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biochem block 3 > eicosanoids > Flashcards

eicosanoids Flashcards

1
Q

what is the only type of cell in the body that does not produce eicosanoids?

A

RBCs

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2
Q

6 general roles of eicosanoids in the body

A

inflammatory response, fever/pain, blood pressure, blood clotting, reproductive functions, sleep/wake cycle

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3
Q

what is the most important eicosanoid in humans?

A

arachidonic acid (20:4w6)

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4
Q

what is arachidonic acid synthesized from? how?

A

linolenic acid

elongation and desaturation by microsomal enzymes in the ER

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5
Q

where is arachidonic acid found in phospholipids?

A

A2

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6
Q

what is the MOA of glucocorticoids?

A

inhibit the formation of arachidonic acid by inhibiting the transcription of phospholipase A2

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7
Q

what are the 3 direct products from arachidonic acid?

A
  • PGG2 (cycloxygenase)
  • HPETE (lipoxygenase)
  • Epoxides (cytochrome P450)
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8
Q

which pathway is used to form prostaglandins and thromboxane?

A

cyclic pathway

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9
Q

what is prostacyclin a type of?

A

prostacyclin= PGI2

is a type of prostaglandin

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10
Q

what enzyme is responsible for synthesis of PGI2?

A

prostacyclin synthase

PGH2 –> PGI2

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11
Q

what enzyme is responsible for synthesis of TXA2?

A

thromboxane synthase

PGH2 –> TXA2

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12
Q

what is the relationship between PGI2 and TXA2?

A

inverse actions

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13
Q

PGI2: produced by/roles

A

vascular endothelium

NO production, inhibits plt aggregation, hyperalgesia, BP control in kidney

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14
Q

TXA2: produced by/roles

A

platelets

platelet aggregation, vasoconstrictions

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15
Q

PGF2a, PGD2 and PGE2 are all produced by-

A

myocardium

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16
Q

which prostaglandin causes bronchconstriction and myometrial contraction?

A

PGF2a

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17
Q

which prostaglandin acts on macrophages to cause vasodilation and hyperalgesia?

A

PGE2

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18
Q

which prostaglandin acts on mast cells to cause vasodilation and inhibition of platelet aggregation?

A

PGD2

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19
Q

what is another name for cyclooxygenase?

A

prostaglandin synthase (PGH2 synthase)

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20
Q

what is the immediate precursor for all of the series 2 PG and thromboxane?

A

PGH2

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21
Q

what are the 2 catalytic activities of COX?

A
  • cyclooxygenase = adds 2 O2

- peroxidase = converts OOH to OH using glutathione

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22
Q

2 COX isoforms

A

COX1- ubiquitious, physiologic regulation

COX2- inducible, involved in inflamm

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23
Q

general MOA of NSAIDs

A

inhibit COX1/2, specifically cyclooxygenase activity

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24
Q

what makes aspirin an irreversible inhibitor?

A

aspirin will acetylate the enzyme at serine residues that are not directly involved in the catalytic site but will result in blocking access of arachidonic acid to the catalytic site (covalent changes = irreversible)

25
Q

why are platelets effected but vascular endothelial cells unaffected by low dose aspirin therapy?

A

Aspirin will irreversibly inhibit COX. Platelets are only in circulation for 10 days, so once inhibition occurs, they do not have time to synthesize more enzyme. Vascular endothelial cells are more long-lived and can synthesize new COX, thus are less affected by aspirin

26
Q

why are COX-2 inhibitors sometimes prescribed?

A

selective for COX2 = limit damage to GI lining

27
Q

how are prostaglandins released from cells following synthesis?

A

using facilitative transporter (PGT)

28
Q

what second messenger do prostaglandins use inside cells?

A

cAMP via GaS mechanism

29
Q

what technique can be used to measure prostaglandin breakdown products in cells?

A

radioimmunoassay

30
Q

how are prostaglandin inactivated in the body? excreted?

A

inactivated by 15-hydroxyprostaglandin dehydrogenase to 15-keto prostaglandins, these are then further oxidized to more polar molecules that are excreted

31
Q

prostaglandin receptors are ___

A

G-protein coupled

32
Q

example- receptor for PGI2 is-

A

IP

33
Q

what type of enzyme is used in the linear pathway?

A

lipoxygenases are used to convert arachidonic acid to HPETEs in the linear pathway

34
Q

what are the 3 possible products of the linear pathway?

A

1- leukotrienes (5-LPO)
2- hepoxins (12-LPO)
3- lipoxins (15-LPO)

35
Q

what are the “peptido-leukotrienes”?

A

LTC4, LTD4, LTE4

36
Q

in what process do “peptido-leukotrienes” play a role?

A

part of the slow reacting substances of anaphylaxis, immediate hypersensitivity runs, inflammation and MI

37
Q

what are leukotrienes related to asthma?

A

will cause bronchoconstriction of small airways and increase mucus secretion

38
Q

what is the general effect of leukotrienes?

A

constriction of smooth mm (vascular, respiratory, intestinal)

39
Q

what is the general pathway for LT production?

A
  • arachidonic acid –> 5-HPETE by 5-LPO
  • 5- HPETE –> LTA4
  • LTA4 –> LTC4 + LTB4
  • LTC4 –> LTD4
  • LTD4 –> LTE4
40
Q

when are the LTs moved out of the cell?

A

LTC4 and LTB4 are moved out of the cell

41
Q

what is the role of LTB4 in the body?

A

chemotaxis of WBCs to sites of infection

42
Q

describe the 2 types of LTB4 receptors

A 
B-LT1 = high affinity, on WBCs
B-LT2= low affinity, ubiquitous
43
Q

CysLT1 receptors

A

bind LTC4 and LTD4

found on airway smooth mm and enodthelium

44
Q

CysLT2 receptors

A

bind LTD4

on heart, adrenals and spleen

45
Q

which receptor is targeted by LT- receptor antagonists like monteleukast? used for?

A

CysLT1

asthma control

46
Q

what does 5-lipoxygenase require for proper functioning?

A

FLAP- 5-lipoxygenase activating protein

47
Q

what are the 2 actions of FLAP?

A
  • faciliates enzyme/substrate rxn

- faciliates interaction between enzyme and membrane

48
Q

how are isoprostanes formed?

A

isoprostanes are formed non-enzymatically following exposure of arachidonic acid to free radicals and subsequent cleavage from the phospholipid by phospholipase A2

49
Q

what is the significance of isoprostanes?

A

isoprostane’s physiologic role is unknown, bu urine measurements can be used to indicate level of oxidative stress

50
Q

example of endocannabinoid

A

ananamide

51
Q

how is ananamide formed?

A

transfer of arachidonic acid to phos-ethanolamide and then release from membrane by phospholipase D

52
Q

what enzyme breaks down ananamide?

A

fatty acid amide hydrolase (thus inhibition of this enzyme would prolong the effects of ananamide)

53
Q

marine lipids are rich in:

A

EPA (w3)

54
Q

EPA inhibits-

A

formation of TXA2

55
Q

EPA is the precursor for-

A

series 5 LTs

56
Q

what is the significance of series 5 LTs

A

series 5 are less active that series 4

57
Q

what are the benefits of dietary EPA?

A
  • inhibit neutrophil aggregation/chemotaxis

- decrease cholesterol/trigs if high

58
Q

which type of PUFA are assoc with inflammation? anti-inflammation? importance?

A

w6 = inflammation (arachidonic acid)
w3= anti-inflammatory (EPA, DHA)
thus lipid mediator switching from w6 to w3 promotes homeostasis

biochem block 3 (7 decks)

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