATP.
Needed for the metabolism of carbohydrates, proteins and fats
Transketolase in Pentose Phosphate Pathway of glucose metabolism……… used to transform:
Approximately 90% of total thiamine in blood is in erythrocytes synthesized by colonic bacteria but this does not become available to the host. It is combine with phosphate within mucosal cells of the intestine and transported via the portal vein into the general circulation Maybe found in liver, heart, brain and muscle tissue
Thiamine is present in the outer layer of rice grains ….. Increase carbohydrate intake…( more requirement of thiamine). . 1) interfere with absorbtion 2)in TPP synthesis In parboiled & milled rice , thiamine is not lost with polishing. Thiaminase containing diet :tea, coffee, raw fish and shell fish destroy it
Decreased transketolase activity………This is the earliest indicator and reliable diagnostic test to assess thiamine deficiency. Carbohydrate metabolism is impaired.acc of pyruvate in tissues is harmful Inc in plasma and urine pyruvate Inc BBBpermitting the pyruvate to enter brain directly-polyneuritis Lack of nerve impulse transmission RBC transketolase activity is dec, its measurement is diagnostic HPLC measures thiamine and its phosphorylated esters in serum or blood is measured
EarlierNonspecific symptoms Increased sensitivity of the oral mucosa, burning tongue, and loss or diminution of taste
Edema does not occur :nerve degeneration, Peripheral w eakness infantile Characterized by dyspnea, cyanosis and cardiac failure
in chronic alcoholics in whom the body’s demand for thiamine increases
Stored in paper, opaque plastic containers Ribose ….. the sugar whose reduced form, ribitol, forms part of its structure……. flavin…. the ring-moiety which imparts the yellow color to the oxidized molecule
Milk and milk products, meat, eggs, liver are rich sources. Cereals, fruits, vegetables and fish are moderate sources Average intake is above RDA but toxicity not documented
synthesized by colonic bacteria but this does not become available to the host. It must be phosphorylated (combined with phosphate) in the intestinal tract before it can be absorbed
The principal growth promoting factor in the vitamin B complex in the many chemical reactions involved in the m etabolism of carbohydrates, proteins and fats , including; oxidation-reduction reactions and electron transport chain .
Because of wide distribution (many sources), dietary deficiency is not common Gastrointestinal disease that causes vomiting and hypermotility of the gastrointestinal tract Lab measurement of RBC and urinary riboflavin, erythrocyte glutathoine reductase deficiency Rda 1.2-1.7mg, higher dose by .5mg by day are advised for pregnancy lactation Galactoflavin is antimetabolite of riboflavin
Glossitis…… swelling, smooth (loss of pappilae), colour changes, painless or painful, difficulty with chewing, swallowing & speaking Cheilosis...... inflammatory lesion at the labial commissure, or corner of the mouth, and often occurs bilaterally Stomatitis…. inflammation of the mucous lining of any of the structures in the mouth sore and raw tongue, lips, throat, ulcers in mouth; vascularization of cornea. Dry scaly skin, loss of hair; anaemia and neuropathy develop later
active coenzyme forms of niacin are formed in the liver Nicotinic acid (niacin) - Pyridine derivative …………….. amide form - nicotinamide (niacinamide) NAD and NADP participates in >200 metabolic reactions in the body little cooking loss
Tryptophan forms Niacin in the presence of B6 60 mg of Tryptophan forms 1mg of Niacin Thus, daily requirement of niacin is affected by the amount of tryptophan in diet
The large doses needed for hypolipidaemic action are poorly tolerated. Only about half of the patients are able to take the full doses. Nicotinic acid is a cutaneous vasodilator: marked flushing, heat and itching (especially in the blush area) occur after every dose. This can be minimized by starting with a low dose taken with meals and gradually increasing as tolerance develops. Aspirin taken daily largely prevents the reaction (PGs may be involved). Dyspepsia is very common; vomiting and diarrhoea occur when full doses are given. Peptic ulcer may be activated. Dryness and hyperpigmentation of skin can be troublesome. Other long-term effects are: Hyperglycaemia, precipitation of diabetes (should not be used in diabetics) . Hyperuricaemia and gout, atrial arrhythmias. It is contraindicated during pregnancy and in children. It is highly efficacious in hypertriglyceridaemia (type III, IV, V) whether associated with raised CH level or not. It is mosth· used to lower VLDL and raise HDL levels, and as an adjunctive drug to statins/ fibrates. Nicotinic acid is the most effective drug in reducing plasma TG levels and controlling pancreatitis in genetic type IV and type V disorders. Long-term use prevents further attacks of pancreatitis. Given over long-term in post-Ml patients, it has been found to reduce recurrences of MI and overall mortality. However, because of marked side effects, use of nicotinic acid is restricted to high-risk cases only.
