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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
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
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
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
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
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
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
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
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
50. Involved in one-carbon metabolism
nucleotide synthesis
growth
reduction in homocysteine levels
Most common vitamin deficiency
Commonly supplemented during pregnancy
50
VITAMINB9: FOLICACID
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
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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
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
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
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
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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
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