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WATER SOLUBLE VITAMINS
1
Dr. Deeksha K , Ph.D
Assistant Professor
Department of Basic Sciences
Yenepoya School of Allied Health Sciences
REVIEWED BY : PPT REVIEW
COMMITTE, YSAHS
Identify the nutritional supplement given when a patient is on
2
3
SPECIFICLEARNING OBJECTIVES
4
At the end of the session student should be able
 To classify water soluble vitamins and name them
correctly
 To describe the major biochemical functions of
water soluble vitamins
 To list the rich and moderate sources and RDA of
water soluble vitamins appropriately
 To describe the deficiency manifestations of
water soluble vitamins
Characteristic Fat soluble
vitamins
Water soluble vitamins
Solubility Organic solvent Water
Digestion & absorption
With lipids
Requires bile
salt
Absorption is
simple Not require
bile salts
Carrier proteins Present No
Storage Liver No appreciable storage
Excretion Not excreted Excreted
Deficiency
Manifests only when
stores are depleted
Manifests rapidly as
there is no storage
Toxicity Hyper vitaminosis Unlikely
Treatment of deficiency Single large dose Regular dietary intake
5
VITAMINS
VITAMINS
Synonyms
Coenzyme Forms
Functions
Nutritional Aspects: Sources
RDA
Deficiency Manifestations
Antivitamins
6
Vitamin B complex -
Thiamine (VitaminB1)
Riboflavin (Vitamin B2)
Niacin(Vitamin B3)
Pantothenic acid(Vitamin B5)
Pyridoxine (Vitamin B6)
Biotin(Vitamin B7)
Folic acid(Vitamin B9)
Cobalamin (Vitamin B12)
Vitamin C
7
WATER SOLUBLE VITAMINS
WATER SOLUBLE VITAMINS
8
Vitamin Coenzyme form Groups transferred
Thiamine(B1)
Thiamine
pyrophosphate(TPP)
Aldehyde
Riboflavin(B2) FMN & FAD Hydrogen/electron
Niacin(B3) NAD & NADP Hydrogen/electron
Pantothenic acid Co enzyme A
Acyl group(Fatty
acid)
Pyridoxine(B6)
Pyridoxal
phosphate(PLP)
Amino group, CO2
Biotin Biotin CO2
Folic acid (B9) Tetrahydrofolate(THF)
1 carbon- methyl,
formyl, methenyl
Cobalamine(B12) Methyl cobalamine methyl
VITAMINB1(THIAMINE)
Involved mainly in carbohydrate metabolism
AMP
ATP
Thiamine TPP
TPP transferase
Thiamine pyrophosphate(TPP)
9
Aneurine, Anti beri-beri factor
Coenzyme form:
VITAMINB1(THIAMINE) -FUNCTIONS
Oxidative decarboxylation reactions
pyruvate dehydrogenase
α-ketoglutarate dehydrogenase
α-keto acid dehydrogenase
Transketolase reactions in HMP pathway
Neurotransmission
10
VITAMINB1(THIAMINE) -FUNCTIONS
11
Thiamine is essential in 3 main systems
• Nervous system- transmission of nerve impulse
• Cardiovascular system-normal functioning of heart
muscles
• GIT- normal maintenance of GIT
VITAMINB1(THIAMINE)
Sources
Vegetarian :Outer layer of cereals –
unpolished (parboiled) rice, whole wheat flour
Pulses, Oil seeds, nuts and yeast
Animal sources: egg, fish, meat
RDA:
Image source: google images-eclinical
works.adam.com
12
VITAMINB1DEFICIENCY
Low dietary intake
Intake of polished cereals
Chronic alcoholism
Other factors
Carbohydraterich diet
Impairedintestinal absorption
Excessive demand – pregnancy & lactation
13
Beri Beri
VITAMIN B1DEFICIENCY
Dry Beri Beri
-Neuropsychiatric
manifestations
Peripheral
neuropathy,
psychosis,
Muscular
weakness
Wet Beri Beri
-cardiovascular
manifestations
Palpitations,
Breathlessness
edema
Infantile Beri
Beri
2-5 months
child
Restlessness
Sleeplessnes
convulsions,
vomiting
Cerebral
( Wernicke’s
–korsakoff
syndrome)
- Chronic
alcholics
14
- Psychosis
- encephal
opathy
VITAMINB1
Antivitamins:
Tannin: excessive tea consumption
 Pyrithiamine and oxythiamine (sulfa drugs-
antibiotics)
15
Flavokinase FAD synthase
FAD
Riboflavin FMN
ATP ADP ATP PPi
Intestinal mucosal cell liver
FMN: Flavin adenine mononucleotide
FAD : Flavin adenine dinucleotide
16
VITAMIN B2 (RIBOFLAVIN)
Two co-enzyme forms
RIBOFLAVIN- FUNCTIONS
Enzyme cofactor for:
• Oxidation – reduction reactions
Metabolism of lipids / carbohydrates Drug
metabolism
• Involved in tissue protein building and cell
respiration
• Helps in conversion of trytophan to niacin
17
Meat Fish Yeast
Animal:
Egg
Veg:
Cereals
Fruits
Pulses Milk
Green Leafy Vegetables
RDA:
Increased in pregnancy and lactation
VITAMIN B2: SOURCES
18
Symptoms involves skin and mucosal membranes
Cheilosis (inflamed lips)
Angular stomatitis
Glossitis
Seborrheic dermatitis
Corneal vascularization
VITAMIN B2: DEFICIENCY
Ariboflavinosis
Image source: https://www.google.com
inlifehealthcare.com 19
Isoriboflavin
Galactoflavin
Araboflavin
ANTIVITAMINS
20
Pellagra preventing factor of Goldberger
Nicotinamide adenine dinucleotide (NAD+ )
Nicotinamide adenine dinucleotide phosphate (NADP + )
NAD+ collects reducing equivalents for ATP production in the
mitochondria by oxidative phosphorylation
VITAMIN B3- NIACIN :
COENZYME FORM
21
NIACIN : Funtions
22
1. It acts as a co-enzyme in oxidation reduction reactions:
v. Catabolic Rxn: in form of NAD+/NADH
v. Anabolic Rxn: in form of NADP+/NADPH
Therefore, it is required for functions of >200 enzymes dealing
with the biosynthesis of several compounds e. g. fatty acids,
steroids and catabolism of fuel molecules for energy.