This action is unrelated to its vitamin activity and not present in nicotinamide. When nicotinic acid is given, TGs and VLDL decrease rapidly, followed by a modest fall in LDL-CH and total CH. Nicotinic acid is the most effective drug to raise HDL-CH; Nicotinic acid reduces production of VLDL in liver by inhibiting TG synthesisIt inhibits intracellular lipolysis in adipose tissue and increases the activity of lipoprotein lipase that clears TGs. A cell surface G-protein coupled receptor which negatively regulates adipocyte adenylyl cyclase has been found to selectively bind nicotinic acid, and has been called 'niacin receptor'. Nicotinic acid appears to inhibit lipolysis in adipose tissue by decreasing hormone stimulated intracellular cAMP formation through this receptor. Hepatic VLDL production is believed to be decreased due to reduced flow of fatty acids from adipose tissue to liver.
Deficiency leads to hemolytic anemia.
These pyridine nucleotides act as hydrogen acceptors In the electron transport chain in tissue respirati on, glycolysis and fat synthesis. Flavoproteins regenerate them by oxidizing N ADH and NADPH. Nicotinic acid (but not nicotinamide) in large doses is a vasodilator, particularly of cutaneous vessels. It also lowers plasma lipids
Oennatitis-sunburn like dermal rash on hands, legs and face which later turn black, crack and :'eaL Diarrhoea-with enteritis, stomatitis, glossitis, oalivation, nausea and vomiting. Dementia-with hallucinations preceded by headache, insomnia, poor memory, motor and sensory disturbances. Anaemia and hypoproteinaemia are common in pellagra. Chronic alcoholics are particularly at risk of developing pellagra, because in addition to dietary deficiency, niacin absorption is impaired in them. Other B vitamin deficiencies are often associated.
Conversion of Tryptophan to Niacin is dependent on pyridoxal phosphate Anti-tubercular drug which inhibits pyridoxal phosphate formation.
and small quantities of pantothenic acid are found in nearly every food.
impaired energy production, due to low CoA levels Acetylcholine synthesis is also impaired.....Insulin receptors are acylated with palmitic acid when they do not want to bind with insulin nearly all symptoms can be reversed with the return of pantothenic acid...........
because raw egg white contains the protein avidin which binds biotin at an extraordinarily high affinity, thus causing deficiency. Biotin is covalently bound to lysine in the enzymes to form ” Biocytin ”…active form Biotinidase allows the body to use and to recycle biotin.........The enzyme biotinidase cleaves biocytin and makes biotin available to be reused by other enzymes
Widespread in foods
Break down of leucine
Dermatitis……Red, scaly rash around the eyes, nose & mouth Toxicity symptoms : none reported
Pyridoxine---plant source………….rest-----food of animal origin
Non-citrus fruits Daily Value set at 2 mg……..Average intake is more than the RDA
Low levels of folate can also lead to homocysteine accumulation
A complete lack of dietary folate takes months before deficiency develops as normal individuals have about 500–20,000 µg of folate in body stores. NTD is an opening in the spinal cord or brain that occurs very early in human development……….all women… 0.4 mg/day
Makes it difficult to diagnose b12 deficiency
A vitamer of a particular vitamin is any of a number of chemical substances, each of which shows vitamin activity. Very commonly each "vitamin" is not a single chemical, but rather multiple chemical substances called vitamers , each of which is defined by its different biological activity.
Average intake exceeds RDA…….stored in the liver………… Non-toxic Vegans are at risk of deficiency
elevated levels of MMA, a myelin destabilizer
Takes ~20 years on a deficient diet to see nerve destruction…………… Injection of B-12 needed Pernicious……… is one of many types of the larger family of megaloblastic anemias .
The name given to the vitamin that the fruit provided, ascorbic acid, literally means “no scurvy acid” Excess excreted……………Easily lost through cooking
Average intake ~72 mg/day…………Fairly nontoxic (at <1 gm)……….Upper Level is 2 g/day Warning to people with hemochromatosis, oxalate kidney stones
Deficient for 20-40 days ………….. Most scurvy symptoms are due to collagen breakdown Rebound scurvy……………… immediate halt to excess vitamin C supplements Who is at risk?................ Infants, elderly men Alcoholics, smokers
Salts of ascorbic …….. no indigestation Larger amounts of Vitamin C lower Manganese levels and aid greater insulin production acid…..
metabolic role and therapeutic use of b complex vitamins
‘An organic substance that occurs in foods in
small amounts and is necessary for normal
metabolic functioning of the body’
VITAMIN” means “vital for life”
May be water soluble or fat soluble
Do not contribute directly to the structure of the body, nor do
they supply energy.
