Water – soluble VitaminsWater – soluble Vitamins

folic acid

folic acid

cobalamin

cobalamin

ascorbic acid

ascorbic acidpyridoxine

pyridoxine

Thiamine

Thiamine

Riboflavin

Riboflavin

niacinniacin

biotinbiotin

pantothenic acid

pantothenic acid

Water – soluble VitaminsWater – soluble Vitamins

VitaminsVitamins : : areare– chemically unrelated organic compoundschemically unrelated organic compounds– cannot be synthesized by humans cannot be synthesized by humans – must be supplied by the diet. must be supplied by the diet.

water-solublewater-soluble VitaminsVitamins;;– folic acid - cobalamin (B12) folic acid - cobalamin (B12) – ascorbic acid (C) - pyridoxine (B6) ascorbic acid (C) - pyridoxine (B6) – Thiamine (B1) - niacin (B3) Thiamine (B1) - niacin (B3) – Riboflavin (B2) - biotin Riboflavin (B2) - biotin – pantothenic acid pantothenic acid

Many of the water-soluble vitamins are precursors Many of the water-soluble vitamins are precursors of coenzymes for the enzymes of intermediary of coenzymes for the enzymes of intermediary metabolism. metabolism.

FOLIC ACID FOLIC ACID (Folate)(Folate)

Plays a key role in one-carbon metabolism.Plays a key role in one-carbon metabolism.

Essential for the biosynthesis of AA, purines, thymine...etc. Essential for the biosynthesis of AA, purines, thymine...etc.

Folic acid deficiency is the most common vitamin deficiency Folic acid deficiency is the most common vitamin deficiency in the United States, particularly among pregnant women in the United States, particularly among pregnant women and alcoholics.and alcoholics.

Serine, glycine, and histidine Serine, glycine, and histidine one-carbon fragments one-carbon fragments to Tetrahydrofolate to Tetrahydrofolate transfers them to intermediates transfers them to intermediates in the synthesis of amino acids, purines, and thymine - in the synthesis of amino acids, purines, and thymine - a pyrimidine found in DNA. a pyrimidine found in DNA.

Function of Folic acidFunction of Folic acid

Nutritional anemiasNutritional anemias • Low blood [Hb] O2 transport Anemia

a) Microcytic anemia (MCV<80 m3):

• caused by lack of iron• the most common form of

nutritional anemia.

b) Macrocytic anemias (MCV>100 m3):

• due to folic acid or vit B12 def.• called megaloblastic because folic acid or vit B12 def. accumulation of large, immature red cell precursors

(megaloblasts) in the bone marrow.

Nutritional anemias : classified according to RBC size or MCV.

Folate and anemiaFolate and anemia : :

– The causes of the megaloblastic anemia should be evaluated prior to The causes of the megaloblastic anemia should be evaluated prior to instituting therapy because vitamin Binstituting therapy because vitamin B1212 deficiency deficiency indirectly causes indirectly causes this disorder.this disorder.

Causes of Causes of serum serum folate levelsfolate levels

increased demandincreased demand::• PregnancyPregnancy• LactationLactation

poor absorptionpoor absorption::• pathology of gutpathology of gut• AlcoholismAlcoholism• ttt with : Methotrexate ttt with : Methotrexate (DHF reductase inhibitor)(DHF reductase inhibitor)

folate-free dietfolate-free diet

Results of Results of folic acid deficiencyfolic acid deficiency

megaloblastic anemia due to synthesis of purines and thymidine DNA synthesis and cell division.

Folate and neural tube defects in the fetusFolate and neural tube defects in the fetus::

Spina bifidaSpina bifida and and anencephalyanencephaly, the most common neural , the most common neural tube defects.tube defects.

affect ~ 4000 pregnancies in USA / year. affect ~ 4000 pregnancies in USA / year.

Folic acid supplementation before conception and during Folic acid supplementation before conception and during the first trimester ( 0.4 mg/day) the first trimester ( 0.4 mg/day) the risk of neural tube the risk of neural tube defects in the fetus. defects in the fetus.

The U.S. FDA has authorized the addition of folic acid to The U.S. FDA has authorized the addition of folic acid to enriched grain products, ( about 0.1 mg day). enriched grain products, ( about 0.1 mg day).

This supplementation will allow ~ 50% of all reproductive-This supplementation will allow ~ 50% of all reproductive-aged women to receive 0.4 mg of folate from all sources. aged women to receive 0.4 mg of folate from all sources.

