Prostaglandins

Front 1

eicosanoids

Back 1

1) prostaglandins
2) thromboxanes
3) leukotrienes

origin of polyunsaturated twenty carbon fatty acids

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difference between true hormones and eicosanoids

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1) produced in small amounts by almost all tissues rather than specialized glands
2) act locally rather than after transport in the blood to distant sites
3) not stored, extremely short half-life

Front 3

how are the biological function of eicosanioids mediated

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by plasma and nuclear membrane receptors, which are different in each organ system

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dietary precursor of prostoglandins

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linoleic acid (essential)
which is then elongated and desaturated to form arachidonic acid

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nomenclature prostoglandins

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PG + (third letter)
third letter designates the type and functional arrangement of the functional groups in the molecule
Thromboxanes (TX)
Leukotrienes (LT)

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when is arachadonic acid released and by-product

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released from membrane-bound phospholipids by
PHOSPHOLIPASE A2
lysophospholipid is a bi-product

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Phospholipase A2

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releases arachidonic acid

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regulation of Phospholipase A2

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inhibition corticosteroids
(cortisol)

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first step in the sythesis of PGH2

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oxidative cyclization of free arachidonic acid to yeild PGH2
by prostaglandin ENdoperoxide sythase

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prostaglandin ENdoperoxide sythase

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microsomal protein
Contains tow catalytic activities:
COX and Peroxidase

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Fatty acid cyclooxygenase

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COX
catalytic activity of prostoglandin endoperoxide sythase
requires two molecules of O2

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Peroxidase

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catalytic acivity of prostoglandin endoperoxide sythase
dependent on reduced glutathione

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isozymes of prostaglandin endoperoxide synthase

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denoated COX-1 and COX-2

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COX-1

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made constitutively in most tissues
required for the maintenance of healthy gastic tissue, renal hemostasis, and platelet aggregation

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COX-2

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inducible in a limited number of tissues in response to products of activated immune and inflammatory cells

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physiological manefestation of induced COX-2

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increased COX-2 induction leased to
1) pain, heat, redness, and swelling of inflammmation
2) fever of infection

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Cortisol

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inhits COX-2 and not COX-1

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inihibitors specific to COX-2

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celecoxib
reduce pathological inflammatory processes while maintaining physio function of COX-1

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inhibitors of COX-1 and COX-2

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aspirin, indomethacin, phenylbutazone

derivatives of NSAIDS

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activator of COX-2

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Cytokines
endotoxin
growth factors
tumor promoters

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synthesis of PGH2 requires

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1) cyclooxygenase 1 or 2
and
2)perodixase

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PGH2 derives

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1) TXA2
2) PG12
3) PGFalpha
4) PGE2

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COX-1 and COX-2 make

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PGG2

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TXA2

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Thromboxane A2
1) produced primarily via platelets
2) promotes platelet aggregation
3) vasoconstriction
4) mobilizes intracellular calcium
5) contraction of smooth muscle
6) promotion of the thrombi

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PG12

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opposing force to TXA2
1) produced by primarily vascular endothelial cells
2) vasodialation
3) inhibits platelet aggregation
4) thus impedes thrombogenesis

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platelet homeostatis

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prostaglandin
TXA2 promotes the formation of clots
PGI2 impedes
limits thrombi formation at the site of vascular injury

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Aspirin

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irreversible inhibitor of TXA2 synthesis from Arachidonic by inhibiting COX-1

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irreversible inhibition of COX-1

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Aspirin
cannot be overcome via anucleate platelets
but can be overcome via endothelial cells, due to the fact that they have a nucleus and can make more enzyme

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low-dose aspirin theory

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since asprin also has a antithrombogenic effect is it used to lower the risk of stroke and heart attacks by decreasing the formation of thrombi vacularly

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Leukotriene synthesis steps

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1) arachidonic acid released by phospholipid via phoshpolipase A2
2) 5-lipoxygenase froms 5-HPETE

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5-HPETE

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5-hydroxy
6,8,11,14
eicosatetraenoic acid

precursor to LT

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Lipoxygenases

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not affected by NSAIDs
mediators to allergic response and inflammation

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treatment of asthma

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inhibitors of 5-lipoxygenase and leukotriene receptor antagonists

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PGF2 alpha

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produced by most tissues
vasoconstriction
contraction of smooth muscle
stimulates uterine contractions

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PGE2

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produced by most tissues, especially kidney
opposing effects of PGF2 alpha
vasodialation
relaxes smooth muscle

used to induce labor

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LTA4

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Leukotriene A4
produced in leukocytes, platelets, mast cells, and heart and lung vascular tissues

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LTC4

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precursor to LTD4 and LTE4

contraction of smooth muscle
bronchoconstriction
vasoconstriction
increases vascular permeability
components of slow-reacting substance of anaphylaxis (SRS-A)

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LTB4

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increased chemotaxis of polymorphonuclear leukocytes
release of lysosomal enzymes
adhesion of white blood cells

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A class of prostoglandins

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contain 1 keto group, and 1 double bond

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E class of prostoglandins

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contian 1 keto group, and 1 hydroxy group

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classes of prostaglandins

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A: 1 keto, 1 double bond
E: 1 keto, 1 hydroxyl
F: 2 hydroxylgroups

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F class of prostaglandins

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2 hydroxyls

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Traditional NSAIDS

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inhibited both COX-1 and COX-2
which lead to gastrointestinal and potential kidney problems

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Specific COX-2 inhibitors

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celecoxib (celebrex)
rofecoxib (Vioxx)
Meloxicam (Mobic)

*COX-2 was primary drug target b/c they wanted to relieve pain without gastro/kidney side effects

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cardiovascular problems that potentially could arise with the inhibition of COX-2

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due to differential inhibition of COX-1 and COX-2

could potentially increase the TXA2/ PG12 ratio

aggregate thrombotic response

Front 46

what is the alcohol in sphingosine

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choline

Front 47

how many fatty acids does sphingosine have

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1

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how many fatty acids does glycerophospholipids have

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2

Front 49

what enzyme catalyzes glycerophospholipid degredation

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phospholipase

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what enzymes catalyzes sphingomyelin degredation

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sphingomyelinase

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Niemanmn-Pick Disease

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characterized by the deficiency in sphinomyelinase

1) lipid accumulation in liver and spleen
2) neurodegeneration

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eiconasoids that make vascular smooth muscle contract

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PGF2 and TXA2

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econiasoids that make female reproductive organs contract

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PGF2 and PGE

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econaisoids that make vacular smooth muscle relax

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PG12 and PGE2

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male PGE1 makes reproductive organs ___

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relax

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opposing effects on platelet aggregation

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TXA2 (promotes)
PG12 (inhibits

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Gi activation

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increase Calcium
thus makes it contract

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Gq activation

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decrease calcium
makes it relax
coupled with leukotriene receptors in order to activate

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4 main actions of asprin

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Analgeic
antipyretic
anti-inflammatory
antiplatelet

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Advantages of COX 2 selective inhibitors vs. non-selective

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1) don't inhibit platelet function (good for hemophiliacs)
2) don't cause ulcers or GI problems
3) cox-2 inhibitors are specific to inflammation sites, while cox-1 is everywhere
4) Cox-2 inhibitors reduce feve (antipyretic) b/c of COx-2 block to brain