2. DNA replication and repair: It is vital for synthesis of DNA-
bound nuclear proteins (histones)
NIACIN : Funtions
23
3. Antioxidant functions: It plays an important role in antioxidant
systems, particularly in the liver.
4. Blood sugar regulation: It is a component of the glucose
tolerance factor (GTF), which together with insulin, helps to
control blood glucose.
5. Fat and cholesterol metabolism: It lowers levels of total and
LDL cholesterol in the blood, while increasing levels of HDL
cholesterol (the healthy, protective form of cholesterol).
• Meat
• Legume
• Sweet
• Potato
• Yeast
• Fish
• Cereals (outer
coats)
• Peanuts
- Niacin is formed in humans during catabolism of tryptophan.
It provides only 10% of the requirement. Remainder must
come from the diet
Every 60 mg of tryptophan =1 mg of niacin
RDA: 20 mg/day
24
NIACIN : SOURCES
1. Diet poor in niacin & tryptophan
- seen in populations dependant on maize as staple food.
Maize deficient in tryptophan, niacin present.
in bound form in maize →niacin unavailable
2. Hartnups disease: defective intestinal absorption and renal
tubular reabsorption of tryptophan
NIACIN : DEFICIENCY
25
NIACIN: DEFICIENCY
Pellagra : Disease of 3Ds( involves skin, GIT &
CNS)
Dermatitis: bright red erythema and increase
pigmentation around neck(Casal’s necklace), ankle,
feet and face exposed to sunlight
Diarrhea: chronic inflammation of intestinal mucosa
Dementia: degeneration of nervous tissue –
irritability, inability to concentrate, poor memory
26
NIACIN: DEFICIENCY
Image source:
https://www.google.com
msdmanuals.com
infonetbiovision.org
27
NIACIN : ANTAGONISTS
28
 3 Acetyl pyridine
 Isoniazid
VITAMINB5 -PANTOTHENICACID
29
 Used in synthesizing two important acyl
carriers (Carrier of acyl groups)
1. Coenzyme A ( CoASH)
2. Acyl carrier protein( ACP of fatty acid
synthase complex)
It has 2 active forms
1.Coenzyme A (CoA / CoA-SH)
Coenzyme (CoA) participates in several enzymatic reactions
of carbohydrate, lipid and amino acid .
Important CoA derivatives:
Acetyl CoA, Succinyl CoA, HMG CoA, Malonyl CoA, Palmityol
CoA, Propionyl CoA
2. Acyl carrier protein (ACP)
- Pantothenic acid is required for the synthesis of
phosphopantotheine of complex
- carry acyl groups in fatty acid synthesis
30
PANTOTHENICACID: FUNCTIONS
Whole cereals
Legumes
Egg yolk
Liver
yeast
Also synthesized by bacterial flora in the intestine
RDA: 10mg/day
31
PANTOTHENICACID: SOURCES
PANTOTHENICACID: DEFICIENCY
 It is
prisoners of war and during famine
manifested as:
-Painful burning sensations(Paresthesia) in feet
-Staggering gait
-impaired coordination & sleep disturbance
32
SUMMARY
33
 The coenzyme form of thiamine is thiamine
pyrophosphate ( TPP)
 TPP is essential for PDH, transketolase, alpha-
ketoglutarate dehydrogenase
 Deficiency of thiamine leads to Beriberi
SUMMARY
34
 The coenzyme forms of riboflavin are FMN
and FAD
 Examples of FAD dependent enzymes are
succinate dehydrogenase and acyl-CoA
dehydrogenase
 Deficiency of riboflavin leads to glossitis,
cheilosis and angular stomatitis
REFERENCES
35
 Textbook of Biochemistry for Medical
Students, Ninth Edition-Vasudevan
 Textbook of Biochemistry, Fifth Edition –
Pankaja Naik
 Harper’s Illustrated Biochemistry, 31 st
edition.
