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Biochemistry > Eicosanoids > Flashcards

Eicosanoids Flashcards

1
Q

Are eicosanoids long lived or short lived signaling molecules?

A

Eicosanoids are degraded rapidly, so they must function locally (paracrine, autocrine)

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2
Q

What are eicosanoids derived from?

A

20-carbon unsaturated essential fatty acids

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3
Q

Name the types of eicosanoids?

A
  1. Prostaglandin
  2. Prostacyclin (prostaglandin with extra ring)
  3. Thromboxane
  4. Leukotriene
  5. Epoxide
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4
Q

Where are the following Eicosanoids produced in?

  1. Prostanoids (PG, PGI, TX)?
  2. Leukotrienes?
  3. Epoxides?
A
  1. Prostanoids: Most cells
  2. Leukotrienes: WBC
  3. Epoxides: Macrophages
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5
Q

What does the 2 represent in the Eicosanoid name PGH2

A

Series (denotes # of double bonds in linear portion of the molecule)

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6
Q

Linolenic is what type of omega fatty acid?

A

w-3

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7
Q

Linolenic is metablized into what fatty acid that becomes incorporated into plasma membrane phospholipids?

A

Eicosapentaenoic acid (EPA) (20:5, w-3)

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8
Q

Linoleic acid is what type of omega fatty acid?

A

w-6

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9
Q

Linoleic acid is metabolized into what type of fatty acid?

A
  • Arachidonic Acid (AA) (20:4; w-6)
  • Dihomo y-linolenic acid (DGLA) (20:3; w-6)
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10
Q

What are the series numbers for DGLA, EPA, and AA?

A
  • DGLA: Series 1
  • EPA: Series 3
  • AA: Series 2 (more inflammatory)
  • 1+3=4 good health
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11
Q

Release of fatty acids from membrane is done by what molecule?

A

Phospholipase A2 (PLA2); rate-limiting enzyme

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12
Q

What type of protein receptor is required in the activation of PLA2

A

Gq-protein coupled receptor

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13
Q

In the activation of PLA2, G-alpha (q) activates….List the process

A
  1. G-alpha (q) activates PLC
  2. PLC cuts PIP into DAG (remains in membrane) and IP3
  3. IP3 binds to Ca2+ channel at the endoplasmic reticulum and causes release of Calcium into the cytosol
  4. Ca2+ Binds with PLA2 and brings it to the cell membrane where it hydrolyzes fatty acid
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14
Q

What enzyme converts Arachidonic Acid (AA) into Leukotrienes?

A

5-lipoxygenase

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15
Q

AA are converted to two types of leukotrienes: Name these

A
  1. Leukotriene A4
  2. A family of LTs called Cysteinyl Leukotrienes
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16
Q

Cysteinyl Leukotrienes act at cell-surface receptors on target cells to cause what?

A
  1. Contract bronchial and vascular smooth muscle
  2. Enhance mucus secretion in airway and gut
  3. Recruit Leukocytes to site of inflammation
  4. Increase capillary permeability
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17
Q

What is the action and purpose of the drug Zyflo?

A
  • 5-lipoxygenase inhibitor therefore inhibits leukotriene formation
  • Used for prophylactic and chronic treatment of asthma
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18
Q

What is the action and purpose of the drug Singulair?

A
  • Cysteinyl leukotriene receptor antagonist; prevents binding to bronchial smooth muscle cells and inflammatory cells
  • Used for chronic treatment of bronchospasms (asthma) and allergic rhinitis
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19
Q

Synthesis of Prostanoids (Prostaglandins and Thromboxanes) is catalyzed by?

A

Prostaglandin endoperoxide synthase (PGH synthase)

20
Q

PGH synthase is one polypeptide with what two catalytic activities?

A
  1. Fatty acid cyclooxygenase (COX) 1 or 2 depending on tissue type
  2. Peroxidase: provides reducing power to produce PGH
21
Q

PGH synthase acts on which fatty acids to create PGH(1-3)

A

PGH synthase can act on AA, EPA, and DGLA to produce PGH(series #)

22
Q

PGH(series #) converts fatty acids into what eicosanoids?

A
  • PGH converts fatty acids (AA, EPA, DGLA) into Prostaglandins and/or Thromboxanes
  • Conversion is dependent upon enzymes that are expressed in the particular cell
  • Cells of a particular tissue synthesize only one or two types of prostanoids
23
Q

What happens to Prostanoids after they become nonfunctional?

A

Prostanoids become nonfunctional near their site of release and are then degraded in the capillary beds on the lungs

24
Q

Platelets synthesize and secrete what type of Eicosanoid? What is its action?

