The Correct Answer is B: Thromboxane A2 (TXA2)
The cyclo-oxygenase (COX) enzyme in the arachidonic acid pathway controls the production of Thromboxane A2 (TXA2) in the platelet cytoplasm. 1
Biochemical Pathway in Platelets
The arachidonic acid metabolic pathway in platelets follows this specific sequence:
Arachidonic acid is liberated from membrane phospholipids by phospholipases when platelets are activated by various stimuli 1
COX-1 enzyme converts arachidonic acid to prostaglandin G2 (PGG2), which is then converted to prostaglandin H2 (PGH2) - these are unstable intermediate compounds called prostaglandin endoperoxides 1, 2
Thromboxane synthase then converts PGH2 to thromboxane A2 (TXA2) specifically in platelets 1, 3
TXA2 is the major COX product in platelet cytoplasm and serves as a potent platelet activator and vasoconstrictor 4, 5
Why TXA2 is the Answer
TXA2 provides an amplification mechanism for platelet activation by being synthesized and released in response to various platelet agonists, creating a self-sustaining activation loop 1, 4
The evidence is unequivocal across multiple authoritative guidelines:
The American College of Chest Physicians explicitly states that "activated platelets can synthesize prostanoids, primarily thromboxane A2 (TXA2), from arachidonic acid released from membrane phospholipids through rapid coordinated activation of phospholipases, cyclooxygenase (COX)-1, and TX synthase" 1
The European Society of Cardiology confirms that "prostaglandin (PG) H-synthase is responsible for the formation of PGH2, the precursor of TXA2" 1
Why Other Options Are Incorrect
Prostaglandin I2 (PGI2/prostacyclin) is NOT produced in platelets - it is synthesized primarily in vascular endothelium, not platelet cytoplasm, and actually has opposite effects (vasodilation and platelet inhibition) 3, 5
ATP is not controlled by COX - it is produced through cellular respiration pathways, not the arachidonic acid pathway 1
PF-4 (platelet factor 4) is not a COX product - it is a chemokine stored in platelet alpha granules and released upon activation, but not synthesized via the arachidonic acid pathway 1