Vitamins relationship

Vitamins & Cofactors Interrelationship Between Vitamins

Isfahan University of Medical Science, School of Pharmacy
Department of Clinical Biochemistry

June 26, 2012 Total slides : 22 1

Vit amins
interrelationship

(An overview)

By:
A.N. Emami Razavi


O u t lin e s

 In t r o d u c t io n
 B c o m p l e x in t e r a c t io n s
 In t e r r e l a t io n s h ip b e t w een t h ia m in a n d r ib o f l a v in
 In t e r r e l a t io n s h ip b e t w een v it . B 1 2 a n d v it .E
 In t e r r e l a t io n s h ip b e t w een v it . B 1 2 a n d f o l a t e
 In t e r r e l a t io n s h ip b e t w een v it . B 1 2 a n d v it .C
 In t e r r e l a t io n s h ip b e t w een v it . B 1 2 a n d v it .B 5
 In t e r r e l a t io n s h ip b e t w een v it . E a n d v it .C
 In t e r r e l a t io n s h ip b e t w een v it . E a n d v it .A
 In t e r r e l a t io n s h ip b e t w een v it . K a n d v it .D



Introduction
The effects of a deficiency of one vitamin would not ordinarily
be expected to be highly dependent on the presence or absence
of another vitamin in the diet, since the symptoms of
deficiency of each vitamin are usually quite distinct.
Nevertheless, antagonistic or synergistic interactions between
vitamins may occur to a greater or less extent. While several
mechanisms can be proposed whereby vitamins can be
synergistic, it is more difficult to conceive of one which could
explain vitamin antagonism.



B complex interactions
Positive interactions
 Certain vitamins of the B-complex (niacin, riboflavin, biotin)
may act synergistically with pyridoxine.

Negative interactions
 Pyridoxine requires riboflavin, zinc and magnesium to fulfil
its physiological function in humans. It has been claimed that
women taking oral contraceptives may have an increased
requirement for pyridoxine.



 Interactions between the vitamins thiamine, riboflavin,
pyridoxine and pantothenate were sought by comparing the
growth of rats on diets deficient in two vitamins with diets
deficient on a single vitamin. No antagonistic interactions
were found. Thiamine and riboflavin and thiamine and
pyridoxine had some synergistic action on growth, but the
only marked interaction found was a synergistic effect of
pyridoxine and pantothenate.

 No evidence of interaction between the 4 principal B vitamins
and niacin, biotin, inositol, p-aminobenzoic acid, folie acid,
choline and vitamin B12 and K was obtained. Penicillin in the
diet increased growth in all single and combined deficiences,
while 5% of ascorbic acid increased growth in all cases except
pyridoxine and combined pyridoxine and pantothenate
deficiencies.


 Sure and Ford ('42) reported that in thiamine deficiency there
is a pronounced disturbance in riboflavin metabolism.

 It is apparent from the results of the experiments submitted by
Barnett Sube that a definite thiamine-riboflavin
interrelationship exists in chronic as well as in acute thiamine
deficiency.



Interrelationship between thiamin and riboflavin

 The riboflavin concentration in the liver was found to be
significantly increased in thiamine-deficient rats, and
riboflavin-deficient rats had an increased concentration of
thiamine in the liver. Furthermore, withdrawal of all B
vitamins except choline resulted in a rapid loss of thiamine,
but the level of riboflavin in the liver remained relatively
stable for a long period.
 On the other hand, the level of thiamine and of riboflavin in
the liver of animals severely depleted in pyridoxine,
pantothenic acid, or biotin failed to show significant
deviations from that of control animals receiving adequate
amounts of these vitamins.



Possible interrelationship between vitamin E and
B12
 The disturbance in 2-methylmalonate metabolism resulting in its increased
urinary excretion observed in vitamin E deficiency is not caused by
increased formation of methylmalonate from propionate as is evident from
the activity of the enzyme propionyl-CoA carboxylase (EC 6.4.1.3), but
can be traced to an impairment in the conversion of methylmalonate into
succinate by the vitamin B12-requiring enzyme, methylmalonyl-CoA
mutase (EC 5.4.99.2) in rat liver.

 It is shown that the decrease in the activity of methylmalonyl-CoA mutase
in vitamin E deficiency is not a consequence of a secondary vitamin B12
deficiency. Peroxidative destruction of the coenzyme in vitamin E
deficiency was also ruled out. The results suggest a defect in the
conversion of cyanocobalamin into its coenzyme form.



Interrelationship between vitamin B12 and folate.