 Internet images from google.com
ASSIGNMENT
36
1.Explain the following aspects of thiamine.
a)Coenzyme form b) Biochemical functions/
metabolic role and c) Deficiency
2.Explain the biochemical basis: Intake of
polished cereals as staple food may cause
Beriberi
1. Write the coenzyme forms of and one reaction for
each of them for Niacin
2. Deficiency manifestations of Niacin.
2. Pellagra is more common in population dependent on
maize as the staple food. Explain.
37
ASSIGNMENT
VITAMINB6: PYRIDOXINE
Pyridoxal Pyridoxal phosphate(PLP)
ATP ADP
Active form of vitamin B6
Pyridoxal phosphate
Pyridoxal kinase
38
Protein
metabolism:
transamination
decarboxylation
 Lipid metabolism
sphingomyelin synthesis
Carbohydrate metabolism
glycogenolysis
 Heme synthesis
39
PLP FUNCTIONS
PYRIDOXINE: SOURCES
Egg, fish, meat milk, (rich sources)
Beans, nuts, wheat, yeast, green leafy vegetables
RDA: 1-2mg/day
40
PYRIDOXINE: DEFICIENCY
Deficiency of vitamin B6 may occur
- During lactation
- In alcoholics
- During isoniazid therapy
 Neurological symptoms: Depression, irritability,
nervousness, mental confusion and convulsions.(
decreased synthesis of GABA, serotonin, epinephrine
and norepinephrine, as PLP is involved in their synthesis).
 PLP is involved in the synthesis of sphingolipids, so B6
deficiency demyelination of nerves peripheral neuritis
neurological manifestation
41
PYRIDOXINE: DEFICIENCY
Image source:
https://www.google.com
Wellness lab health info.blogspot.com
42
PYRIDOXINE-ANTIVITAMINS
43
 Isoniazid
 Deoxypyridoxine
 Methoxypyridoxine
VITAMINB7: BIOTIN
Sulfur containing vitamin
Anti egg white injury factor/Vitamin H
Synthesized by intestinal flora
Coenzyme for carboxylases
44
widely distributed
Liver
Peanuts
Milk
Yeast
Soyabeans
Egg yolk
Vegetables( tomato, carrot, cabbage, cucumber)
intestinal bacteria can synthesise biotin
RDA: 30 – 100μg/ day
45
BIOTIN:SOURCES
BIOTIN-FUNCTIONS
These functions are dependent on a biotin-containing enzymes:
• Glucose synthesis (The key initial step in gluconeogenesis).
• Fat metabolism (synthesis and breakdown of fatty acids as
well as the essential fatty acid metabolism such as conversion
of linoleic acid to various eicosanoids)
• Amino acid metabolism (breakdown of amino acids, such as
threonine, isoleucine, and methionine, for use as energy).
• Cell division and growth (Biotin plays an important role in
DNA synthesis)
Prolonged use of antibiotics
High consumption of raw eggs cause deficiency
Manifestations
Dermatitis(erythematous rash: face)
Atrophic glossitis
Anorexia
Neurological symptoms: hallucination, depression,
lethargy, Hyperesthesia, Muscle pain
47
BIOTIN: DEFICIENCY
Avidin
Present in egg white
binds with biotin
Prevent the absorption of biotin biotin deficiency
• Boiling of egg neutralize the inhibitory activity
BIOTINANTAGONIST
48
BIOTIN- ANTAGONISTS
49
 Avidin
 Desthiobiotin
 Biotin sulphonic acid
Involved in one-carbon metabolism
nucleotide synthesis
growth
reduction in homocysteine levels
Most common vitamin deficiency
Commonly supplemented during pregnancy
50
VITAMINB9: FOLICACID
Contains three components
-Pteridine ring
-Para amino benzoic acid (PABA)
-Glutamic acid (1-7 residues)
51
VITAMIN B9: FOLIC ACID
FOLICACID
Coenzyme
(active) form
Tetrahydrofolate
[THF]
Folate reducatse
Folic acid
NADPH+H+ NADP+
Folate reducatse
Dihydrofolate THF
NADPH+H+ NADP+
52
FOLICACID: SOURCES
Sources: abundant in green leafy vegetables(spinach,
cauliflower)
Yeast, liver, egg, vegetables, cereals, pulses and
oil seeds, Beans, peas
RDA: 200µg/day
400µg/day in pregnancy
Image source:
https://www.google.com
naturespharmacy.biz 53
Actively involved in one carbon metabolism
Carrier of one carbon units –
Formyl (-CHO)
Formimino (-CH=NH)
Methenyl (-CH=)
Methylene (-CH2-)
Hydroxymethyl (-CH2OH)
Methyl (-CH3)
• Bind with THF @ N5 & / N10 of pteroyl structure
54
FOLICACID: FUNCTIONS
1. Biochemical functions
FOLICACID: FUNCTIONS
that occur
2.Folic acid
during fetal development.
