Vitamins

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Vitamin B
thiamine (B1),
– riboflavin (B2),
– nicotinamide (niacin),
– pyridoxine (B6),
– folate (pteroylglutamate),
– the vitamin B12 complex (cobalamins),
– biotin and pantothenate,
T
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(
B
1
)
Humans cannot synthesize thiamine.
It is found in many dietary components;
food grains, rice ,
 
Function of Thiamine B1
is a component of thiamine pyrophosphate,
which is an essential cofactor for
Decarboxylation of 2-oxoacids
;
    pyruvate                     acetyl coenzyme A.
In thiamine deficiency, pyruvate cannot be metabolized and
accumulates in the blood.
Transketolase
 in the pentose–phosphate
pathway.
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Adequate amounts are present in a normal diet and deficiency is
most common
 1
.  
Beriberi 
“weakness”. 
        
Wet beriberi
: 
Here cardiovascular manifestations are
prominent , death occurs due to heart failure.
      
Dry beriberi
: 
In this condition, CNS manifestations are the
major features.
     
Infantile beriberi
: 
It occurs in infants born to mothers suffering
from thiamine deficiency. Restlessness and sleeplessness are
observed.
    Cerebral beriberi 
: 
Clinical features are those of
encephalopathy plus psychosis. It is seen only when the nutritional
status is severely affected.
2. 
Polyneuritis:
 I
t is common in chronic alcoholics.
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the estimation of 
erythrocyte transketolase
activity  .( Reduced activity)
Other tests may be useful, including the
measurement of both 
blood and urinary
thiamine concentrations,
a raised 
blood pyruvate concentration 
is
suggestive as is a lactic acidosis
 
R
i
b
o
f
l
a
v
i
n
 
(
B
2
)
Sources
       Riboflavin is found in large amounts in yeasts
and germinating plants such as peas and beans,
and in smaller amounts in fish, poultry and meat.
Functions    it is incorporated in the form of
 flavine mononucleotide (
FMN
)
flavine adenine dinucleotide (
FAD
).
     Both FMN and FAD are reversible electron
carriers in 
biological oxidation systems
, which are,
in turn, oxidized by cytochromes
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)
deficiency of riboflavin  is
 
uncommon,
because riboflavin is synthesized by the
intestinal flora
.
 Riboflavin deficiency usually 
accompanies
other 
deficiency diseases 
such as 
beriberi
,
pellagra 
and
 
Kwashiorkor.
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1- The finding of a low erythrocyte activity of
glutathione reductase
(Riboflavin acts as a cofactor for this enzyme,
which increases by about 30 per cent after the
addition of FAD, suggests riboflavin deficiency.
 A low 
urinary riboflavin concentration
 may also
be a useful marker of deficiency. The treatment
for deficiency is to give riboflavin. Riboflavin
excess is very rare.
N
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(
n
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)
Nicotinamide is the active constituent of
  Nicotinamide adenine dinucleotide 
(NAD+)
 and its
phosphate  (
NADP+
),
     which are important cofactors in oxidation–
reduction reactions such as glycolysis and oxidative
phosphorylation, and for many synthetic processes.
Not : Reduced NAD+ and NADP+ are,  in turn,
re-oxidized by flavoproteins, and the functions
of riboflavin and nicotinamide are closely
linked
.
Sources
Nicotinamide can be formed in the body
from
   1- nicotinic acid.
  2-Some nicotinic acid can also be
synthesized in humans from tryptophan.
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Pellagra
Pellagra is an Italian word, meaning “rough
skin”.
Pellagra is caused by the deficiency of
Tryptophan as well as Niacin.
Pellagra is seen more in women; this may
be because tryptophan metabolism is
inhibited by estrogen metabolites.
The symptoms of pellagra are Dermatitis,
Diarrhea, Dementia
C
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 Dietary deficiency of nicotinamide
Deficient synthesis:
 
Isoniazid (INH): 
It is an antituberculous drug, which
inhibits pyridoxal phosphate formation. Hence, there is block
in conversion of tryptophan to NAD+.
Hartnup disease: 
Tryptophan absorption from intestine is
defective in this congenital disease.
    Moreover, tryptophan is excreted in urine in large quantities.
Carcinoid syndrome: 
The tumor utilizes major portion of
available tryptophan for synthesis of
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measuring urinary N-methylnicotinamide
concentration, which is low in deficiency.
Pyridoxine (B6)
Structure
Vitamin B6
Vitamin B6
 consists of a mixture of three different closely
related pyridine derivatives namely:
1
. 
. 
Pyridoxine
Pyridoxine
2. Pyridoxal
2. Pyridoxal
3. Pyridoxamine
3. Pyridoxamine
.
.
       All the three have 
equal vitamin activity,
equal vitamin activity,
 as they can
be interconverted in the body.
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V
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B
6
Pyridoxal phosphate (PLP)
Pyridoxal phosphate (PLP)
     