 The metabolism and intracellular recycling of methionine
requires vitamin B12 as cofactor and methyltetrahydrofolate
as coreactant.



 The biochemical basis of the interrelationship between folate
and cobalamin is the maintenance of two functions, nucleic
acid synthesis and the methylation reactions. The latter is
particularly important in the brain and relies especially on
maintaining the concentration of S-adenosylmethionine
(SAM) which, in turn, maintains the methylation reactions
whose inhibition is considered to cause cobalamin deficiency
associated neuropathy. SAM mediated methylation reactions
are inhibited by its product S-adenosylhomocysteine (SAH).

 This occurs when cobalamin is deficient and, as a result,
methionine synthase is inhibited causing a rise of both
homocysteine and SAH. Other potential pathogenic processes
related to the toxic effects of homocysteine are direct damage
to the vascular endothelium and inhibition of N-methyl-
Daspartate receptors.



Control of entry of folate into cells and the interrelation of
intracellular folate and cobalamin. Reactions: 1, methionine synthase; 2,
S-adenosylmethionine synthetase; 3, S-adenosylhomocysteine hydrolase,
4, methylene tetrahydrofolate reductase; 5, serine hydroxy methyl
transferase; 6, tetrahydrofolate glutamate ligase; 7, dihydrofolate reductase.



Reactions involving folate and cobalamin interrelationships with particular reference to the
brain. Reactions present and active in the brain have solid lines, those not present or inactive in the
brain are shown as dotted lines. Reactions 1-7 are as in the caption to Figure 1. Other reactions: 8,
thymidylate synthetase; 9, cystathionine synthetase; 10, cystathionine lyase; 11, betaine methyl
transferase; and 12, glycine methyl transferase.



Metabolic Interrelationship between Vitamin B12
and Ascorbic Acid in Pernicious Anemia

 Subnormal plasma ascorbic acid concentration and rapid
plasma ascorbate clearance have been found in patients with
vitamin B12 deficiency despite adequate intake of vitamin C.

 In this patient despite long term administration of high doses
of vitamin C, the plasma ascorbate concentration did not
become normal until MMA excretion was abolished.These
data suggested that the plasma ascorbate concentration is
related to the excretion of MMA and is directly or indirectly
related to vitamin B12 stores.



Metabolic Interrelationships Between Vitamin BI2
and Pantothenic Acid
 Interrelationships between pantothenic acid and vitamin B12in
the nutrition of different species of animals have been re
ported.

 Boxer et al. observed a fivefold increase in the coenzyme-A
concentration of liver in vitamin B12-deficient chicks.

 Further studies with rats, although confirming the earlier
observations, revealed that increases were also observable in
the kidney, although not in the brain. It was also evident that
the increase was due neither to a decreased destruction of
coenzyme A in the deficient tissues, nor to a shift in the ratio
of the oxidized to the active reduced form of coenzyme A.


 Similar observations have since been reported by others and it
has been suggested that since the vitamin B12-deficient animal
cannot utilize carbohydrate efficiently , the increase in liver
coenzyme A may be a physiological adaptive mechanism that
increases energy production by providing more two carbon
fragments from fatty acid oxidation.

 The vitamin Bi2-deficient animal showed greater in vivo
synthesis of coenzyme A from intraperitoneally administered
precursors, than the vitamin-supplemented animal. Prior
administration of vitamin B12 to the deficient animal
decreased the coenzyme A synthesis.



Vitamin E, vitamin C, and exercise
 Exercise increases the generation of oxygen free radicals and
lipid peroxidation.

 Vitamin C (ascorbic acid), which is water soluble and present
in the cytosolic compartment of the cell, serves as an electron
donor to vitamin E radicals generated in the cell membrane
during oxidative stress.

 The positive health benefits of using vitamins E and C may
suggest an additive or synergistic effect when combined with
regular exercise.



Interrelationship between vitamins E and A in calves

 dietary tocopherol may increase as well as decrease the
utilization of vitamin A in the dairy calf. Tocopherol caused
increases in utilization of vitamin A at the highest intake of the
latter, decreases at the lowest intake of vitamin A, and little
change at the middle intake of this vitamin.

 Whether or not toeopherol acts on vitamin A only in the
alimentary tract or in the body proper is controversial.

 Evidence indicated that the majority of the activity occurs in
the alimentary tract and some of its activity occurs within the
body proper.



Vitamin K and Osteoporosis:
 it was shown that vitamin D and vitamin K treatments had
synergistic effects in treating the disease.


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