It may also work through PGHS, particularly in areas of the brain with high concentrations of fatty acid amide hydrolase. AM404 exerts effect through cannabinoid receptors. p-Aminophenol is conjugated with arachidonic acid by fatty acid amide hydrolase to form AM404.
Alternatively, paracetamol effects may be mediated by an active metabolite (p-aminophenol). Peroxide tone and swamping explain lack of peripheral analgesic effect, platelet effect, and anti-inflammatory effect by paracetamol. This effect can be reduced in the presence of hydroperoxide-generating lipoxygenase enzymes within the cell (peroxide tone) or by swamping the POX site with substrate such as PGG(2). Paracetamol acts as a reducing cosubstrate on the POX site and lessens availability of the ferryl protoporphyrin IX radical cation. Prime examples are progesterone and prostaglandin E 1 that activate CatSper without involving classical nuclear and G protein-coupled receptors, respectively. It may reduce the production of prostaglandins, which are chemicals that cause inflammation and. PGJ2 and its metabolites exert their actions by different mechanisms. Formation of a ferryl protoporphyrin IX radical cation from the reducing agent Fe(3+) at the POX site is essential for conversion of tyrosine-385 to its radical form. The sperm-specific Ca 2+ channel CatSper registers chemical cues that assist human sperm to fertilize the egg. The exact mechanism of action of acetaminophen is unknown. PGJ2 and its metabolites exit the cell via diffusion or poorly defined transporters, and can enter cells or the nucleus via active transporters at the plasma or nuclear membranes. The conversion of arachidonic acid to PGG(2) is dependent on a tyrosine-385 radical at the COX site.
PGHS comprises of two sites: a cyclooxygenase (COX) site and a peroxidase (POX) site. The two major forms of this enzyme are the constitutive PGHS-1 and the inducible PGHS-2. Prostaglandin H(2) synthetase (PGHS) is the enzyme responsible for metabolism of arachidonic acid to the unstable PGH(2). Debate exists about its primary site of action, which may be inhibition of prostaglandin (PG) synthesis or through an active metabolite influencing cannabinoid receptors. MUCOSAL DEFENSE Mucosal defense is a term used to describe the various factors and components that permit the mucosa to remain intact despite its frequent exposure to substances with a wide range of temperature, pH, and osmolarity, as well as to substances with detergent or cytotoxic actions, and bacterial products capable of causing local and systemic inflammatory reactions (). Arachidonic acid, released from phospholipids by the action of phospholipase A 2, is converted by the cyclooxygenase enzymes to prostaglandin H 2.Prostaglandin H 2 is, in turn, the precursor of multiple prostaglandins. Paracetamol has a central analgesic effect that is mediated through activation of descending serotonergic pathways. Prostaglandins are potent and ubiquitous lipid messenger molecules.
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