A
  • Thromboxane (TXA)
  • Stimulates neighboring platelets and enhance platelet aggregation
25
Q

To prevent platelet aggregation in undamaged area of vasculature, endothelial cells synthesize and secrete what? How does it work?

A
  • The prostaglandin Prostacyclin (PGI)
  • PGI binds to platelets and interferes with thromboxane signaling
26
Q

If AA is used to synthesie TXA2 and PGI2 what type of response will be favored in terms of platelet aggregation?

A
  • Stronger Platelet Aggregation
  • TXA2 will have a stronger aggregation effect
  • PGI2 will have weak antiplatelet effect
27
Q

If EPA is used to synthesis TXA or PGI, what will be the response in terms of platelet aggregation?

A
  • Weaker platelet aggregation
  • TXA3 will have weak aggregation effect
  • PGI3 will have stronger antiplatelet effect
28
Q

Where is Cox-1 expressed and what is its function?

A
  • Cox-1 is constitutively expressed in most tissues
  • Required for maintenance of health gastric tissues, renal homeostasis, and platelet function
29
Q

Where is Cox-2 expressed? What is its function?

A
  • Cox-2 is expressed in a limited number of tissues (including inflammatory cells)
  • Mediates inflammation, sensitivity to pain, and fever
30
Q

Drugs that inhibit Cox-1 (e.g. NSAIDS) can have what side effect?

A
  • Can impair protective signaling of gastric mucosa
  • causing stomach ulcers and GI bleeding with extended use
31
Q

Glucocorticoids (steriod hormones) increase the synthesis of what protein?

A

Lipocortin (Annexin- 1) which prevents PLA2 from hydrolyzing fatty acids at the membrane

32
Q

Glucocorticoids ALSO decrease synthesis of Cox-1 or Cox-2

A

Decrease synthesis of Cox-2 (but not Cox-1)

33
Q

What are the two classes of competitive inhibitors?

A
  1. Irreversible inhibitors: Create a new covalent bond as a result of binding that permanently inactivates enzyme activity (Ex: ASA)
  2. Reversible inhibitors: Bind reversibly to active site of enzyme; can compete with substrate for binding (Ex: Ibuprofen)
34
Q

Drugs that inhibit COX activity are primarly what?

A

Competitive inhibitors: interferes with active site of enzyme so substrate is unable to bind

35
Q

Aspirin has what mechanism of action? What is the clinical benefit?

A
  1. Irreversibly inhibits COX-1 and COX-2 (acetylates serine in active site)
  2. Benefit: Anti-inflammatory, analgesic, antipyretic; anti-platelet activity
36
Q

Why is low dose Aspirin therapy used to reduce the risk of heart attacks?

A
  • ASA inhibits COX-1 and COX-2 thus inhibiting the formation of TXA -> decreased aggregation of platelets
  • Platelets do not contain nuclei thus they can’t synthesize new COX enzymes after ASA administration whereas other cells can continue to produce COX
  • Anti-platelet activity of ASA lasts longer than its antiflammatory activity
37
Q

What is the mechanism of action and clinical benefit of Ibuprofen/Naproxen?

A
  • NSAIDs that reversibly (competitively) inhibit COX-1 and COX-2
  • Beneift: Anti-inflammatory, Analgesic, Antipyretic
  • Brand name: Advil
38
Q

What is Celebrex’s mechanism of action? Clincal Benefit?

A
  • NSAID that is a reversible, competitive, inhibitor of COX-2 (not COX-1) at sites of inflammation
  • Benefit: Inhibits inflammation without GI side effects
  • *increased risk of heart attack has been associated
39
Q

Where does Acetaminophen act? Clincal benefit?

A
  • Brand name: Tylenol
  • Acts in the CNS (does not inhibit COX-1 or COX-2)
  • Benefit: reduces pain/fever, minimal anti-inflammatory effects
  • Does not affect platelet function
40
Q
  1. Linoleic acid (w-6) comes from eating what types of food?
  2. Linolenic (w-3) comes from eating what types of food?
A
  1. Linoleic: Nuts
  2. Linolenic: Fatty fish
41
Q

What drug prevents transcription of COX-2

A

Glucocorticoid

42
Q

What drug blocks the substrate channel of COX-2 but not COX-1?

A

Celebrex

43
Q

What drug acetylates the active site of COX-1 and COX-2 enzymes?

A

Aspirin

44
Q

What drug inhibits 5-lipoxygenase?

A

Zyflo

45
Q

What drug blocks substrate channel of both COX-1 and COX-2?

A

Ibuprofen

Biochemistry (7 decks)

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