Arachidonic Acid Metabolism Flashcards
What is AA?
poly-saturated long fatty acid tail found in the cell wall
polar parts (OH group and double bond O group) stick out of wall to get pulled on by enzymes
part compound of lots of things
made from phospholipids?
What are the 4 main derivative pathways of AA?
Prostaglandins
Leukotriene
Thromboxane A2
HETE’s/EET’s
Prostaglandins
- PGE2 (prostaglandin E2)
- PGI2 (prostaglandin I2/prostacyclin)
- PGF 2a (prostaglandin F2 alpha)
ramp up the pain signals
Thromboxane A2
TXA2
mediates healing/bleeding of vessel injury by vasospasm
released during blood vessel injury along with the clotting cascade
COX
cycloxygenase
-catalyzes 2 reactions in a row
-enzyme that produces prostaglandins and TXA2
What is TXA2 more specific from?
COX 1
What two reactions are catalyzed by COX1 and COX2
PGG2 (prostaglandin G2) precursor compound
PGH2 (prostaglandin H2)
What specialized enzymes direct the COX compounds into difference pathways?
ex: prostaglandinE2-ase
COX 1
present throughout the body
lots of tissues can produce prostaglandins and TXA2
less pain control, over the counter
(aspirin ->bleeding)
COX 2
- more inducible form
- the isoform that gets turned on in response to pain
-stronger pain control (Naproxen less bleeding risk) - not only involves pain but also CV and other organs
(ex: Vioxx leading to CV events)
What enzyme takes AA and turns it into leukotriene
lipoxygenase… turns LT4 into
LT4 turns into LTC4, LTD4, LTE4
Function of Leukotriene pathway?
immune mediated inflammation
- lungs swell
- mucus production
What drug is a leukotriene receptor antagonist?
Singular
HETE’s/ EET’s
large fatty compound stays in cell wall because it doesn’t change much from AA
- short living
- mediator involved in kidney failure
- not many drugs attack tis pathway bc unstable , short living, and hang in cell wall… hard to manipulate
