Abdullah Fadl Al-Moalmy

_ Vitamin's Function Deficiency Requirements

Name
A  Vision: Retinal is essential for night vision  Eye: a. Night blindness and Xero-ophthalmia • 5000 IU/day
(retinoids)  Reproduction: Retinol is essential for reproduction  Growth retardation • Excess of vitamin A
 Growth: Retinol is essential for normal growth and  Skin and mucous membrane: roughness of skin and mucous causes increase of retinol
bone, teeth formation membranes of different body system. This lead to infection. witch exceeds the capacity
 Maintenance of epithelial cells of RBP lead to the toxic
 Antioxidant (anticancer) action effect Headache, nausea,
bone pain and loss of hair.
D (calciferol)  Normalization of serum calcium:  Rickets in children 400IU/day
_ On intestine: it stimulates synthesis of calcium binding  Osteomacia in adults Excess of vitamin D leads
protein (calbindin) that responsible for calcium absorption  Renal Rickets to
_ On bones: it stimulates calcium responsible for bones renal stone.
_ It increases renal reabsorption of calcium
 Mineralization of bones:
_In small doses: calcitriol helps the bone mineralization
_ In large doses: the reverse occurs, where calcium and
phosphate move from bone to blood.
 Absorption of phosphate from intestine
K ( Synthesis of some clotting factors in liver: prothrombin,  It leads to impairment of blood clotting
quinones
factor II and factors VII, IX and X  deficiency occurs in :
/anti
Synthesis of osteocalcin (calcium binding protein) in bones  New born infant
hemorrhagic  Long use of antibiotic
V)  Long use of dicumarol and warfarin
E  Antioxidant: vitamin E prevent non-enzymatic oxidation __occurs usually in premature infants 15 IU/day
(tocopherol of cell components  Haemolysis of RBCs and anaemia: due to lack of protection
)  Vitamin E removes peroxide formation in against peroxides
polyunsaturated fatty acids.  Muscle breakdown.
 Protection against heart disease.
C  Formation of collagen protein (scurvy): 60mg/day
(Ascorbic  Absorption and mobilization of iron:  decreased collagen formation (bleeding) ,Defective formation Excessive vitamin c:
acid)  Ascorbic acid acts as coenzyme for many hydroxylase of bone and teeth ,Defective healing of wounds and, Necrosis lead to stone formation.
enzymes in the pathway of : of gums and loss of teeth
 Bile acids synthesis ,Osteocalcin synthesis ,and  Anaemia: due to decreased absorption of iron and bleeding
Epinephrine synthesis  decreased neurotransmitters : Severe emotional
disturbances and Severe emotional disturbances
 decrease carnitine and fatty acid oxidation: General weakness.
 Abdullah Fadl Al-Moalmy

Vitamin,s Function Deficiency Requirement

Name
B1  Oxidative decarboxylation of αketoacids by : Beriberi .5 mg/day.
(Thiamine) a. Pyruvate dehydrogenase enzyme  Decrease TPP (thiamine pyrophosphate) lead to :
b. Α ketoglutarate dehydrogenase a.Decrease energy production lead to impaired cellular functions
 Transketolation reactions :Transketolase in pentose especially of nervous system.
phosphate path way b. Increase lactate production lead to lactic acidosis
 Thiamine is also essential for the process of nerve conduction  Three B1 deficiency syndromes can be recognized:
and structure of nerve membrane. a. Chronic bri bri : (Peripheral neuritis and Muscle wasting and
hyperesthesia)
b- Shosine pri pri :( Heart failure and Oedema)
c. Wernicke- korsakoff syndrome (Encephalopathy , Psychosis
,Ocular (eye) disturbance ,Loss memory)
B2 1. Both FMN and FAD are coenzyme for flavo enzymes  Ocular disturbances: Photophobia --abnormal sensitiveness of
(Riboflavin) they act as hydrogen or electron carriers in oxidation reduction the eye to light and Vascularization of cornea
reactions FMNH2 and FADH2  Cheilosis : fissuring at the corners of the mouth
 Glossitis : inflammation of tongue which appear smooth and
purplish
 Dermatitis: inflammation of skin.
B3  Formation of NAD and NADP hydrogen carrier -----Pellagra 20mg/day
(Niacin)  Lowering plasma cholesterol  Pellagra called a disease of 3 Ds (diarrhoea, dermatitis,  Hypervitaminosis
 Formation of ADP-ribose for ribosylation of protein and DNA dementia) of niacin may
 Causes: cause liver
a) Deficiency of niacin, tryptophan, and vitamin B6 damage.
B) Corn is a deficient in both niacin and tryptophan
 Hartnup ُs disease
B6 1. In protein metabolism: it acts as a coenzymes for amino acids  Pellagra may occur 2mg/day
(Pyridoxine) metabolism in the following reactions:( a. Transamination e , b.  convulsions in young infant  Intake of more
Deamination e. , c. Decarboxylation e., d. Heme synthesis e, e.  Anemia (microcytic hypochromic) than 200 mg/day
Trans- sulphonation e,and f. Pyridoxal phosphate  Disturbance in amino acids metabolism B6 may cause
2. In carbohydrate metabolism : pyridoxal phosphate acts as a  Cancer breast, uterus, and prostate neurological
coenzyme of glycogen phosphorylase Glycogen break down in to  Homosysteinuria: damage
glucose (glycogenolysis)
3. In lipids metabolism: pyridoxal phosphate is important in steroid
hormone action
Abdullah Fadl Al-Moalmy

