V i t a m i n s vitamins - PowerPoint Presentation

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Vitamins

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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,

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

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Function of Thiamine B1is 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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Clinical effects of thiamine deficiencyAdequate 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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Laboratory diagnosis of thiamine deficiencythe 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

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Riboflavin (B2)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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Riboflavin Deficiency(riboflavinosis) 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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diagnosis of riboflavin deficiencyLaboratory1- 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. 

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Nicotinamide (niacin)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

.

 

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SourcesNicotinamide 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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Clinical effects of nicotinamide deficiencyPellagra

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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

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Causes of nicotinamide deficiency Dietary deficiency of nicotinamideDeficient 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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Laboratory diagnosis of nicotinamide deficiencymeasuring urinary N-methylnicotinamide concentration, which is low in deficiency.  

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Pyridoxine (B6)StructureVitamin B6 consists of a mixture of three different closely related pyridine derivatives namely:1. Pyridoxine2. Pyridoxal

3.

Pyridoxamine

.

All

the three have

equal vitamin activity,

as they can

be

interconverted

in the body.

 

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Active Form of Vitamin B6Pyridoxal phosphate (PLP) is the active form of vitamin B6 . PLP is formed from phosphorylation of all three forms of vitamin B6. 

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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

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DeficiencyAs pyridoxine occurs in most foods, the dietary deficiency of vitamin B6 is rare.Deficiency ManifestationsNeurologicalDermatological HematologicalNot Doses over 100 mg may lead to

sensory neuropathy

Further excess is manifested by

imbalance, numbness, muscle weakness

and nerve damage.

 

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Folic Acid 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

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

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

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

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• Megaloblastic or macrocytic anemiaimpairement 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 

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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    

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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 chainActive Form of BiotinEnzyme-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.

 

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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. 

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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

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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).

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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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Deficiency ManifestationsNo clearcut case of pantothenic acid deficiency has been reported. (becuase the substance is widely distributed in foods) except in malnourished prisoners of war  

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Cobalamin VIT B12

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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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