Lipid mediators cyclooxygenase enzymes

The alteration of lipid mediators by PUFA has been reviewed in great detail (Stulnig, 2003) and is mentioned only briefly here. The function of cells of the immune system can be exquisitely sensitive to lipid mediators such as prostaglandins and leukotrienes. Those mediators are normally produced by the action of specific enzyme systems on the AA substrate that is released from membrane phospholipids pools. Thus, cyclooxygenase (COX-1 or COX-2) converts AA to prostaglandins, and lipoxygenase (e.g., 5-LOX) converts AA to HETEs and leukotrienes. The amount of substrate, the activity of the enzymes, and the amount and potency of the lipid mediators appear to be regulated by FA composition and, thus, the dietary intake of PUFA. Specifically, EPA is and DHA is not a substrate for COX and LOX and can competitively inhibit AA metabolism. In addition, DHA can inhibit... 

The prostaglandins are lipid mediators implicated, not only in inflammation, but also, in other pathological processes, such as edema, fever, hyperalgia, cancer or Alzheimer s disease. The cyclooxygenase (COX) is the rate-limiting enzyme in the synthesis of PGE2, TXB2 and prostacyclines from arachidonic acid. 

The biological membranes that surround cells and form the boundaries of intracellular organelles contain polyunsaturated fiitty acids, which are susceptible to oxidation. This reaction is used under controlled conditions by enzymes, such as the lipoxygenases or cyclooxygenases, within cells to produce oxygenated lipids, which can act as mediators of inflammation (Smith and Marnett, 1991 Yamamoto, 1992). Such compounds are characterized by their high potency and specificity in their interaction with cells (Salmon, 1986). While these enzymatic reactions... 

Lipid hydroperoxides are also generated in singlet molecular oxygen mediated oxidations and by the action of enzymes such as lipoxygenases and cyclooxygenases. Chemiluminescence (CL) arising from lipid peroxidation has been used as a sensitive detector of oxidative stress both in vitro and in vivo . Several authors have attributed ultra-weak CL associated with lipid peroxidation to the radiative deactivation of O2 and to triplet-excited carbonyls (63, 72) (equations 35 and 36) " . It has been proposed that the latter emitters arise from the thermolysis of dioxetane intermediates (61, 62) (equation 35), endoperoxide (73) (equation 37) and annihilation of aUtoxyl, as well as peroxyl radicals ... 

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