Folic acid intake should not exceed ~ 1 mg/day to avoid Folic acid intake should not exceed ~ 1 mg/day to avoid misdiagnosis of vit Bmisdiagnosis of vit B1212 deficiency. deficiency.

COBALAMIN (VITAMIN B12)COBALAMIN (VITAMIN B12)

• Required in humans for Required in humans for 2 essential enzymatic 2 essential enzymatic reactions:reactions: A) Methionine synthesisA) Methionine synthesis

B)B) isomerization of isomerization of methylmalonyl CoAmethylmalonyl CoA (produced during the (produced during the degradation of some AA, degradation of some AA, and fatty acids with odd and fatty acids with odd numbers of carbon atoms)numbers of carbon atoms)

Deficiency of B12Deficiency of B12

accumulation of accumulation of

abnormal fatty acidsabnormal fatty acids

incorporated into cell incorporated into cell

membranes, including membranes, including

nervous systemnervous system

neurologic neurologic

manifestationsmanifestations . .

A. Structure of cobalamin and its coenzyme formsA. Structure of cobalamin and its coenzyme forms

cyanide is cyanide is replaced by replaced by CH3 groupCH3 group

cyanide is replaced with cyanide is replaced with 5-deoxyadenosine5-deoxyadenosine

CobaltCobalt is held in the center of the corrin is held in the center of the corrin ring by four coordination bonds from the ring by four coordination bonds from the nitrogens of the pyrrole groupsnitrogens of the pyrrole groups

differs from the porphyrins in differs from the porphyrins in that two of the pyrrole rings are that two of the pyrrole rings are linked directly rather than linked directly rather than through a CH3 bridgethrough a CH3 bridge

CoordinationCoordination bondsbonds

Distribution of vit B12Distribution of vit B12: :

Vitamin B12 is synthesized only by Vitamin B12 is synthesized only by microorganisms.microorganisms.

It is not present in plants. It is not present in plants.

Animals obtain the vitamin preformed from:Animals obtain the vitamin preformed from:– their natural bacterial flora. their natural bacterial flora. – by eating foods derived from other animals. by eating foods derived from other animals.

• liver liver • whole milk whole milk • eggs eggs • oysters oysters • fresh shrimp fresh shrimp • chicken chicken

B12 is present in:B12 is present in:

Folate trap hypothesisFolate trap hypothesis: :

need both Nneed both N55-N-N1010-methylene & -methylene & NN1010- formyl forms of THF for - formyl forms of THF for nucleotides synthesis required nucleotides synthesis required for DNA replication.for DNA replication.

• the erythropoietic tissue of bone marrow the erythropoietic tissue of bone marrow • the mucosal cells of the intestinethe mucosal cells of the intestine

B12 deficiency affects:B12 deficiency affects:

BB1212 deficiency deficiency is hypothesized to is hypothesized to deficiency of the deficiency of the THF forms needed in purine and thymine synthesis, THF forms needed in purine and thymine synthesis, megaloblastic anemiamegaloblastic anemia..

• Methylated form of THF cannot be converted directly to Methylated form of THF cannot be converted directly to other forms other forms accumulation of he N accumulation of he N55-methyl form & -methyl form & of of other forms.other forms.

• In BIn B1212 deficiency, the N deficiency, the N33-methyl form of tetrahydrofolate is -methyl form of tetrahydrofolate is

not efficiently used.not efficiently used.

Clinical indications for vitamin B12Clinical indications for vitamin B12

Unlike other water-sol Vitamins, significant amounts of Unlike other water-sol Vitamins, significant amounts of vitamin B12 (4 - 5 mg) are stored in the body.vitamin B12 (4 - 5 mg) are stored in the body.

SO,SO,

Development of clinical symptoms of B12 deficiency take Development of clinical symptoms of B12 deficiency take several years in individuals with partial or total gastrectomy several years in individuals with partial or total gastrectomy (intrinsic factor-deficient with loss of B12 absorption)(intrinsic factor-deficient with loss of B12 absorption)..

Pernicious anemiaPernicious anemia : :• Vitamin B12 deficiency is Vitamin B12 deficiency is rarely due to dietary rarely due to dietary insufficiency.insufficiency.

• Deficiencies are more Deficiencies are more common in patients with common in patients with intestinal malabsorption of the intestinal malabsorption of the vitamin vitamin pernicious anemia. pernicious anemia.

