MadSci Network: Medicine
Query:

Re: How does acetaminophen work differently from asprin to relieve pain?

Date: Mon Feb 19 11:44:05 2001
Posted By: Michael Parker, Research Chemist
Area of science: Medicine
ID: 982516495.Me
Message:

Velma,
You have asked a good question that brings up some interesting science.

Aspirin, or acetyl salicylic acid, acts as an inhibitor of an enzyme 
called cyclooxygenase, often abbreviated as COX.  COX  mediates the 
conversion of arachidonic acid to prostaglandin H2.  Prostaglandins in 
general are involved in the processes that cause pain and inflammation.  
By inhibiting the COX enzymes, aspirin prevents the synthesis of 
prostaglandins, and thereby reduces both pain and inflammation.  (If you 
want to know the chemical structures of arachidonic acid and 
prostaglandins, or want to know more about how they are synthesized 
biochemically, any good college-level biochemistry textbook should have 
plenty of information for you, so I won't go into detail here.)

About ten years ago, scientists discovered that there are actually two 
forms of the cyclooxygenase enzyme, termed COX-1 and COX-2.  It was 
determined that COX-1 is found throughout the body and performs 
many “housekeeping” functions.  COX-2 is found mainly in inflamed tissues, 
and is more specifically associated with causing inflammation.  Aspirin 
inhibits both COX-1 and COX-2. Since COX-1 is found throughout the body, 
especially in the gastrointestinal tract, kidneys, and platelets, it is 
believed that inhibition of this enzyme leads to the unwanted side effects 
such as gastrointestinal damage (ulcers), renal dysfunction, and platelet 
abnormalities.  Newer anti-inflammatory drugs, such as rofecoxib (Vioxx) 
and celecoxib (Celebrex) were designed by pharmaceutical researchers to 
specifically inhibit COX-2 and not COX-1, so they have fewer side effects. 

The mechanism of action of acetaminophen, the active ingredient in the 
Tylenol brand, however is not fully understood.  It also inhibits the COX-
1 and COX-2 enzymes just like aspirin does, but not very strongly, so 
there must be something more important going on.  Since it only weakly 
inhibits COX-2, there is little anti-inflammatory effects.  Acetaminophen 
seems to exert its pain-reducing effect more directly on the central 
nervous system by reducing the threshold of pain.  This effect is believed 
to be due inhibition of the actions of chemical mediators that sensitize 
the pain receptors to mechanical or chemical stimulation.  The antipyretic 
(fever-reducing) activity is exerted by blocking the effects of the 
chemical pyrogen on the hypothalamic heat-regulating center.  Additional 
mechanisms of action have also been suggested for acetaminophen, including 
inhibition of nitric oxide formation that results from activation of 
substance P and N-methyl-D-aspartate (NMDA) receptor stimulation.  Active 
research is underway now in many laboratories to more specifically 
determine the mode of action of acetaminophen.



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