They regulate metabolism by releasing energy from fats
They are involved in amino acid metabolism and also assist
in forming blood, bones and tissues
Essential Vitamins For Human Being
water -soluble lipid-soluble
Vit C Vit B A,D,E,K
B1, B2, B6, B12, PP, patothenic acid ，
folic acid,biotin ,lipoic acid
Overview of Water Soluble Vitamins
Heterogeneous( differ chemically)
Dissolve in water
Readily excreted through urine
Continuous supply needed
Function as a coenzyme
Generally deficiencies due to water soluble
vitamins are multiple rather than individual with
• The water soluble vitamins form coenzymes
(active form of the vitamin).
Thiamine- Vitamin B-1
• “thio”-vitamin (sulfur-containing vitamin)
• Ist vitamin to be identified
• Other names
– Anti neuretic
– Anti Beri Beri
• Only synthesized by bacteria, fungi & plants
• Animals must obtain it from their diet
• Relatively unstable
-Destroyed with heat and in alkaline environment
-Lost by milling flour, leaching into cooking liquids
and in thawing frozen food
• Co-enzyme: helps release energy from carbohydrates
RDA and Toxicity
• 1to 1.5 mg/day
• Requirement increases in pregnancy &
lactation(2mg), old age & alcoholism.
• Daily intake depends on carbohydrate metabolism
• Upto 50mg/d can brought to control
The Active Form
• Thiamine contains an aminopyrimidine
ring and a thiazole ring.
• Active forms - Thiamine Pyrophosphate
• The TPP reaction is catalyzed by enzyme
thiamine pyrophosphate transferase.
• Activation occurs mainly in liver.
Needed for the metabolism of
carbohydrates, proteins and fats
Thiamine pyrophosphate (TPP) is
involved with the energy releasing
reactions of carbohydrate metabolism.
10–15 % of total
energy in the
form of ATP.
85–90% of total
energy in the
form of ATP. GLYCOLYSIS
Pyruvate Dehydrogenase (PDH)
α Ketoglutarate Dehydrogenase.
Transketolase.in HMP shunt
pentose sugar (ribose) hexose
sugar (glucose) which is then
used to produce energy in the
form of ATP.
Reactions requiring TPP
The branched chain aminoacid dehydrogenase
Leucine, isoleucine , valine to form keto acid.
Pts of Maple syrup disease(defect in decarboxylation
reaction) are treated with large dose of thiamine
Transmission of nerve impulse
TPP is required for acetylcholine synthesis and
ion translocation of neurnal tissue. Thiamine
triphosphate form is also involved.
Absorption, Transport & Metabolism
• Absorbed in the upper small intestine
– Low concentration = carrier mediated
– High concentration = passive diffusion
• Transported by RBC in the blood(90% of
total thiamine of blood )
• Excreted in the urine
• Inadequate Diet (polished rice)
• chronic illness(liver cirrhoses,
disease affecting absorbtion in small intestine,cancer)
• Pregnancy and lactation
• Thiaminase ( in raw fish) inactivates thiamine by breaking
the thiazole ring.
Women with hyperemesis
gravidarum and anorexia
• Pt on parental glucose
• Pt on chronic diurectic therapy
• Maternal thiamine def in breast fed child, Infantile
• Increased Carbohydrate intake
• Increased metabolic activity due to Hyperthyroidism and fever
Carbohydrate metabolism is impaired.acc of pyruvate in
Increased pyruvate concentration and is excreted in urine.
Increased pyruvate in plasma Lactate Lactic acidosis
Inc permeability of Blood Brain Barrier. Pyruvate entry & brain
directed poly neuritis
The transketolase activity in erythrocytes is decreased.
Who is at Risk For Deficiency?
Poor , Alcoholics, Elderly, Diet consisting of highly processed
Deficiency leads to Beri-beri which is of three types.
Wet Beri-beri: CVS manifestations are prominent
Edema of legs, face & trunk
Pleural effusion & ascites
Breathlessness and palpitation. systolic murmurs
Fast and bouncing pulse
Weak heart muscles resulting in death due cardiac
Dry Beri-beri: CNS manifestations prominent.