is the active form of vitamin B6 
 .  
PLP is
formed from 
phosphorylation of all three
forms of vitamin B6
.
F
F
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s
(
PLP
) acts as 
coenzyme 
in large number of
reactions 
of amino acid 
metabolism. For
example:
– Transamination
– Decarboxylation
– Nonoxidative deamination
– Trans-sulfuration
– Condensation reactions of amino acids
D
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As pyridoxine occurs in most foods, the dietary deficiency
of vitamin B6 is rare.
Deficiency Manifestations
Neurological
Dermatological
 Hematological
Not 
    
Doses over 100 mg 
may lead to 
sensory
neuropathy 
Further excess is manifested by 
imbalance,
numbness,  muscle weakness
 and nerve damage.
F
o
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A
c
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Active Form of Folic Acid
 
Tetrahydrofolate (THF) 
is the active
form of folic acid.
Folate is enzymatically reduced in a two-
stage process in tissues to yield the
dihydro and then tetrahydrofolate,  which
requires vitamin C
 
 
 
function of folic acid (THF)
THF acts as a carrier of one carbon units. The one
carbon units are
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P
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Neurological Manifestations;
Dermatological Manifestations and
 Hematological Manifestations
 
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Folate deficiency frequently occurs
particularly I pregnant women and in
alcoholics.
Clinical symptoms of folic acid deficiency
include:
Megaloblastic or macrocytic anemia
impairement
 of synthesis of 
DNA
 
and impairs the
maturation of erythrocytes.
 Consequently
 
Accumulation and excretion of FIGLU in the urine:
Folate deficiency blocks the last step of histidine catabolism,
due to lack of THF. This results in accumulation of FIGLU in
body, which leads to increased excretion of FIGLU in urine
Hyperhomocysteinemia:
 Due to folic acid deficiency the
methylation of homocysteine to methionine is impaired
which leads to hyperhomocysteinemia. Increased level of
homocystein is a risk factor for cardiovascular disease.
Neural tube defect in fetus:
     Since, folate is required for the formation of neural tube
in early stage of gestation, the folate deficiency during early
stage of pregnancy increases the risk of neural tube defect
B
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t
i
n
Biot  
was known formerly as vitamin H.
Biotin is an imidazole derivative It consists of a
tetrahydrothiophene 
ring bound to an imidazole ring
and a 
valeric acid 
side chain
Active Form of Biotin
Enzyme-bound biotin, 
biocytin 
is an active form of
biotin. Biotin is covalently bound to å-amino group of
lysine of an enzyme to form 
biocytin.
Functions
Biotin is a coenzyme of carboxylase reactions
,
where it is a carrier of CO2.
Deficiency Manifestation
 
• Since biotin is widely distributed in 
plant
 and
animal foods 
and 
intestinal bacterial flora
supply a
dequate amounts of 
biotin,
 the natural
deficiency of biotin is not well characterized
in humans.
But the using of antibiotics, that inhibit the
growth of intestinal bacteria, eliminates this
source of biotin and leads to deficiency of
biotin.
Pantothenic Acid (Vitamin B5)
 The name pantothenic acid is derived
from the 
Greek
 word 
pantothene
,’
meaning from 
“everywhere
and gives an
indication of the wide distribution of the
vitamin in foods
Structure of 
Pantothenic acid 
       
Pantothenic acid is formed by a
combination of 
pantoic acid 
and β
-
alanine 
.
Active form
Active forms of pantothenic acid are:
 Coenzyme-A (CoA-SH)
 Acyl carrier protein (ACP).
Functions
 Pantothenic acid
 
• The thiol (-SH) group of CoA-SH and ACP acts as a 
carrier
of acyl groups
.
Coenzyme-A
 participates in reactions concerned with:
– Reactions of 
citric acid 
cycle
Fatty acid
 synthesis and oxidation
– Synthesis of 
cholesterol
– Utilization of 
ketone bodies
.
ACP 
participate in reactions concerned with
- fatty acid synthesis.
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No clearcut case of pantothenic acid
deficiency has been reported.
  (becuase the substance is widely
distributed in  foods) except in
 
malnourished prisoners of war
C
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V
I
T
 
B
1
2
Thus, cobalamin exists in 
three forms 
that
differ in the 
nature of the chemical group
attached to cobalt
.
Cynocobalamin 
is the commercial available
form of vitamin B
12
.
Methylcobalamin
 
Deoxyadenosylcobalamin
 
 
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Vitamins play vital roles in the body, with each type serving specific functions. Explore the importance of vitamins such as Thiamine (B1) and Riboflavin (B2), their food sources, functions, clinical effects of deficiencies, and laboratory diagnosis methods. Learn how these essential nutrients support overall health and wellbeing.

