Vitamins relationship

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Interrelationship Between Vitamins Vitamins & Cofactors Total slides : 22 1 June 13, 2022 Isfahan University of Medical Science, School of Pharmacy Department of Clinical Biochemistry

description

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.

Transcript of Vitamins relationship

Page 1: Vitamins relationship

Interrelationship Between VitaminsVitamins & Cofactors

Total slides : 22 1April 12, 2023

Isfahan University of Medical Science, School of Pharmacy

Department of Clinical Biochemistry

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Vitamins interrelationship

Vitamins interrelationship

(An overview)(An overview)

By:

A.N. Emami Razavi

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Outlines Outlines

Introduction B complex interactions Interrelationship between thiamin and riboflavin Interrelationship between vit. B12 and vit.E Interrelationship between vit. B12 and folate Interrelationship between vit. B12 and vit.C Interrelationship between vit. B12 and vit.B5 Interrelationship between vit. E and vit.C Interrelationship between vit. E and vit.A Interrelationship between vit. K and vit.D

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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.

Introduction

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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.

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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.

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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.

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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.

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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.

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Interrelationship between vitamin B12 and folate.

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

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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.

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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.

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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.

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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.

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Metabolic Interrelationships Between Vitamin BI2and 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.

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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.

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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.

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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.

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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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