3.Folic acid is effective in
concentration in patients with coronary
artery disease.
55
Insufficient dietary intake
malabsorption
Increased demand-
pregnancy and lactation
Administration of
antifolate drugs
56
Megaloblastic anemia
Homocysteinuria
Neural tube defects
GIT manifestations: Vomiting, Diarrhea, Abdominal
pain
Anorexia, Weakness, Fatigue
57
FOLICACID: MANIFESTATION
Normocytes
B12 deficiency)
Delayed maturation of
erythroblasts ( nucleus)
Megaloblasts(folic acid,
Image source:
https://www.google.com
emedicine.medscape.com
58
In babies of pregnant women with folate deficiency
Congenital malformations of spine (spina bifida)
NEURALTUBE DEFECTS
Image source :
https://www.google.com
pedclerk.bsd.uchicago.edu
Neuropathology-web org 59
SUMMARY
60
 Biotin acts as coenzyme for carboxylation reactions.
Examples include acetyl-CoA carboxylase, propionyl
CoA carboxylase, pyruvate carboxylase.
 Avidin, a protein present in egg white has great affinity
for biotin. Hence intake of raw ( unboiled ) egg may
cause biotin deficiency.
SUMMARY
61
 Tetrahydrofolic acid ( THFA) is the carrier of one-carbon
groups.
 Megaloblastic anemia is the most characteristic feature
of folate deficiency.
 Folate antagonists are sulfonamides, methotrexate and
pyrimethamine
REFERENCES
62
 Textbook of Biochemistry for Medical
Students, Ninth Edition-Vasudevan
 Textbook of Biochemistry, Fifth Edition –
Pankaja Naik
 Harper’s Illustrated Biochemistry, 31 st
edition.
 Internet images from google.com
Extrinsic factor of castle(EF)
Antipernicious anemia factor
Contains cobalt
No plant sources
63
VITAMINB12: COBALAMIN
VITAMINB12: COBALAMIN

1.Methyl cobalamin(major form present in blood)
64
2. Deoxy adenosylcobalamin ( storage form)
Only animal sources –
Liver
Meat
Fish
Egg
Curd (lactobacillus)
RDA: 1-2µg/day
Image source :
https://www.google.com
glowpeople.com
COBALAMIN: SOURCES
65
COBALAMIN: FUNCTIONS
66
COBALAMIN: DEFICEIENCYCAUSES
Lack of IF - common cause- Auto antibodies against
parietal cells (Pernicious anemia)
Malabsorption - Gastrectomy, Ileal resection
Prolonged antibiotic therapy
Reduced intake- elderly people, Pregnancy
67
1. Megaloblastic anemia – d/t folate trap- large RBCs
2. Neurological disorders→non availability of methionine
→no conversion of ethanolamine to choline →defective
myelin sheath→demyelination & neurological lesions-
Subacute combined degeneration
3. Homocystinuria
4. Methyl malonic aciduria
68
COBALAMIN: MANIFESTATIONS
COBALAMIN: MANIFESTATIONS
 Pernicious anemia associated with nerve
degeneration and paralysis
-Cell division is sluggish but
cytoplasmic development is normal
-Nucleated RBC s are seen
medium.com
69
COBALAMIN: MANIFESTATIONS
Image source :https://www.google.com 115
VITAMINC (ascorbic acid)
-The structure of ascorbic acid closely resembles
that of a hexose.
-It is a strong reducing agent. The reducing property
of vitamin C depends on the double bonded carbons
(enediol).
- L-ascorbic acid undergoes oxidation to form
dehydroascorbic acid and this reaction is reversible.
71
Antioxidant function
Maintaining iron or copper in the reduced state- Absorption
of iron
Reduces cataract formation
Role in iron absorption
Regeneration of hemoglobin
Synthesis of collagen, Epinephrine, Bile acids Immune
functions
Helps in wound healing
VITAMIN C(ASCORBIC ACID) :
FUNCTIONS
72
Gooseberry(amla), Citrus fruits, Cabbage-type vegetables
- Broccoli
Strawberries, Tomatoes, Papayas, Mangoes
Milk is a poor source
RDA: 75mg/day
VITAMIN C : SOURCES
Image source :
https://www.google.com
studyandscore.com 129
VITAMINC: DEFICIENCY
 Cause:
- Intake of foods devoid of fresh fruits and vegetables
 Manifestations:
Scurvy
- Due to
1. Formation of defective collagen
2. Low absorption of iron
130
Defective collagen formation results in:
Fragile capillaries
Weak & brittle bones
Decreased scar tissue formation
Manifestations:
Oral cavity: Painful, swollen, spongy bleeding gums,loose
teeth
Subcutaneous hemorrhage
VITAMIN C DEFICIENCY - SCURVY
Image source :
https://www.google.com
Vitamin C 18
slideshare.net &
wikem.org 131
VITAMINCDEFICIENCY- SCURVY
 Bone: frequent fractures
Infections &Delayed wound healing
Low iron absorption results in
Microcytic hypochromic anemia
76
Assignment
77
1. Explain the biochemical basis:
a) Vitamin C deficiency may result in bleeding gums,
frequent fractures and delayed wound healing.
b) Vitamin C facilitates iron absorption in the intestine.
