Vitamins biological properties along with their coenzyme forms are presented. Deficiency leading to diseases is discussed.Structure is given

1. Vitamins,
their classification and
mechanism of action.
Structure and
biochemical properties of
water-soluble vitamins (coenzyme forms of vitamins)
In The Name of Allah, The Most Merciful, The Most
Compassionate
Mahira Amirova
Associate Professor
Biochemistry Department
Azerbaijan Medical University
Year 2021

2. All B vitamins help the body convert food carbohydrates (glucose)
to fuel: ergo, the body uses these vitamins to produce energy. The
B vitamins, often referred to as B-complex vitamins, also help
the body to metabolize fats and proteins.

3. B1 – thiamine takes part in oxidative decarboxylation of pyruvate and α-
ketoglutarate, which play a key role in energy metabolism and are particularly
important in tissues of the nervous system. In thiamine deficiency, the activity of these
two dehydrogenase-catalyzed reactions is decreased, resulting in a decreased
production of ATP and, thus, impaired cellular function. Thiamine deficiency is
diagnosed by a reduce in erythrocyte transketolase activity.
B1, Thiamine
(ANEYRIN, ANTI-BERI-BERI), sourses

4. 1. Beri-beri is a severe thiamine-deficiency syndrome found in areas
where polished rice is the major component of the diet. The deficiency
syndrome can have a rapid onset in nursing infants, whose mothers
are deficient in thiamine. Adult beri-beri is characterized by dry skin,
irritability, disordered thinking, and progressive paresis and paralysis.
Thiamine deficiency: Beri-beri

5. Dry beri-beri
Dry beriberi causes wasting and
partial paralysis resulting from damaged
peripheral nerves.
By the way, high doses of vitamin B1
reduce kidney disease in people with Type II
diabetes.

7. Wernicke–Korsakoff syndrome is also form
of dry beriberi
Wernicke-Korsakoff syndrome is a thiamine
deficiency, which happens in association with chronic
alcoholism and is due to dietary insufficiency of
vitamine, or impaired intestinal absorption of vitamin
B1. The neurologic consequences of Wernicke's
syndrome may be treatable with thiamine
supplementation.

8. Wernicke's encephalopathy, Korsakoff
syndrome are manifested with alcohol
amnestic disorder
The thiamine deficiency
state in drunks is characterized by
apathy, loss of memory,
ataxia, and a rhythmic
to-and-fro motion of the
eyeballs (nystagmus).

9. nystagmus
Anterograde and retrograde amnesia
Drunks symptoms

10. Wet beriberi
Disease results in
• vasodilation leading to decreased systemic
vascular resistance
• Dilated cardiomyopathy - a condition in which
the heart becomes enlarged and cannot pump
blood effectively. Symptoms vary from none to
feeling tired, leg swelling, and shortness of
breath. It may also result in chest pain or fainting.
Complications can include heart failure and an
irregular heartbeat.

11. Gastrointestinal beriberi
Gastrointestinal beri-beri is characterized by:
• Abdominal pain
• Nausea
• Vomiting
• Lactic acidosis

12. Infants
Infantile beriberi usually occurs
between two and six months of age in
children whose mothers have inadequate
thiamine intake. It may present as either
wet or dry beriberi.
For example, signs of infantile beriberi
include tachycardia, vomiting,
convulsions, and, if not treated, death.

13. B2 coenzymes FMN and FAD are each
capable of reversibly accepting two hydrogen
atoms, forming FMN-H2 and FAD-H2.
FMN and FAD are bound tightly—sometimes
covalently—to flavoenzymes, that catalyze the
oxidation or reduction of a substrate.
B2 – riboflavin, GROWTH FACTOR

14. STRUCTURE of VITAMIN B2
Isoalloxazine ring
Ribitol

15. STRUCTURE of FMN and FAD, coenzyme forms
of vitamin B2

16. SOURSES OF VITAMIN B2

17. Riboflavin deficiency
symptoms include dermatitis,
cheilosis and glossitis.

18. cheilosis (painfull fissuring at the
corners of the mouth)

19. B2 deficiency: inflamed tongue and
mouth glossitis (the tongue appearing
smooth and purplish)
Glossitis refers to inflammation of the
tongue. The condition causes the tongue
to swell in size, change in color, and
develop a different appearance on the
surface.

