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22 Cards in this Set

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What is Phosphatidylinositol (PIP2) hydrolyzed/degraded by and what is released?
- PI-Phospholipase C (PI-PLC)
- DAG and IP3 are released (secondary messengers)
- IP3 releases intracellular stores of Ca
What do DAG and Ca activate? What does this product do?
- Calcium-Dependent Protein Kinase C (PKC)
- Phosphorylates multiple intracellular proteins
How is DAG recycled back into PIP2?
- DAG phosphorylated by ATP
- Produces Phosphatidic Acid
- CTP added to create CDP- Diglyceride
- Inositol added to create PI
- PI phosphorylated twice to create PIP2
What are the major and minor pathways to liberate Arachindonic Acid from Membrane Phospholipid?
Major:
- Stimulus binds to receptor
- PLA2, activated with Ca, modifies Phosphatidylcholine to Arachindonic Acid

Minor
- Stimulus binds to receptor
- PLC modifies Phosphatidylinositol bisphosphate to DAG
- DAG lipase creates Arachidonic Acid and Monoacylglycerol
- Monoacylglycerol lipase modifies monoacylglycerol to Aranchindonic Acid
What are Cyclooxygenase's (COX) 2 Activities?
Cyclooxygenase Activity: adds O2
Peroxidase Activity (synthesizes PGH2)
What are Eicosanoids?
Family of oxygenated arachidonic acid derivatives that interact with specific receptors to amplify/propagate flow of biological information
Pathway to synthesize Prostacyclin (PGI2) from Arachindonic Acid
- Add COX (O2 activity) to Arachidonic Acid
- PGG2
- Add COX (peroxidase activity) to PGG2
- PGH2
- Add PGI synthase to PGH2
- Prostacyclin
Pathway to synthesize Thromboxane (TXA2) from Arachindonic Acid
- Add COX (O2 activity) to Arachidonic Acid
- PGG2
- Add COX (peroxidase activity) to PGG2
- PGH2
- Add Thromboxane synthase to PGH2
- Thromboxane
What does Prostacyclin (PGI2) do?
- produced by endothelial cells (as is PGE2)
- increases vasodilation and decreases platelet aggregation
What does Thromboxane (TXA2) do?
- produced by platelets
- increases vasoconstriction and platelet aggregation
NSAIDS
- Activity of Aspirin
- Inhibits platelet COX 1 (prevents platelet aggregation, TXA2)
- creates irreversible covalent bond by acetylation, so COX is a dead end product
NSAIDS
- Activity of Ibuprofen
- Inhibits the binding of Arachidonic Acid to COX 1 and II (the O2 activity)
- competitive inhibition, thus reversible
- Celebrex/Vioxx works same way
Activity of Acetominophen (not an NSAID)
- Inhibits COX by acting on CNS
- Rapidly degraded, so not an anti-inflammatory
NSAID uses and drawbacks
- Treats inflammation and pain
- May cause ulcers
Purpose of COX I and II in GI tract
- mediate the secretion of bicarbonate and mucous
Low doses of Aspirin
- Inhibits the platelets from making thromboxane (doesn't effect endothelial cells)
- Less Thromboxane but high PIP2
- Increases platelet turnover and prevents MI
PIP2 vs TXA2
- Antagonistic properties regarding aggregation of platelets and vascular tone
- important in hemostatic response and atherosclerosis
Synthetic Pathway for Leukotrienes
- 5-Lipoxygenase modifies Arachidonic Acid into 5-HPETE
- 5-HPETE reduced to 5-HETE
-5-HETE to LTA4
- With addition of glutathione residue to LTA4 it breaks into LTC4 and LTB4
- LTC4 can break into its derivatives LTD4 and LTE4
What are the Peptidoleukotrienes?
LTC4
LTD4
LTE4
What does LTB4 do in anaphylaxis?
- Increases vascular permeability (swelling) and T-cell proliferation (inflammation), etc
What does LTC4 and LTD4 do in anaphylaxis?
- Increases bronchoconstriction and vascular permeability
What biological function do leukotrienes (LT) participate in?
anaphylaxis