Edema not commonly seen.
Neurological manifestation resulting from accumulation of
pyruvate in the nerves.
polyneuritis with numbness , loss of nerve transmission
resulting in 'wrist drop', 'foot drop', irritability, poor
arm/leg coordination even paralysis of whole limb.
mental changes, sluggishness, poor memory, loss of
appetite and constipation
Seen in infants born to mothers suffering from thiamine deficiency.
Sleeplessness, restlessness, vomiting, convulsions and finally death.
Wernicke-Korsakoff syndrome: Seen in chronic
alcoholics and is characterized by:
Loss of memory
Apathy (absence of emotions)
Nystagmus (rhythmical to-and-fro motion of the eyeballs)
Ataxia (Unstable gait)
Opthalmoplegia (paralysis of the eye muscles)
Encephalopathy: Congestion and hemorrhages in parts of
Lack of nerve impulse transmission
RBC transketolase activity is dec, its
measurement is diagnostic This is the earliest
indicator and reliable diagnostic test to assess
HPLC measures thiamine and its
phosphorylated esters in serum or blood is
• 1 . Prophylactically (2-10 mg daily) in infants,pregnant women,
chronic diarrhoeas, patients on parenteral alimentation. Glucose
infusion unmasks marginal thiamine deficiency.
• 2. Beriberi-100 mg/day i.m. or i.v. till symptoms regress-then
maintenance doses orally.
• 3. Acute alcoholic intoxication: thiamine 100 mg is added to each
vac of glucose solution infused. Most neurological symptoms in
chronic alcoholics are due to thiamine deficiency-peripheral
neuritis, Wernick's encephalopathy, Korsakoff'spsychosis: give 100
mg/ day parenterally.
4. In neurological and cardiovascular disorders, hyperemesis
gravidarum, chronic anorexia and obstinate constipation-
thiamine has been used even without definite proof of its
deficiency.symptoms improve dramatically if thiamine
deficiency has been causative.
5. Maple syrup disorder
Thiamine is nontoxic. Sensitivity reactions sometimes occur on
Riboflavin (Vit. B2)
• The name "riboflavin" comes from “ribose” and “flavin”
– Flavin mononucleotide (FMN)
– Flavin adenine dinucleotide (FAD)
• Stable to heat but sensitive to light (photosensitive). When
exposed to UV rays it gets destroyed
• Oxidation-reduction reactions
• Electron transport chain
• Citric Acid Cycle
• Drug and steroid metabolism, including detoxification
reaction (called the drug vitamin)
Absorption, Transport, & Metabolism
• HCL in the stomach releases riboflavin from its
– Active or facilitated transport during low to
– Passive absorption during high intake
• Transported by a protein carrier in the blood
• Excess riboflavin is excreted unchanged in the
Active Coenzymes of Riboflavin
• FMN: Flavin mononucleotide:
Formed in the intestine by phosphorylation of Riboflavin in the
presence of enzyme ‘Flavokinase’
• FAD: Flavin adenine dinucleotide:
Formed in the liver from FMN by the transfer of an AMP from
FAD = FMN + AMP
•Growth promoting factor:
–Repair & development of body tissues - healthy skin
•Act as “coenzymes” in many reactions including the oxidation-reduction
reactions and electron transport chain.
by serving as an acceptor of two hydrogen atoms (with electrons)
Accepts electrons Electron Transport Chain
Citric Acid Cycle
Assist in the metabolism carbohydrates, protein and fats
Who is at Risk For Deficiency?
Rare, usually with other vit b deficiency
Low milk/dairy intake
Gastrointestinal disease that causes vomiting
and hypermotility of the gastrointestinal tract
Phototherapy (neonatal jaundice)
Pregnancy & lactation
Long term phenobarbital &
– Glossitis, cheilosis & angular stomatitis
– Sore & raw tongue
– seborrheic dermatitis
– Loss of appetite
– Dry scaly skin, loss of hair
– anaemia and neuropathy
– vascularization of cornea
– Occurs within 2 months
– Most often seen in association
with protein energy malnutrition
– Also in cases of alcoholism
• Deficiency can be seen in anorexia , malabsorbtion.
• Drugs eg. Barbiturates (microsomal oxidation of
• Symptoms of ariboflavinosis are relatively mild and
not life threatening because
• 1 riboflavin are associated with protein diet.
