Acetaminophen works primarily in the central nervous system to reduce pain and fever, though its exact mechanism is not fully understood. It is thought to inhibit a cyclooxygenase (COX) enzyme variant in the brain, reducing the production of prostaglandins which sensitize nerve endings to pain and play a role in fever. Unlike NSAIDs, acetaminophen has minimal anti-inflammatory effects. It may also activate the endocannabinoid system, contributing to its analgesic effects. Overall, it raises the body's pain threshold and acts on the brain's thermoregulatory center to reduce fever.
Details on Mechanism of Action
- Acetaminophen inhibits COX activity in the central nervous system but not significantly in peripheral tissues, differentiating it from NSAIDs.
- It is proposed to act on a COX-3 variant or by altering the oxidation state of COX enzymes, though the involvement of COX-3 is debated.
- Analgesic effects also involve modulation of descending serotonergic pathways and possibly cannabinoid receptors via a metabolite called AM404.
- The drug does not bind directly to the active site of COX enzymes but reduces their activity through other mechanisms.
Effects in the Body
- Reduces fever by acting on the hypothalamic thermoregulatory center.
- Provides relief from mild to moderate pain such as headaches, toothaches, and muscle aches.
- It does not have peripheral anti-inflammatory properties like NSAIDs, so its pain relief is limited to certain types of pain.
This complex mechanism, involving central COX inhibition and other pathways, explains why acetaminophen is effective yet distinct from typical anti- inflammatory pain relievers.