  • Vitamins
  • Health
  • Thiamine
  • Riboflavin
  • Nutrients

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  1. Vitamins

  2. vitamins

  3. Vitamin B thiamine (B1), riboflavin (B2), nicotinamide (niacin), pyridoxine (B6), folate (pteroylglutamate), the vitamin B12 complex (cobalamins), biotin and pantothenate,

  4. Thiamine (B1) Humans cannot synthesize thiamine. It is found in many dietary components; food grains,rice ,

  5. Function ofThiamine B1 is a component of thiamine pyrophosphate, which is an essential cofactor for Decarboxylation of 2-oxoacids; pyruvate acetyl coenzymeA. In thiamine deficiency, pyruvate cannot be metabolized and accumulates in the blood. Transketolase in the pentose phosphate pathway.

  6. Clinical effects of thiamine deficiency Adequate amounts are present in a normal diet and deficiency is most common 1. Beriberi weakness . Wet beriberi: Here cardiovascular prominent ,death occurs due to heart failure. Dry beriberi: In this condition, CNS manifestations are the major features. Infantile beriberi:It occurs in infants born to mothers suffering from thiamine deficiency. Restlessness and sleeplessness are observed. Cerebral beriberi : Clinical encephalopathy plus psychosis. It is seen only when the nutritional status is severely affected. manifestations are features are those of 2.Polyneuritis: It is common in chronic alcoholics.

  7. Laboratory diagnosis of thiamine deficiency the estimation of erythrocyte transketolase activity .( Reduced activity) Other tests may be useful, including the measurement of both blood and urinary thiamine concentrations, a raised blood pyruvate concentration is suggestive as is a lactic acidosis

  8. Riboflavin (B2) Sources and germinating plants such as peas and beans, and in smaller amounts in fish,poultry and meat. Riboflavin is found in large amounts in yeasts Functions flavine mononucleotide (FMN) flavine adenine dinucleotide (FAD). it is incorporated in the form of Both FMN and FAD are reversible electron carriers in biological oxidation systems,which are, in turn,oxidized by cytochromes

  9. Riboflavin Deficiency (riboflavinosis) deficiency of riboflavin because riboflavin is synthesized by the intestinal flora. is uncommon, Riboflavin deficiency usually accompanies other deficiency diseases such as beriberi, pellagra and Kwashiorkor.

  10. diagnosis of riboflavin deficiency Laboratory 1- The finding of a low erythrocyte activity of glutathione reductase (Riboflavin acts as a cofactor for this enzyme, which increases by about 30 per cent after the addition of FAD,suggests riboflavin deficiency. A low urinary riboflavin concentration may also be a useful marker of deficiency. The treatment for deficiency is to give riboflavin. Riboflavin excess is very rare.

  11. Nicotinamide (niacin) Nicotinamide is the active constituent of Nicotinamide adenine dinucleotide (NAD+) and its phosphate (NADP+), which reduction reactions such as glycolysis and oxidative phosphorylation,and for many synthetic processes. are important cofactors in oxidation Not : Reduced NAD+ and NADP+ are, in turn, re-oxidized by flavoproteins, and the functions of riboflavin and nicotinamide are closely linked.

  12. Sources Nicotinamide can be formed in the body from 1- nicotinic acid. 2-Some nicotinic synthesized in humans from tryptophan. acid can also be

  13. Clinical effects of nicotinamide deficiency Pellagra

  14. Pellagra is an Italian word,meaning rough skin . Pellagra is caused by the deficiency of Tryptophan as well as Niacin. Pellagra is seen more in women; this may be because tryptophan metabolism is inhibited by estrogen metabolites. The symptoms of pellagra are Dermatitis, Diarrhea,Dementia

  15. Causes of nicotinamide deficiency Dietary deficiency of nicotinamide Deficient synthesis: Isoniazid (INH): It is an antituberculous drug, which inhibits pyridoxal phosphate formation. Hence, there is block in conversion of tryptophan to NAD+. Hartnup disease: Tryptophan absorption from intestine is defective in this congenital disease. Moreover,tryptophan is excreted in urine in large quantities. Carcinoid syndrome: The tumor utilizes major portion of available tryptophan for synthesis of

  16. Laboratory diagnosis of nicotinamide deficiency measuring urinary N-methylnicotinamide concentration,which is low in deficiency.