Autoimmune destruction of Autoimmune destruction of the gastric parietal cells the gastric parietal cells synthesis of the synthesis of the intrinsic intrinsic factorfactor (Glycoprotein)(Glycoprotein)..

NormallyNormally, dietary vitamin B12 , dietary vitamin B12 binds to intrinsic factorbinds to intrinsic factor in the intestine in the intestine cobalamin - intrinsic factor complexcobalamin - intrinsic factor complex travels through the gut travels through the gut binds to specific receptorsbinds to specific receptors on the surface of mucosal cells of the ileum on the surface of mucosal cells of the ileum transported into the mucosal cell transported into the mucosal cell general circulation general circulation carried by carried by B12-binding proteins. B12-binding proteins.

– Lack of intrinsic factorLack of intrinsic factor prevents vitamin B12 prevents vitamin B12

absorption absorption pernicious anemiapernicious anemia. .

– Neuropsychiatric symptoms Neuropsychiatric symptoms develops laterdevelops later . .

– CNS symptoms may occur in the absence of anemia. CNS symptoms may occur in the absence of anemia.

– The The CNS effectsCNS effects are are irreversibleirreversible. .

– by giving high-dose B12 orally, or cyanocobalamin IM.by giving high-dose B12 orally, or cyanocobalamin IM.

– Therapy must be continued throughout the lives of Therapy must be continued throughout the lives of patients with pernicious anemia. patients with pernicious anemia.

TreatmentTreatment

Folic acid administration aloneFolic acid administration alone reverses the hematologic abnormality reverses the hematologic abnormality masks the B12 deficiencymasks the B12 deficiency severe neurologic dysfunction and pathologysevere neurologic dysfunction and pathology; ;

therefore, therefore, megaloblastic anemiamegaloblastic anemia should be treated with a should be treated with a combination of combination of folate and vitamin B12folate and vitamin B12

ASCORBIC ACID (VITAMIN C)ASCORBIC ACID (VITAMIN C)

The active form of vitamin C is ascorbic acid.The active form of vitamin C is ascorbic acid.The The main functionmain function is as a is as a reducing agentreducing agent in several different reactions. in several different reactions. Vitamin C has an essential role as a coenzyme in hydroxylation reactions, Vitamin C has an essential role as a coenzyme in hydroxylation reactions, e.g, e.g, hydroxylation of prolyl- and lysyl-residues of collagenhydroxylation of prolyl- and lysyl-residues of collagen . .

Vitamin C is Vitamin C is required forrequired for::– maintenance of normal connective tissuemaintenance of normal connective tissue– wound healingwound healing– facilitates the absorption of dietary iron from the intestinefacilitates the absorption of dietary iron from the intestine. .

Deficiency of ascorbic acidDeficiency of ascorbic acid::

Deficiency of ascorbic acid Deficiency of ascorbic acid deficiency in the deficiency in the hydroxylation of collagen hydroxylation of collagen defective connective tissue defective connective tissue scurvy. scurvy.

soresore spongy gumsspongy gums loose teethloose teeth fragile blood vesselsfragile blood vessels swollen jointsswollen joints anemiaanemia

Scurvy

Prevention of chronic diseasePrevention of chronic disease : :

Vitamin CVitamin C , , vitamin Evitamin E and and -carotene-carotene are known as are known as antioxidantsantioxidants..

Consumption of food or supplements rich in these Consumption of food or supplements rich in these compoundscompounds Coronary heart disease Coronary heart disease and certain and certain cancerscancers. .

Supplementation with the isolated antioxidants have low Supplementation with the isolated antioxidants have low

beneficial effects.beneficial effects.

PYRIDOXINE (VITAMIN B6)PYRIDOXINE (VITAMIN B6)

They differ only in the nature of the They differ only in the nature of the functional groupfunctional group attached to the ring attached to the ring

primarily in plantsprimarily in plants

in animal in animal foods foods

All three compoundsAll three compounds can serve as can serve as precursors of the biologically precursors of the biologically active coenzymeactive coenzyme, , pyridoxal pyridoxal phosphate.phosphate.

PyridoxinePyridoxine pyridoxalpyridoxal pyridoxamine, pyridoxamine,

DerivativesDerivatives of of pyridinepyridine..