Vitamin's Function Deficiency Requirement

Name
B5  coenzyme A (CoASH):  deficiency of pantothenic acid causes no effect in human 5-10mg/day.
(Pantothenic is formed of phosphpantothein attached to biphosphoadenosine
acid) which act in the transfer of acyl groups e.g. acyl CoA. Succinyl
CoA and other carboxylic acids
 Acyl carrier protein (ACP): Is formed of : pantothenic acid
connected to phosphate and protein in one side and
thioethyl amine in the other side
which component of fatty acid synthase enzyme required
for fatty acid synthesis.
B7  CO2 fixation:  Deficiency of biotin does not occur in man because due to:
(Biotin)  Biotin is a CO2 carrier acts as coenzyme for carboxylase The intestinal bacteria and widely distributed in food.
enzymes that catalyse carboxylation reactions  deficiency may result dut to :
 Regulation of cell cycle a. ingestion avidin
b.Deficiency of holocarboxylase synthetase enzyme in children
 The manifestations of biotin deficiency include: muscle
pain, dermatitis, glossitis, loss of appetite and nausea.
B12  Synthesis of methionine :  Megaloblastic anemiia (macrocytic hyperchromic anemia 4ug/day
(cobalamin) acts as coenzyme of methionine synthase enzyme. due to abnormal replication of DNA in hematopoietic
N⁵-methyl tetrahydrofolate acts as a source of methyl group it tissues and direct insufficiency of folate or indirectly to
transfers (CH3) to cobalamin then then methylcobalamin transfer cobalamin insufficiency)
(CH3) to homocysteine to form methionine  Neurological manifestations due to the lack of myelin
which is important for: I: synthesis of phospholipids which inter sheath formation
in the structure of myelin , sheath prevention of fatty liver and
important for cell division
 Isomerization of methyl-malonyl COA
B9  The active form is tetrahydrofolic (H4 folate ) functions as a  Pancytopenia: all blood cells are affected 200ug/ day
(Folic acid(= carrier for one carbon groups  Megaloblastic anemia (macrocytic anemia)  increase during
folate =  The one carbon group may be carried on N⁵ or N10 or both  Leucopenia: decrease WBCs late pregnancy,
folacin) of H4 folate  Thrombocytopenia : decrease platelets formation lactation and old
 Folate is essential for synthesis of purines  Impaired growth and neural tube defects in foetus ages.
Abdullah Fadl Al-Moalmy
Name's Function Deficiency Requirement
Vitamin
Choline  It enters in the formation of lecithin and sphingomyelin
 It has a lipotropic action prevents fatty liver
 It enters in the formation of acetylcholine
 Oxidation of choline produce Betaine which has a function as
methyl donor in transmethylation reactions
Inositol  It is enters in the structure of phosphatidyl inositol which acts
as lipotropic factor
 Inositol triphosphate acts as a second hormone messenger .
(see mode of hormone action)
Lipoic acid  acts as coenzyme in oxidative decarboxylation of α ketoacids
e,g pyruvic acid