  17. Pyridoxine (B6) Structure Vitamin B6 consists of a mixture of three different closely related pyridine derivatives namely: 1.Pyridoxine 2.Pyridoxal 3.Pyridoxamine. All the three have equal vitamin activity, as they can be interconverted in the body.

  18. Active Form of Vitamin B6 Pyridoxal phosphate (PLP) is the active form of vitamin B6 . PLP is formed from phosphorylation of all three forms of vitamin B6.

  19. Functions (PLP) acts as coenzyme in large number of reactions of amino acid metabolism. For example: Transamination Decarboxylation Nonoxidative deamination Trans-sulfuration Condensation reactions of amino acids

  20. Deficiency As pyridoxine occurs in most foods, the dietary deficiency of vitamin B6 is rare. Deficiency Manifestations Neurological Dermatological Hematological Doses over 100 mg may lead to sensory Not neuropathy Further excess is manifested by imbalance, numbness, muscle weakness and nerve damage.

  21. Folic Acid Active Form of FolicAcid Tetrahydrofolate (THF) is the active form of folic acid. Folate is enzymatically reduced in a two- stage process in tissues to yield the dihydro and then tetrahydrofolate, which requires vitamin C

  22. function of folic acid (THF) THF acts as a carrier of one carbon units. The one carbon units are

  23. Deficiency Manifestations of Pyridoxine Neurological Manifestations; Dermatological Manifestations and Hematological Manifestations

  24. Deficiency Manifestations Folate particularly I pregnant women and in alcoholics. Clinical symptoms of folic acid deficiency include: deficiency frequently occurs

  25. Megaloblastic or macrocytic anemia impairement maturation of erythrocytes. Consequently of synthesis of DNA and impairs the Accumulation and excretion of FIGLU in the urine: Folate deficiency blocks the last step of histidine catabolism, due to lack of THF. This results in accumulation of FIGLU in body,which leads to increased excretion of FIGLU in urine

  26. Hyperhomocysteinemia: Due to folic acid deficiency the methylation of homocysteine to methionine is impaired which leads to hyperhomocysteinemia. Increased level of homocystein is a risk factor for cardiovascular disease. Neural tube defect in fetus: Since, folate is required for the formation of neural tube in early stage of gestation, the folate deficiency during early stage of pregnancy increases the risk of neural tube defect

  27. Biotin Biot was known formerly as vitamin H. Biotin is an imidazole derivative It consists of a tetrahydrothiophene ring bound to an imidazole ring and a valeric acid side chain Active Form of Biotin Enzyme-bound biotin, biocytin is an active form of biotin. Biotin is covalently bound to -amino group of lysine of an enzyme to form biocytin. Functions Biotin is a coenzyme of carboxylase reactions, where it is a carrier of CO2.

  28. Deficiency Manifestation Since biotin is widely distributed in plant and animal foods and intestinal bacterial flora supply adequate amounts of biotin, the natural deficiency of biotin is not well characterized in humans. But the using of antibiotics, that inhibit the growth of intestinal bacteria, eliminates this source of biotin and leads to deficiency of biotin.

  29. PantothenicAcid (Vitamin B5) The name pantothenic acid is derived from the Greek word pantothene, meaning from everywhere and gives an indication of the wide distribution of the vitamin in foods

  30. Structure of Pantothenic acid Pantothenic combination of pantoic acid and - alanine . acid is formed by a Active form Active forms of pantothenic acid are: Coenzyme-A (CoA-SH) Acyl carrier protein (ACP).

  31. Functions Pantothenic acid The thiol (-SH) group of CoA-SH and ACP acts as a carrier of acyl groups. Coenzyme-A participates in reactions concerned with: Reactions of citric acid cycle Fatty acid synthesis and oxidation Synthesis of cholesterol Utilization of ketone bodies. ACP participate in reactions concerned with - fatty acid synthesis.

  32. Deficiency Manifestations No clearcut case of pantothenic acid deficiency has been reported. (becuase distributed in foods) except in malnourished prisoners of war the substance is widely

  33. CobalaminVIT B12

  34. Thus, cobalamin exists in three forms that differ in the nature of the chemical group attached to cobalt. Cynocobalamin is the commercial available form of vitamin B12. Methylcobalamin Deoxyadenosylcobalamin

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