20. Pantothenic acid is a component of
Coenzyme A (HS-CoA), which functions
in the transfer of acyl groups. HS-CoA
comprises a thiol group, that carries acyl
compounds in activated form. Examples
of such structures are acetyl CoA, fatty
acyl CoA and succinyl CoA. Pantothenic
acid is also a component of the acyl
carrier protein (ACP), that participates in
fatty acid synthesis.
B3 - Pantothenic acid

21. Pantothenic acid structure:
(𝜷 − 𝒂𝒍𝒂𝒏𝒊𝒏𝒆 +
2,4−Dihydroxy 3,3−dimethyl butiric acid)
2
4 3

22. +ATP
OH (Acetyl-CoA

23. Coenzymes NAD+ and NADP+ serve in
oxidation-reduction reactions. These coenzymes
pyridine ring undergoes reduction by accepting a
hydride ion (hydrogen atom plus one electron). The
reduced forms of NAD+ and NADP+ are NADH2
and NADPH2 respectively.
Niacin

24. PROVITAMIN
A deficiency of niacin causes pellagra, a disease
involving the skin, gastrointestinal tract, and CNS. The
symptoms of pellagra progress through the three Ds:
dermatitis, diarrhea, dementia—and, if untreated, death.
VITAMIN PP (pellegra-
preventive)
pyridine ring

25. NUCLEOTIDE-CONTAINING
NAD+ and NADP+

26. PP

27. Niacin deficiency (pellagra)
(dermatitis, diarrhea,
dementia)

28. Niacin in treatment of hyperlipidemia: Niacin at doses of
1.5 g/day or 100 times the Recommended Dietary
Allowance (RDA), strongly inhibits lipolysis in adipose
tissue—the primary producer of circulating free fatty
acids. The liver normally uses these circulating fatty acids
as a major precursor for triacylglycerol synthesis. Thus,
niacin causes a decrease in liver triacylglycerol synthesis,
which is required for very-low-density lipoprotein
(VLDL) production. Low-density lipoprotein (LDL, the
cholesterolrich lipoprotein) is derived from VLDL in the
plasma. Thus, both plasma tri acylglycerol (in VLDL) and
cholesterol (in VLDL and LDL) are lowered. Therefore,
niacin is particularly useful in the treatment of Type IIb
hyperlipoproteinemia, in which both VLDL and LDL are
elevated. Niacin also raises HDL level.

29. B6 VITAMIN AND COENZYME STRUCTURE
COENZYME PALP –
pyridoxal 5-phosphate,

30. B6 coenzyme Pyridoxal phosphate and Pyridoxamine phosphate
They function in a large number of enzymes, particularly those that
catalyze reactions involving amino acids. Reactions, vitamin B6
participates, are shown below. Reaction type and example:
B6 – Pyridoxine, Pyridoxal, Pyridoxamine
(vitamers)
1.Transamination:
Oxaloacetate+glutamate aspartate+ α ketoglutarate
2. Deamination:
Serine → pyruvate
3. Decarboxylation:
Histidine → histamine (biogenic amine)
4. Condensation:
Glycine + succinyl CoA → δ-aminolevulinic acid
(to heme synthesis)
-NH3
-CO2

31. Vitamin B6 deficiency
1
• Rough skin
• Insomnia (lovered
2
• Anemia
• Hb ↓
3
• Biogenic amines formation ↓
GABA (𝛾 𝑎𝑚𝑖𝑛𝑜 −
𝑏𝑢𝑡𝑖𝑟𝑖𝑐 𝑎𝑐𝑖𝑑)

32. Pyridoxine is the only water-soluble vitamin
with significant toxicity. Neurologic
symptoms as sensory neuropathy occur at
intakes above 200 mg/day, an amount 100
times more than normal. Substantial
improvement, but not complete recovery,
occurs when the vitamin is discontinued.

33. ACTION OF vitamin B9
(THFA)

34. VITAMIN B9 (FOLIC ACID) chemical
structure

35. THFA (Tetra hydro folic acid)
B9 receives one-carbon fragments from donors such as
serine, glycine, and histidine and transfers them to
intermediates in the synthesis of amino acids, purines, and
thymidine mono phosphate (TMP)—a pyrimidine found in
DNA.