Pyridoxal phosphatePyridoxal phosphate functions as a functions as a coenzyme coenzyme catalyze reactions catalyze reactions involving amino acidsinvolving amino acids

Reaction typeReaction typeExampleExample

Transamination Transamination Oxaloacetate + glutamate Oxaloacetate + glutamate aspartate + α-ketoglutarateaspartate + α-ketoglutarate

Deamination Deamination Serine Serine pyruvate + NH3 pyruvate + NH3

Decarboxylation Decarboxylation Histidine Histidine histamine + CO2 histamine + CO2

Condensation Condensation Glycine + succinyl CoAGlycine + succinyl CoA δ- δ-aminolevulinic acid aminolevulinic acid

Clinical indications for pyridoxineClinical indications for pyridoxine::

Isoniazid Isoniazid (isonicotinic acid hydrazide),(isonicotinic acid hydrazide), [a drug frequently [a drug frequently used to treat TB]used to treat TB] B6 deficiencyB6 deficiency by forming an inactive by forming an inactive derivative with pyridoxal phosphate. derivative with pyridoxal phosphate.

Dietary supplementation with B6Dietary supplementation with B6 is important with is important with isoniazide treatment. isoniazide treatment.

Dietary deficiencies in pyridoxine are Dietary deficiencies in pyridoxine are rarerare but observed inbut observed in::– newborn infants fed formulas low in vitamin B6newborn infants fed formulas low in vitamin B6– women taking oral contraceptives women taking oral contraceptives – alcoholics. alcoholics.

Toxicity of pyridoxineToxicity of pyridoxine::

intakes of greater than 2 g/day intakes of greater than 2 g/day

Neurologic symptomsNeurologic symptoms

Substantial improvement, but Substantial improvement, but not not complete recoverycomplete recovery, occurs when the , occurs when the vitamin is discontinuedvitamin is discontinued

Thiamine Thiamine pyrophosphate pyrophosphate (TPP) is:(TPP) is:

the biologically active the biologically active form of the vitamin,form of the vitamin,

formed by the formed by the transfer of a transfer of a pyrophosphate group pyrophosphate group from ATP to thiaminefrom ATP to thiamine

THIAMINE (VITAMIN B1)THIAMINE (VITAMIN B1)

PP from ATP

Thiamine pyrophosphate (TPP)Thiamine pyrophosphate (TPP) serves serves as a coenzymeas a coenzyme in : in :

the oxidative decarboxylationthe oxidative decarboxylation of pyruvate and α -keto acidsof pyruvate and α -keto acids

Important for CNSImportant for CNS

the formation or degradation ofthe formation or degradation of α-ketols by transketolaseα-ketols by transketolase

Clinical indications for thiamineClinical indications for thiamine::

Thiamine deficiencyThiamine deficiency:: activity of dehydrogenase reactions activity of dehydrogenase reactions

ATP ATP impaired cellular function. impaired cellular function.

Thiamine deficiencyThiamine deficiency is is diagnosed by:diagnosed by: erythrocyte transketolase erythrocyte transketolase activityactivity observed on addition of TPP. observed on addition of TPP.

Beri beriBeri beri::

– Severe thiamine-deficiency syndrome.Severe thiamine-deficiency syndrome.– Found in areas where polished rice is the major Found in areas where polished rice is the major

component of the diet. component of the diet. – Rapid onset in nursing infants whose mothers are Rapid onset in nursing infants whose mothers are

deficient in thiamine. deficient in thiamine.

– tachycardiatachycardia

– vomitingvomiting

– convulsionsconvulsions

– death death (if untreated)(if untreated)

- dry skindry skin- irritabilityirritability- disorderly thinkingdisorderly thinking- progressive paralysisprogressive paralysis

Adult beriberiAdult beriberiinfantile beriberiinfantile beriberi

Wernicke-Korsakoff syndromeWernicke-Korsakoff syndrome::

– In the United States, thiamine deficiency, which is In the United States, thiamine deficiency, which is seen primarily with chronic alcoholism, is due to:seen primarily with chronic alcoholism, is due to:

dietary insufficiency. dietary insufficiency.

impaired intestinal absorption of the vitamin. impaired intestinal absorption of the vitamin.

