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datty117 datty117
wrote...
Posts: 94
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11 years ago
& also, how might a signal pathway be turned off?
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wrote...
11 years ago
The enzyme THROMBOXANE is affected by Aspirin, thereby reducing coagulative capability of platelets.
wrote...
11 years ago
Aspirin is a non narcotic analgesic i.e. a pain killer that is not addictive in nature. Aspirin is actually a derivation of salicyclic acid and in fact is a prodrug of salicylic acid. I mean prodrug as aspirin becoming salicyclic acid in the body once consumed.

Salicyclic acid ( what aspirin becomes in the body upon consumption ) is a non competitive inhibitor of cyclo oxygenase enzyme (COX) that is needed to turn arachidonic acid into prostaglandins.

Prostaglandins are hormones made at sites of cell death or injury and are responsible for the transmission of pain information to the brain. They also regulate the hypothalamic thermostat and are responsible for the symptoms of inflammation. That is why aspirin is described as analgesic ( pain killer), antipyretic ( reduces or mitigates fever ), and anti inflammatory.

Hence, aspirin once converted to salicyclic acid in the body binds to a site other than the active site of COX (COX-1 and COX-2) and causes a conformational change in the 3D shape of the enzyme. Active site is lost and this enzyme-inhibitor complex can no longer bind to arachidonic acid to convert it into protaglandins.

The arachidonic acid pathway constitutes one of the main mechanisms for the production of pain and inflammation, as well as controlling homeostatic function. ( does this answer your last question ?)
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