Summarise all the water soluble vitamins in a tabular
form under the headings:
Name of
Vitamin
Biochemical
functions
Dietary
sources
RDA Deficiency
manifestations
78

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Water Soluble Vitamins -Dr. Deeksha K.pptx

  • 1. WATER SOLUBLE VITAMINS 1 Dr. Deeksha K , Ph.D Assistant Professor Department of Basic Sciences Yenepoya School of Allied Health Sciences REVIEWED BY : PPT REVIEW COMMITTE, YSAHS
  • 2. Identify the nutritional supplement given when a patient is on 2
  • 3. 3
  • 4. SPECIFICLEARNING OBJECTIVES 4 At the end of the session student should be able  To classify water soluble vitamins and name them correctly  To describe the major biochemical functions of water soluble vitamins  To list the rich and moderate sources and RDA of water soluble vitamins appropriately  To describe the deficiency manifestations of water soluble vitamins
  • 5. Characteristic Fat soluble vitamins Water soluble vitamins Solubility Organic solvent Water Digestion & absorption With lipids Requires bile salt Absorption is simple Not require bile salts Carrier proteins Present No Storage Liver No appreciable storage Excretion Not excreted Excreted Deficiency Manifests only when stores are depleted Manifests rapidly as there is no storage Toxicity Hyper vitaminosis Unlikely Treatment of deficiency Single large dose Regular dietary intake 5 VITAMINS
  • 6. VITAMINS Synonyms Coenzyme Forms Functions Nutritional Aspects: Sources RDA Deficiency Manifestations Antivitamins 6
  • 7. Vitamin B complex - Thiamine (VitaminB1) Riboflavin (Vitamin B2) Niacin(Vitamin B3) Pantothenic acid(Vitamin B5) Pyridoxine (Vitamin B6) Biotin(Vitamin B7) Folic acid(Vitamin B9) Cobalamin (Vitamin B12) Vitamin C 7 WATER SOLUBLE VITAMINS
  • 8. WATER SOLUBLE VITAMINS 8 Vitamin Coenzyme form Groups transferred Thiamine(B1) Thiamine pyrophosphate(TPP) Aldehyde Riboflavin(B2) FMN & FAD Hydrogen/electron Niacin(B3) NAD & NADP Hydrogen/electron Pantothenic acid Co enzyme A Acyl group(Fatty acid) Pyridoxine(B6) Pyridoxal phosphate(PLP) Amino group, CO2 Biotin Biotin CO2 Folic acid (B9) Tetrahydrofolate(THF) 1 carbon- methyl, formyl, methenyl Cobalamine(B12) Methyl cobalamine methyl
  • 9. VITAMINB1(THIAMINE) Involved mainly in carbohydrate metabolism AMP ATP Thiamine TPP TPP transferase Thiamine pyrophosphate(TPP) 9 Aneurine, Anti beri-beri factor Coenzyme form:
  • 10. VITAMINB1(THIAMINE) -FUNCTIONS Oxidative decarboxylation reactions pyruvate dehydrogenase α-ketoglutarate dehydrogenase α-keto acid dehydrogenase Transketolase reactions in HMP pathway Neurotransmission 10
  • 11. VITAMINB1(THIAMINE) -FUNCTIONS 11 Thiamine is essential in 3 main systems • Nervous system- transmission of nerve impulse • Cardiovascular system-normal functioning of heart muscles • GIT- normal maintenance of GIT
  • 12. VITAMINB1(THIAMINE) Sources Vegetarian :Outer layer of cereals – unpolished (parboiled) rice, whole wheat flour Pulses, Oil seeds, nuts and yeast Animal sources: egg, fish, meat RDA: Image source: google images-eclinical works.adam.com 12
  • 13. VITAMINB1DEFICIENCY Low dietary intake Intake of polished cereals Chronic alcoholism Other factors Carbohydraterich diet Impairedintestinal absorption Excessive demand – pregnancy & lactation 13
  • 14. Beri Beri VITAMIN B1DEFICIENCY Dry Beri Beri -Neuropsychiatric manifestations Peripheral neuropathy, psychosis, Muscular weakness Wet Beri Beri -cardiovascular manifestations Palpitations, Breathlessness edema Infantile Beri Beri 2-5 months child Restlessness Sleeplessnes convulsions, vomiting Cerebral ( Wernicke’s –korsakoff syndrome) - Chronic alcholics 14 - Psychosis - encephal opathy
  • 15. VITAMINB1 Antivitamins: Tannin: excessive tea consumption  Pyrithiamine and oxythiamine (sulfa drugs- antibiotics) 15
  • 16. Flavokinase FAD synthase FAD Riboflavin FMN ATP ADP ATP PPi Intestinal mucosal cell liver FMN: Flavin adenine mononucleotide FAD : Flavin adenine dinucleotide 16 VITAMIN B2 (RIBOFLAVIN) Two co-enzyme forms
  • 17. RIBOFLAVIN- FUNCTIONS Enzyme cofactor for: • Oxidation – reduction reactions Metabolism of lipids / carbohydrates Drug metabolism • Involved in tissue protein building and cell respiration • Helps in conversion of trytophan to niacin 17
  • 18. Meat Fish Yeast Animal: Egg Veg: Cereals Fruits Pulses Milk Green Leafy Vegetables RDA: Increased in pregnancy and lactation VITAMIN B2: SOURCES 18