• 2.recycling of riboflavin from FMN & FAD is very
• Lab measurement of RBC and urinary riboflavin
• Measurement of erythrocyte glutathoine reductase
activity (deficiency)as an index of riboflavin status
• To prevent and treat ariboflavinosis(2-20 mg/ day oral or
parenteral), generally along with other B complex members.
Niacin (Vit. B3)
• 2 Forms
– Nicotinic acid (niacin)
– Nicotinamide (niacinamide)
• Coenzyme (liver)
– Nicotinamide adenine dinucleotide (NAD)
– Nicotinamide adenine dinucleotide phosphate (NADP)
– oxidation-reduction & oxidative-phosphorylation reactions
• Heat stable
• A peculiar vitamin since it can be synthesized in body (via
tryptophan) 60mg of tryptophan is equivalent to 1 mg of niacin
for the synthesis of niacin coenzyme(B6)
• All protein foods
• Milk, eggs, meat, fish,
• Nuts, Mushrooms
• Can be synthesized
• Tryptophan rich food
• 15 – 20 mg/day
Absorption and Metabolism
• Absorbed in the upper part of the small
• It is stored only sparingly in the kidney, heart,
brain, and liver and is exreted in the urine
Adult 15-20mg/d children 10-15mg/d
Niacin equivalent = 1mg niacin= 60mg tryptophan
ma ize eaters have suffered from pellagra
because corn flour is poor in tryptophan and
it is believed
to contain a niacin antagonist. Thus, daily
requirement of niacin is affected by the
amount of tryptophan in diet
3. Hartnup's disease: in which tryptophan
transport is impaired, and in carcinoid tumours
which use up tryptophan for manufacturing
5-HT, need niacin supplementation.
4. Nicotinic acid (not nicotinamide) has been
used in peripheral vascular disease and as
hypolipidaemic (Ch. 45).
Adverse effects Nicotinic acid, in pharmacological
doses, has many side effects and toxicities
(p. 618). Nicotinamide is innocuous.
• The oxidation–reduction reactions catalyzed by enzymes
belonging to ‘oxido-reductases’
• α- ketoglutarate Succinyl CoA
NAD+ NADH + H+
• Malate Oxaloacetate
NADH + H+
• Forms the active portion of the coenzymes(40) that play an
essential role in cells.
NADPH + H+
• The Oxidative-Phosphorylation: NADH that is produced in TCA cycle, will
undergo oxidative phosphorylation (NADH + H+
) in the Electron
Transport Chain to generate ATP.
• Responsible for major energy production in the form of ATP.
1 NADH = 3 ATP
NADPH is important in Reductive Anabolic Pathways
(Reductive Biosynthesis) by donating reducing equivalents
(NADPH + H+
No energy is produced.
NADPH is also required to maintain the structure of
erythrocyte membrane. (Deficiency leads to hemolytic
• . Flavoproteins regenerate them by
oxidizing N ADH and NADPH.
• Nicotinic acid (but not nicotinamide) in
large doses is a vasodilator, particularly of
• It also lowers plasma lipids(in large doses)
Pellagra [3 D’s]
• scaly dermatitis
• sun exposed surfaces of skin
• starts as red pigmentation which turn to be dark later
• Confused & disoriented
• irritation/inflammation of mucous membranes
– Reduced appetite & weight.
– Occurs in 50-60 days.
– Prevented with an adequate protein diet
• Pellagra – characterized as the disease
• Persistent fatigability
• Soreness and inflammation of the tongue
(glossitis) and mouth (stomatitis)
Causes of Deficiency
Vitamin B6 deficiency
Hartnup Disease: Tryptophan absorption from intestine is
Pregnancy and Lactation
Corn as main staple
Poor diet & alcoholics
Niacin as a Medicine
• Inhibits lipolysis in adipose tissues
• 75-100 x RDA can lower LDL and TG and increase HDL
• Slow/ reverse progression of atherosclerosis with diet and
• Toxicity effects
– Flushing of skin
– Liver damage
– Hyperuricemia (exacerbate gout)
• Vitamin B-5
• Its name derives from the Greek word pantothen meaning
• Easily destroyed by food processing
• Part of coenzyme A, used in energy metabolism
• Essential for metabolism of CHO, fat & protein
•Pantothenic acid contains β alanine and pantoic acid.
•The active Coenzyme A (CoA) differs according to the
group added in place of H in the –SH (sulphahydryl group)
Acetate is added to form acetyl CoA.
Succinate is added to form succinyl CoA.