37. There is well-known microcytic anemia, caused by lack of iron
in the nutrition. But there is also the second major
category of nutritional anemia, macrocytic, or
megaloblastic, which results from a deficiency in
folic acid or vitamin B12. It can be also caused by
1) increased demand in B9 (for example, pregnancy and
lactation),
2) poor absorption caused by pathology of the small intestine,
3) alcoholism, or
4) treatment with drugs that are dihydrofolate reductase
inhibitors, for example, methotrexate.
B9 (THFA) DEFICIENCY

38. anemia

39. Vitamin B12 - cyanocobalamin

40. DEOXY-ADENOSYL-COBALAMIN, a
coenzyme of vitamin B12

42. SAM – S-adenosyl methionine
B9 works along with B12 to produce methionine (SAM)
(СH3-)

43. Patients with B12 deficiency are usually anemic, but later in
the development of the disease they show neuropsychiatric
symptoms. However, central nervous system (CNS) symptoms
may occur in the absence of anemia. The disease is treated by
giving high-dose B12 orally, or intramuscular injection of
cyanocobalamin. Therapy must be continued throughout the
lives of patients with pernicious anemia.
At gastrectomy patients can not absorb the vitamin B12.
Deficiency of vitamin B12 can be measured by the level
of methylmalonic acid in blood, which is elevated in
individuals with low intake or decreased absorption of the
vitamin.
B12 deficiency

44. Bloodstream
Intrinsic factor
absence
At gastrectomy, patients can not
absorb the vitamin B12
due to

45. Addison-Birmer (pernicious) anemia
• Biermer's anemia, better known as
pernicious anemia, is characterized by the
presence in the blood of large, immature,
nucleated cells (megaloblasts) that are
forerunners of red blood cells. (Red blood cells,
when mature, have no nucleus). It is thus a type
of megaloblastic anemia.

46. brittle
nails

47. fatigue
Other manifestations of B12 deficiency

48. Biotin can be considered as a compound
of urea with thiophene and valeric acid.

50. SEBORRHEA

51. Biotin deficiency: stubborn dandruff
Vitamin H - biotin deficiency appears as
Dermatitis, glossitis,
nausea and loss of appetite.

52. Seborrheic dermatitis on the face
• Seborrheic dermatitis is a common skin
condition that mainly affects a scalp. It causes
scaly patches, red skin and stubborn dandruff.
• Seborrheic dermatitis can also affect oily
areas of the body, such as the face, sides of
the nose, eyebrows, ears, eyelids and chest.
scaly
patches

53. VITAMIN C
2
3
Vitamin C (ascorbic acid) is a vitamin needed to form collagen for
blood vessels, cartilage, muscle and bones. Vitamin C is also vital to
healing of damaged areas of the body.

55. The antioxidant action cascade highlighting the
interaction of ascorbic acid (vitamin C) and
tocopherol (vitamin E).
ROS = reactive oxygen species
Damage of cell
Sceme of cell protection from ROS

56. vitamin C, ascorbic acid deficiency
A deficiency of vitamin C results in scurvy, a disease
characterized by sore and spongy gums, loose teeth, fragile
blood vessels, swollen joints, petechiae (spot haemorrages)
and anemia.
Many of the deficiency symptoms can be explained
by a deficiency in the hydroxylation of collagen, resulting
in defective connective tissue.

57. Vitamin C deficiency: unpreventable teeth lose in loose
(sore and spongy) gums

58. Vitamin C deficiency: fragile blood
vessels result in nose bleeding

59. Swollen joints, petechiae (spot
haemorrages), loose of teeth

60. Deficiency can be removed with high
doses of vitamins!
Lemon, orange, tangerin, pomegranate, grapefruit, kiwi are
richest in vitamin C products

61. PP-nicotinamide NAD+, NADP+
B2-riboflavin FAD, FMN
OXIDOREDUCTASES
CoQ,
Lipoic acid
Water-soluble vitamins act mostly as coenzymes of enzymes.
Vitamin Coenzyme Enzyme
Vitamin-like
substances

62. B6-pyridoxal PALP (Pyridoxal phosphate),
PAMP (Pyridoxamine phosphate)
B3 – pantothenic HS-CoA, dephospho-CoA,
acid 4-phospho-pantothenate TRANSFERA
B9-folic acid THFA (tetrahydrofolic acid)
B12-Cobalamin Methyl-Cobalamin

63. Do not have coenzymes - HYDROLASES
B1 TPP (thyamine pyrophosphate)
(in ketoacid decarboxylases)
B3 HS-CoA (Coenzyme A)
in decarboxylases
B6 PALP
B12 DOAC
(deoxyadenosyl-cobalamin)
(Pyridoxal phosphate)

64. B6 PALP
B12 DOAC
(deoxyadenosyl-cobalamin) ISOMERASES
THFA
Biotin Carboxybiotin
LIGASES