  • 19. Symptoms involves skin and mucosal membranes Cheilosis (inflamed lips) Angular stomatitis Glossitis Seborrheic dermatitis Corneal vascularization VITAMIN B2: DEFICIENCY Ariboflavinosis Image source: https://www.google.com inlifehealthcare.com 19
  • 21. Pellagra preventing factor of Goldberger Nicotinamide adenine dinucleotide (NAD+ ) Nicotinamide adenine dinucleotide phosphate (NADP + ) NAD+ collects reducing equivalents for ATP production in the mitochondria by oxidative phosphorylation VITAMIN B3- NIACIN : COENZYME FORM 21
  • 22. NIACIN : Funtions 22 1. It acts as a co-enzyme in oxidation reduction reactions: v. Catabolic Rxn: in form of NAD+/NADH v. Anabolic Rxn: in form of NADP+/NADPH Therefore, it is required for functions of >200 enzymes dealing with the biosynthesis of several compounds e. g. fatty acids, steroids and catabolism of fuel molecules for energy. 2. DNA replication and repair: It is vital for synthesis of DNA- bound nuclear proteins (histones)
  • 23. NIACIN : Funtions 23 3. Antioxidant functions: It plays an important role in antioxidant systems, particularly in the liver. 4. Blood sugar regulation: It is a component of the glucose tolerance factor (GTF), which together with insulin, helps to control blood glucose. 5. Fat and cholesterol metabolism: It lowers levels of total and LDL cholesterol in the blood, while increasing levels of HDL cholesterol (the healthy, protective form of cholesterol).
  • 24. • Meat • Legume • Sweet • Potato • Yeast • Fish • Cereals (outer coats) • Peanuts - Niacin is formed in humans during catabolism of tryptophan. It provides only 10% of the requirement. Remainder must come from the diet Every 60 mg of tryptophan =1 mg of niacin RDA: 20 mg/day 24 NIACIN : SOURCES
  • 25. 1. Diet poor in niacin & tryptophan - seen in populations dependant on maize as staple food. Maize deficient in tryptophan, niacin present. in bound form in maize →niacin unavailable 2. Hartnups disease: defective intestinal absorption and renal tubular reabsorption of tryptophan NIACIN : DEFICIENCY 25
  • 26. NIACIN: DEFICIENCY Pellagra : Disease of 3Ds( involves skin, GIT & CNS) Dermatitis: bright red erythema and increase pigmentation around neck(Casal’s necklace), ankle, feet and face exposed to sunlight Diarrhea: chronic inflammation of intestinal mucosa Dementia: degeneration of nervous tissue – irritability, inability to concentrate, poor memory 26
  • 28. NIACIN : ANTAGONISTS 28  3 Acetyl pyridine  Isoniazid
  • 29. VITAMINB5 -PANTOTHENICACID 29  Used in synthesizing two important acyl carriers (Carrier of acyl groups) 1. Coenzyme A ( CoASH) 2. Acyl carrier protein( ACP of fatty acid synthase complex)
  • 30. It has 2 active forms 1.Coenzyme A (CoA / CoA-SH) Coenzyme (CoA) participates in several enzymatic reactions of carbohydrate, lipid and amino acid . Important CoA derivatives: Acetyl CoA, Succinyl CoA, HMG CoA, Malonyl CoA, Palmityol CoA, Propionyl CoA 2. Acyl carrier protein (ACP) - Pantothenic acid is required for the synthesis of phosphopantotheine of complex - carry acyl groups in fatty acid synthesis 30 PANTOTHENICACID: FUNCTIONS
  • 31. Whole cereals Legumes Egg yolk Liver yeast Also synthesized by bacterial flora in the intestine RDA: 10mg/day 31 PANTOTHENICACID: SOURCES
  • 32. PANTOTHENICACID: DEFICIENCY  It is prisoners of war and during famine manifested as: -Painful burning sensations(Paresthesia) in feet -Staggering gait -impaired coordination & sleep disturbance 32
  • 33. SUMMARY 33  The coenzyme form of thiamine is thiamine pyrophosphate ( TPP)  TPP is essential for PDH, transketolase, alpha- ketoglutarate dehydrogenase  Deficiency of thiamine leads to Beriberi
  • 34. SUMMARY 34  The coenzyme forms of riboflavin are FMN and FAD  Examples of FAD dependent enzymes are succinate dehydrogenase and acyl-CoA dehydrogenase  Deficiency of riboflavin leads to glossitis, cheilosis and angular stomatitis
  • 35. REFERENCES 35  Textbook of Biochemistry for Medical Students, Ninth Edition-Vasudevan  Textbook of Biochemistry, Fifth Edition – Pankaja Naik  Harper’s Illustrated Biochemistry, 31 st edition.  Internet images from google.com
  • 36. ASSIGNMENT 36 1.Explain the following aspects of thiamine. a)Coenzyme form b) Biochemical functions/ metabolic role and c) Deficiency 2.Explain the biochemical basis: Intake of polished cereals as staple food may cause Beriberi
  • 37. 1. Write the coenzyme forms of and one reaction for each of them for Niacin 2. Deficiency manifestations of Niacin. 2. Pellagra is more common in population dependent on maize as the staple food. Explain. 37 ASSIGNMENT
