Quote:
Originally Posted by TheMercenary
(Post 425407)
Acetaminophen (Tylenol) works by inhibiting the synthesis of prostaglandins in the central nervous system and peripherally blocks pain impulse generation through an unknown mechanism. It's antipyretic effect is due to an inhibiting action in the hypothalamus heat regulation center in the brain.
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So you don't know either eh? Your answer was better than the one monster found on Tylenol's site.
The wiki pretty much sums up what a few minutes on google will tell you; no one really knows for sure. But it works, so people take it and give it to their kids, just like arnica. Except you can't damage your liver with arnica...
Quote:
Mechanism of action
The mechanism by which paracetamol reduces fever and pain is still a source of considerable debate[citation needed]. The reason for this confusion has largely been due to the fact that paracetamol reduces the production of prostaglandins, pro-inflammatory chemicals the production of which is also inhibited by aspirin, but, unlike aspirin, paracetamol does not have much anti-inflammatory action. Likewise, whereas aspirin inhibits the production of the pro-clotting chemicals thromboxanes, paracetamol does not. Aspirin is known to inhibit the cyclooxygenase (COX) family of enzymes, and, because of paracetamol's partial similarity of aspirin's action, much research has focused on whether paracetamol also inhibits COX. It is now clear, however, that paracetamol acts via (at least) two pathways.[6][7][8][9]
The COX family of enzymes are responsible for the metabolism of arachidonic acid to prostaglandin H2, an unstable molecule, which is, in turn, converted to numerous other pro-inflammatory compounds. Classical anti-inflammatories, such as the NSAIDs, block this step. The activity of the COX enzyme relies on its being in the oxidized form to be specific, tyrosine 385 must be oxidized to a radical.[10][11] It has been shown that paracetamol reduces the oxidized form of the COX enzyme, preventing it from forming pro-inflammatory chemicals.[7][12]
Further research has shown that paracetamol also modulates the endogenous cannabinoid system.[13] Paracetamol is metabolized to AM404, a compound with several actions; most important, it inhibits the uptake of the endogenous cannabinoid/vanilloid anandamide by neurons. Anandamide uptake would result in the activation of the main pain receptor (nociceptor) of the body, the TRPV1 (older name: vanilloid receptor). Furthermore, AM404 inhibits sodium channels such as anesthetics, lidocaine and procaine.[14] Either of these actions by themselves has been shown to reduce pain, and are a possible mechanism for paracetamol, though it has been demonstrated that, after blocking cannabinoid receptors and hence making any action of cannabinoid reuptake irrelevant, paracetamol no longer has any analgesic effect, suggesting its pain-relieving action is indeed mediated by the endogenous cannabinoid system.[15]
A theory that held some sway, but has now largely been discarded, is that paracetamol inhibits the COX-3 isoform of the cyclooxygenase family of enzymes.[6][16] This enzyme, when expressed in dogs, shares a strong similarity to the other COX enzymes, produces pro-inflammatory chemicals, and is selectively inhibited by paracetamol. However, in humans and mice, the COX-3 enzyme is without inflammatory action, and is not modulated by paracetamol.[6]
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