Some alcoholicsSome alcoholics

Wernicke - KorsakoffWernicke - Korsakoff syndromesyndrome

- apathy, - apathy, - loss of memory - loss of memory - rhythmical to-and-fro motion of the eyeballs- rhythmical to-and-fro motion of the eyeballs

NIACINNIACIN

Niacin, or Niacin, or nicotinic acid, nicotinic acid, is a is a substituted pyridine derivativesubstituted pyridine derivative

The biologically active coenzyme formsThe biologically active coenzyme forms are: are:

1.1. nicotinamide adenine dinucleotide (NAD) nicotinamide adenine dinucleotide (NAD) and its phosphorylated and its phosphorylated derivative,derivative,

2.2. nicotinamide adenine dinucleotide phosphate (NADP)nicotinamide adenine dinucleotide phosphate (NADP)

NicotinamideNicotinamide, , a derivative of nicotinic acid that contains an a derivative of nicotinic acid that contains an amide instead of a carboxyl groupamide instead of a carboxyl group, , deaminated in the deaminated in the bodybody So it is So it is nutritionally equivalent to nicotinic acid.nutritionally equivalent to nicotinic acid.

NADNAD++ and and NADPNADP++

serve as serve as coenzymes incoenzymes in

oxidation-reduction oxidation-reduction

reactionsreactions in which the in which the

coenzyme undergoes coenzyme undergoes

reduction of the pyridine reduction of the pyridine

ring by accepting a ring by accepting a

hydride ion hydride ion (hydrogen (hydrogen

atom plus one electron)atom plus one electron)

The The reduced forms:reduced forms:

NADNAD++ NADHNADH

NADPNADP++ NADPHNADPH

A. Distribution of niacinA. Distribution of niacin

unrefined and enriched grains and cerealsunrefined and enriched grains and cereals milkmilk lean meats especially liver.lean meats especially liver.

Sources

Limited quantitiesLimited quantities of niacin can also be of niacin can also be obtained from obtained from metabolism of tryptophan metabolism of tryptophan..

6060 mgmg tryptophantryptophan 1 mg1 mg nicotinic acidnicotinic acid

tryptophan is metabolized to niacin only when tryptophan is metabolized to niacin only when there is a relative abundance of the amino acidthere is a relative abundance of the amino acid

B. Clinical indications for niacinB. Clinical indications for niacin: :

Deficiency of niacinDeficiency of niacin

PellagraPellagra

DDermatitisermatitisDDiarrheaiarrheaDDementiaementia

DeathDeath

if untreatedif untreated

Treatment of hyperlipidemiaTreatment of hyperlipidemia::

NiacinNiacin is particularly useful in the treatment of is particularly useful in the treatment of type lIb type lIb hyperlipoproteinemia (hyperlipoproteinemia (in which in which VLDL & LDL ). VLDL & LDL ).

inhibits lipolysis in adipose tissueinhibits lipolysis in adipose tissue ( the primary producer of circulating free fatty acids).( the primary producer of circulating free fatty acids).

NiacinNiacin ))at doses of 1.5 g /day or 100 times the RDAat doses of 1.5 g /day or 100 times the RDA((

triacylglycerol synthesis in livertriacylglycerol synthesis in liver

VLDL and LDLVLDL and LDL

RIBOFLAVIN (VITAMIN B2)RIBOFLAVIN (VITAMIN B2)

FMN FMN && FAD FAD are:are: the the 22 biologically active formsbiologically active forms. . formed by transfer of AMPformed by transfer of AMP from ATP from ATP FMN FMN.. capable of capable of reversiblyreversibly acceptingaccepting 2 H atoms2 H atoms FMNH2FMNH2 or or FADH2FADH2 bound tightlybound tightly - sometimes covalently - - sometimes covalently - toto flavoenzymes flavoenzymes that catalyze that catalyze the oxidation or reduction of a substrate.the oxidation or reduction of a substrate.

)FMN( )FAD(

• dermatitis

• cheilosis (fissuring at the corners of the mouth), (fissuring at the corners of the mouth),

• glossitis (the tongue appearing smooth & purplish). (the tongue appearing smooth & purplish). DeficiencDeficiencyy

BIOTINBIOTIN

A coenzyme inA coenzyme in carboxylation reactionscarboxylation reactions, , ( serves as a carrier of activated ( serves as a carrier of activated CO2 ).CO2 ).

Covalently bound to the Covalently bound to the -amino groups of -amino groups of lysine residues of biotin-lysine residues of biotin-dependent enzymes.dependent enzymes.

Required by all Required by all organismsorganisms. .

Can only be synthesized Can only be synthesized by:by: bacteria, yeasts, bacteria, yeasts, molds, algae, and some molds, algae, and some plant species.plant species.