  • 38. VITAMINB6: PYRIDOXINE Pyridoxal Pyridoxal phosphate(PLP) ATP ADP Active form of vitamin B6 Pyridoxal phosphate Pyridoxal kinase 38
  • 39. Protein metabolism: transamination decarboxylation  Lipid metabolism sphingomyelin synthesis Carbohydrate metabolism glycogenolysis  Heme synthesis 39 PLP FUNCTIONS
  • 40. PYRIDOXINE: SOURCES Egg, fish, meat milk, (rich sources) Beans, nuts, wheat, yeast, green leafy vegetables RDA: 1-2mg/day 40
  • 41. PYRIDOXINE: DEFICIENCY Deficiency of vitamin B6 may occur - During lactation - In alcoholics - During isoniazid therapy  Neurological symptoms: Depression, irritability, nervousness, mental confusion and convulsions.( decreased synthesis of GABA, serotonin, epinephrine and norepinephrine, as PLP is involved in their synthesis).  PLP is involved in the synthesis of sphingolipids, so B6 deficiency demyelination of nerves peripheral neuritis neurological manifestation 41
  • 44. VITAMINB7: BIOTIN Sulfur containing vitamin Anti egg white injury factor/Vitamin H Synthesized by intestinal flora Coenzyme for carboxylases 44
  • 45. widely distributed Liver Peanuts Milk Yeast Soyabeans Egg yolk Vegetables( tomato, carrot, cabbage, cucumber) intestinal bacteria can synthesise biotin RDA: 30 – 100μg/ day 45 BIOTIN:SOURCES
  • 46. BIOTIN-FUNCTIONS These functions are dependent on a biotin-containing enzymes: • Glucose synthesis (The key initial step in gluconeogenesis). • Fat metabolism (synthesis and breakdown of fatty acids as well as the essential fatty acid metabolism such as conversion of linoleic acid to various eicosanoids) • Amino acid metabolism (breakdown of amino acids, such as threonine, isoleucine, and methionine, for use as energy). • Cell division and growth (Biotin plays an important role in DNA synthesis)
  • 47. Prolonged use of antibiotics High consumption of raw eggs cause deficiency Manifestations Dermatitis(erythematous rash: face) Atrophic glossitis Anorexia Neurological symptoms: hallucination, depression, lethargy, Hyperesthesia, Muscle pain 47 BIOTIN: DEFICIENCY
  • 48. Avidin Present in egg white binds with biotin Prevent the absorption of biotin biotin deficiency • Boiling of egg neutralize the inhibitory activity BIOTINANTAGONIST 48
  • 49. BIOTIN- ANTAGONISTS 49  Avidin  Desthiobiotin  Biotin sulphonic acid
  • 50. Involved in one-carbon metabolism nucleotide synthesis growth reduction in homocysteine levels Most common vitamin deficiency Commonly supplemented during pregnancy 50 VITAMINB9: FOLICACID
  • 51. Contains three components -Pteridine ring -Para amino benzoic acid (PABA) -Glutamic acid (1-7 residues) 51 VITAMIN B9: FOLIC ACID
  • 52. FOLICACID Coenzyme (active) form Tetrahydrofolate [THF] Folate reducatse Folic acid NADPH+H+ NADP+ Folate reducatse Dihydrofolate THF NADPH+H+ NADP+ 52
  • 53. FOLICACID: SOURCES Sources: abundant in green leafy vegetables(spinach, cauliflower) Yeast, liver, egg, vegetables, cereals, pulses and oil seeds, Beans, peas RDA: 200µg/day 400µg/day in pregnancy Image source: https://www.google.com naturespharmacy.biz 53
  • 54. Actively involved in one carbon metabolism Carrier of one carbon units – Formyl (-CHO) Formimino (-CH=NH) Methenyl (-CH=) Methylene (-CH2-) Hydroxymethyl (-CH2OH) Methyl (-CH3) • Bind with THF @ N5 & / N10 of pteroyl structure 54 FOLICACID: FUNCTIONS 1. Biochemical functions
  • 55. FOLICACID: FUNCTIONS that occur 2.Folic acid during fetal development. 3.Folic acid is effective in concentration in patients with coronary artery disease. 55
  • 56. Insufficient dietary intake malabsorption Increased demand- pregnancy and lactation Administration of antifolate drugs 56
  • 57. Megaloblastic anemia Homocysteinuria Neural tube defects GIT manifestations: Vomiting, Diarrhea, Abdominal pain Anorexia, Weakness, Fatigue 57 FOLICACID: MANIFESTATION
  • 58. Normocytes B12 deficiency) Delayed maturation of erythroblasts ( nucleus) Megaloblasts(folic acid, Image source: https://www.google.com emedicine.medscape.com 58
  • 59. In babies of pregnant women with folate deficiency Congenital malformations of spine (spina bifida) NEURALTUBE DEFECTS Image source : https://www.google.com pedclerk.bsd.uchicago.edu Neuropathology-web org 59
  • 60. SUMMARY 60  Biotin acts as coenzyme for carboxylation reactions. Examples include acetyl-CoA carboxylase, propionyl CoA carboxylase, pyruvate carboxylase.  Avidin, a protein present in egg white has great affinity for biotin. Hence intake of raw ( unboiled ) egg may cause biotin deficiency.
