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PROSTAGLANDINS
1.
2. Postaglandins & their related compounds
prostacyclins (PGI), thromboxanes (TXA),
leukotrienes (LT) & lipoxins are collectively
known as eicosaniods, they all contain 20C.
Structure of prostaglandins:
Prostaglandins are derivatives of 20-carbon
fatty acid - prostanoic acid, hence known as
prostanoids.
3. This has a cyclopentane ring (formed by
carbon atoms 8 to 12) & two side chains, with
carboxyl group on one side.
Prostaglandins differ in their structure due to
substituent group & double bond on
cyclopentane ring.
Most important prostaglandins (PGF2 &
PGF2α), prostacyclins (PGI2), thromboxanes
(TXA2) & leukotrienes (LTA4).
4.
5. Arachidonic acid (5,8,11,14 - eicosatetraenoic
acid) is the precursor for most of the
prostaglandins in humans.
It occurs in the endoplasmic reticulum.
Release of arachidonic acid from membrane
bound phospholipids by phospholipase A2.
It occurs due to a specific stimuli by
hormones – epinephrine or bradykinin.
6. Oxidation & cyclization of arachidonic acid
to PGG2 which is then converted to PGH2 by
peroxidase.
PGH2 serves as the immediate precursor for
the synthesis of a number of prostaglandins,
including prostacyclins & thromboxane.
This is known as cyclic pathway of
arachidonic acid.
7.
8. Cyclooxygenase – a suicide enzyme.
Prostaglandin synthesis can be partly
controlled by suicidal activity of the enzyme
cyclooxygenase.
This enzyme is capable of undergoing self-
catalysed destruction to switch off PG
synthesis.
9. Corticosteroids (e.g. cortisol) prevent the
formation of arachidonic acid by inhibiting
the enzyme phospholipase A2.
Anti-inflammatory drugs inhibit the synthesis
of prostaglandins, prostacyclins &
thromboxane.
They block the action of cyclooxygenase.
Aspirin irreversibly inhibits cyclooxygenase.
10. All the eicosanoids are metabolized rapidly.
Degradation occur in lung & liver.
Two enzymes, namely 15-α-hydroxy PG
dehydrogenase & 13-PG reductase, convert
hydroxyl group at C15 to keto group & then
to C13 and C14 dihydroderivative.
11. Prostaglandins act as local hormones.
PGs are produced in almost all the tissues.
PGs are not stored & they are degraded to
inactive products at the site of their
production.
PGs are produced in very small amounts &
have low half-lives.
12. Regulation of blood pressure:
The prostaglandins (PGE, PGA & PGl2) are
vasodilator in function.
This results in increased blood flow and
decreased peripheral resistance to lower the
blood pressure.
PGs serve as agents in the treatment of
hypertension.
13. Inflammation:
PGEI & PGE2 induce the symptoms of
inflammation (redness, swelling, edema etc.)
due to arteriolar vasodilation.
PGs are natural mediators of inflammatory
reactions of rheumatoid arthritis, psoriasis,
conjunctivitis etc.
Corticosteroids are used to treat these
inflammatory reactions, since they inhibit
prostaglandin synthesis.
14. Reproduction:
PGE2 & PGF2 are used for the medical termination of
pregnancy & induction of Iabor.
Pain and fever:
Pyrogens (fever producing agents) promote
prostaglandin synthesis leading to the formation of
PGE2 in hypothalamus-regulation of body temperature.
PGE2 along with histamine & bradykinin cause pain.
Migraine is also due to PGE2.
Aspirin & other non-steroidal drugs inhibit PG synthesis
& thus control fever & relieve pain.
15. Regulation of gastric secretion:
Prostaglandins (PGE) inhibit gastric secretion.
PGs are used for the treatment of gastric ulcers.
PGs stimulate pancreatic secretion & increase
the motility of intestine which often causes
diarrhea.
Influence on immune system:
Macrophages secrete PGE which decreases the
immunological functions of B-& T-lymphocytes.
16. Effects on respiratory function:
PGE is a bronchodilator whereas PGF acts
as a constrictor of bronchial smooth
muscles.
PGE & PGF oppose the actions of each other
in the lungs.
PGEI & PGE2 are used in the treatment of
asthma.
17. Influence on renal functions:
PGE increases glomerular filtration rate &
promotes urine output.
Excretion of Na+ & K+ is also increased by PGE.
Effects on metabolism:
Prostaglandins influence certain metabolic
reactions, through the mediation of cAMP.
PGE decrease lipolysis, increases glycogen
formation & promotes calcium mobilization.
18. Platelet aggregation & thrombosis:
The prostaglandins – prostacyclins (PGI2),
inhibit platelet aggregation.
Thromboxanes (TXA2) & prostaglandin E2
promote platelet aggregation & blood
clotting that might lead to thrombosis.
Mechanism of action of PGs:
PGE increases cAMP & PGF increases cGMP.
19. They are used in the treatment of gastric
ulcers, hypertension, thrombosis, asthma etc.
Prostaglandins are also employed in the
medical termination of pregnancy,
prevention of conception, induction of labor
etc.
20. Leukotrienes are synthesized by leucocytes,
mast cells, lung, heart, spleen etc., by
lipoxygenase pathway of arachidonic acid.
Leukotrienes (A4, B4, C4, D4 & E4) are
synthesized through the intermediate, 5-
hydroperoxyeicosatetraenoic acid (5-HPETE).
21.
22. Leukotrienes (C4, D4 & E4) are components of
slow-reacting substances of anaphylaxis (SRS-
A), released after immunological challenge.
SRS-A is 100 -1,000 times more potent than
histamine or prostaglandins in its action as a
stimulant of allergic reactions.
Leukotrienes are implicated in asthma,
inflammatory reactions, hypersensitivity
(allergy) and heart attacks.
23. Leukotrienes cause contraction of smooth
muscles, bronchoconstriction,
vasoconstriction, adhesion of white blood
cells & release of lysosomal enzymes.
Lipoxins are involved in vasoactive &
immunoregulatory functions.