Each Each CarboxylaseCarboxylase catalyzes an essential catalyzes an essential

metabolic reaction:metabolic reaction:

Acetyl-CoA carboxylase:Acetyl-CoA carboxylase:

catalyzes the binding of catalyzes the binding of HCO3HCO3-- to acetyl- to acetyl-CoA to form malonyl-CoA required for the CoA to form malonyl-CoA required for the synthesis of fatty acidssynthesis of fatty acids..

Pyruvate carboxylase:Pyruvate carboxylase:

in in gluconeogenesisgluconeogenesis formation of formation of glucose from amino acids and fats.glucose from amino acids and fats.

Methylorotonyl-CoA carboxylase:Methylorotonyl-CoA carboxylase:

in the in the metabolism of leucinemetabolism of leucine, an essential , an essential amino acid.amino acid.

Propionyl-CoA carboxylase:Propionyl-CoA carboxylase:

in the in the metabolism of amino acidsmetabolism of amino acids, , cholesterol,cholesterol, and and odd chain fatty acidsodd chain fatty acids (fatty acids with an odd number of carbon (fatty acids with an odd number of carbon molecules)molecules)

very rare. very rare. does not occur naturally. does not occur naturally. the vitamin is widely distributed the vitamin is widely distributed in food.in food.in humans, big percentage is in humans, big percentage is supplied by intestinal bacteria. supplied by intestinal bacteria.

Biotin deficiencyBiotin deficiency

Human requirementHuman requirement for dietary biotin for dietary biotin inin::

• prolonged IV feeding without prolonged IV feeding without biotin supplementation.biotin supplementation.

• consumption of raw egg whiteconsumption of raw egg white

for a prolonged period .for a prolonged period .

Raw egg white contains a glycoprotein, Raw egg white contains a glycoprotein, avidin avidin tightly binds biotin tightly binds biotin prevents its absorption from the intestine.prevents its absorption from the intestine.

Cooking egg whiteCooking egg white denatures avidindenatures avidin renders it digestable renders it digestable unable to prevent the absorption of dietary biotin.unable to prevent the absorption of dietary biotin.

Addition ofAddition of raw egg-whiteraw egg-white

to the dietto the diet as a sourceas a source of proteinof protein

symptomssymptoms of biotinof biotin

deficiencydeficiency

depressiondepression lethargylethargy hallucinationhallucination numbness numbness tingling of extremities.tingling of extremities.

• dermatitisdermatitis• glossitisglossitis• loss of appetiteloss of appetite• loss of hairloss of hair • nauseanausea• scaly red rashscaly red rash around around the eyes, nose, mouth, the eyes, nose, mouth, and genital area.and genital area.

Neurologic Neurologic symptomssymptoms in adultsin adults

With a normal dietWith a normal diet, , 20 raw eggs / day would be required 20 raw eggs / day would be required to induce a deficiency syndrometo induce a deficiency syndrome..

The Adequate Intake (AI):The Adequate Intake (AI): average intakes of biotin average intakes of biotin (35 (35 mcg to 60 mcg/day)mcg to 60 mcg/day) are meeting the dietary requirement. are meeting the dietary requirement.

Biotin is incorporatedBiotin is incorporated into almost all nutritionally complete into almost all nutritionally complete dietary supplementsdietary supplements and and infant formulasinfant formulas..

In larger dosesIn larger doses, biotin is used to , biotin is used to treat inborn errors of treat inborn errors of metabolismmetabolism such as such as biotinidase deficiencybiotinidase deficiency..

Uses:Uses:

PANTOTHENIC ACIDPANTOTHENIC ACIDA component of A component of

coenzyme A, which coenzyme A, which functions in the transfer of functions in the transfer of acyl groupsacyl groups

Coenzyme A contains a Coenzyme A contains a thiol group that carries acyl thiol group that carries acyl compounds as activated compounds as activated thiol esters. thiol esters.

such structures are such structures are succinyl CoA, fatty acyl succinyl CoA, fatty acyl C0A, and acetyl CoA. C0A, and acetyl CoA.

Pantothenic acid is also a component of Pantothenic acid is also a component of fatty acid synthase fatty acid synthase . .

Sources:Sources:

• Eggs Eggs • Liver Liver • YeastYeast

DeficiencyDeficiency • Is not well characterized Is not well characterized in humans, in humans, • No RDA is established.No RDA is established.