  • 61. SUMMARY 61  Tetrahydrofolic acid ( THFA) is the carrier of one-carbon groups.  Megaloblastic anemia is the most characteristic feature of folate deficiency.  Folate antagonists are sulfonamides, methotrexate and pyrimethamine
  • 62. REFERENCES 62  Textbook of Biochemistry for Medical Students, Ninth Edition-Vasudevan  Textbook of Biochemistry, Fifth Edition – Pankaja Naik  Harper’s Illustrated Biochemistry, 31 st edition.  Internet images from google.com
  • 63. Extrinsic factor of castle(EF) Antipernicious anemia factor Contains cobalt No plant sources 63 VITAMINB12: COBALAMIN
  • 64. VITAMINB12: COBALAMIN  1.Methyl cobalamin(major form present in blood) 64 2. Deoxy adenosylcobalamin ( storage form)
  • 65. Only animal sources – Liver Meat Fish Egg Curd (lactobacillus) RDA: 1-2µg/day Image source : https://www.google.com glowpeople.com COBALAMIN: SOURCES 65
  • 67. COBALAMIN: DEFICEIENCYCAUSES Lack of IF - common cause- Auto antibodies against parietal cells (Pernicious anemia) Malabsorption - Gastrectomy, Ileal resection Prolonged antibiotic therapy Reduced intake- elderly people, Pregnancy 67
  • 68. 1. Megaloblastic anemia – d/t folate trap- large RBCs 2. Neurological disorders→non availability of methionine →no conversion of ethanolamine to choline →defective myelin sheath→demyelination & neurological lesions- Subacute combined degeneration 3. Homocystinuria 4. Methyl malonic aciduria 68 COBALAMIN: MANIFESTATIONS
  • 69. COBALAMIN: MANIFESTATIONS  Pernicious anemia associated with nerve degeneration and paralysis -Cell division is sluggish but cytoplasmic development is normal -Nucleated RBC s are seen medium.com 69
  • 70. COBALAMIN: MANIFESTATIONS Image source :https://www.google.com 115
  • 71. VITAMINC (ascorbic acid) -The structure of ascorbic acid closely resembles that of a hexose. -It is a strong reducing agent. The reducing property of vitamin C depends on the double bonded carbons (enediol). - L-ascorbic acid undergoes oxidation to form dehydroascorbic acid and this reaction is reversible. 71
  • 72. Antioxidant function Maintaining iron or copper in the reduced state- Absorption of iron Reduces cataract formation Role in iron absorption Regeneration of hemoglobin Synthesis of collagen, Epinephrine, Bile acids Immune functions Helps in wound healing VITAMIN C(ASCORBIC ACID) : FUNCTIONS 72
  • 73. Gooseberry(amla), Citrus fruits, Cabbage-type vegetables - Broccoli Strawberries, Tomatoes, Papayas, Mangoes Milk is a poor source RDA: 75mg/day VITAMIN C : SOURCES Image source : https://www.google.com studyandscore.com 129
  • 74. VITAMINC: DEFICIENCY  Cause: - Intake of foods devoid of fresh fruits and vegetables  Manifestations: Scurvy - Due to 1. Formation of defective collagen 2. Low absorption of iron 130
  • 75. Defective collagen formation results in: Fragile capillaries Weak & brittle bones Decreased scar tissue formation Manifestations: Oral cavity: Painful, swollen, spongy bleeding gums,loose teeth Subcutaneous hemorrhage VITAMIN C DEFICIENCY - SCURVY Image source : https://www.google.com Vitamin C 18 slideshare.net & wikem.org 131
  • 76. VITAMINCDEFICIENCY- SCURVY  Bone: frequent fractures Infections &Delayed wound healing Low iron absorption results in Microcytic hypochromic anemia 76
  • 77. Assignment 77 1. Explain the biochemical basis: a) Vitamin C deficiency may result in bleeding gums, frequent fractures and delayed wound healing. b) Vitamin C facilitates iron absorption in the intestine. Summarise all the water soluble vitamins in a tabular form under the headings: Name of Vitamin Biochemical functions Dietary sources RDA Deficiency manifestations
  • 78. 78