• Usually in combination with other deficiencies
Irritability, fatigue & apathy
Neurological symptoms: numbness, paresthesia & muscle
Hypoglycemia d/t increased sensitivity to insulin
Restlessness, malaise, sleep disturbances, nausea,
vomiting & abdominal cramps.
Burning foot syndrome: painful burning sensations of the
• Alcoholics at risk
• Vitamin B-7 & Vitamin H
• Anti Egg White Injury Factor: Avidin, a protein found in raw
egg white, inhibits the absorption of biotin.
• Free and bound form
• Biocytin (protein bound form)
• Biotinidase (allows the body to use and to recycle biotin)
• Organ meats, fish
• Egg yolks
• Whole grains
• Also produced by GI
• 30 µg/day
Active form of Biotin acts as coenzyme for Carboxylation
reactions (addition of carbon in the form of CO2).
Carboxylation of Acetyl CoA ( Biosynthesis of FA)
Acetyl CoA + CO2 Malonyl CoA
Carboxylation of Pyruvate (Gluconeogenesis)
Pyruvate + CO2 Oxaloacetate
Metabolism of fat & amino acids (leucine)
Steady blood sugar level
Hair loss (alopecia)
Depression, lethargy, hallucinations, numbness and
tingling of the extremities
Various forms: [pyridine derivatives]
Pyridoxal phosphate [PLP]
– active coenzyme form
Heat and alkaline sensitive
– 1.3 mg/day for adults
– 1.7 mg/day for men over 50
– 1.5 mg/day for women over 50
Absorption, Transport & Metabolism
• Absorbed passively
• Binds to albumin for transport in the blood
• B-6 is stored in the liver and muscle tissue
• All three forms of B-6 are phosphorylated in
• Excess is excreted in urine
B-6 As A Medicine
• Morning sickness in early pregnancy
• Mental depression
• Cut the risk of parkinson’s disease by half
• Carpal tunnel syndrome
• Can lead to irreversible nerve damage with doses > 2
• From the Latin word “folium” (which means “leaf”)
• Other names
Vitamin B-9, Vitamin M & Vitamin Bc
• Consists of
Para-amino benzoic acid (PABA) and
• Coenzyme form:
Tetrahydorfolic acid (THFA)
Dihydrofolic acid (DHFA)
• Susceptible to heat, oxidation & ultraviolet light
Absorption, Transport & Metabolism
• Absorbed in the monoglutamate form with help of folate
– Active absorption = low to moderate intake
– Passive absorption = high intake
• Delivered to the liver where it is changed back to the
• Mostly stored in the liver
• Excreted in urine and bile (entero-hepatic circulation)
• Synthesis, repair & methylation of DNA
– Transfer of single carbon units
– Synthesis of amino acids, purines &
• Cell division & growth
• Homocysteine metabolism
• Produce healthy red blood cells & prevent
– Anemia (megaloblastic)
– Neural tube defects (in developing embryo)
– Peripheral neuropathy
– Glossitis with peptic and mouth ulcers
– Mental confusion, depression, weakness, fatigue & irritability
– Headache, diarrhea & palpitations
– Cancer development
– Pregnant women
• Risk is low
• Upper limit
1 mg/day – adult men & women
0.8 mg/day – women < 18 yrs of age
Skin & respiratory disorder
• Excess can mask vitamin B-12 deficiency
• Also known as cobalamin
• contains cobalt
• Consists of a class of chemically-related compounds
Cyano-cobalamin (synthetic form)
• Basic structure: Synthesized only by bacteria, fungi and algae
• Heat stable up to 100°C
• Affected by strong acids/alkalis
• Affected by light
– Delayed or failure of normal cell division due to impaired DNA
– Destruction of parietal cells
– Achlorhydria & atrophic gastritis
– defective myelination
– never degeneration
– progressive peripheral weakening
– Tingling/numbness in the extremities (parasthesia)
• Vitamers of vitamin C
– Ascorbic acid (reduced form)
– Salts of ascorbic acid
• Vitamin C is purely the L-enantiomer of ascorbic acid
• Synthesized by most animals (not by human)
• The name is derived from ”a”- (meaning "no")
and ”scorbutus” (scurvy)
90 mg/day for male adults
75 mg/day for female adults
+35 mg/day for smokers
Adverse effects (doses > 2 gms/day):
• Indigestion & diarrhea
• Iron poisoning (in people with iron overload disorders)
• Suppresses the production of progesterone from
• Increases insulin production
• Interference with blood coagulation therapy
• Kidney stones [oxalate]