AA(Arachidonic Acid) ELISA Kit (E-EL-0051)

This ELISA kit uses the Competitive-ELISA principle. The micro ELISA plate provided in this kit has been pre-coated with Universal AA. During the reaction, Universal AA in the sample or standard competes with a fixed amount of Universal AA on the solid phase supporter for sites on the Biotinylated Detection Ab specific to Universal AA. Excess conjugate and unbound sample or standard are washed away, and Avidin-Horseradish Peroxidase (HRP) conjugate are added to each micro plate well and incubated. Then a TMB substrate solution is added to each well. The enzyme-substrate reaction is terminated by the addition of stop solution and the color turns from blue to yellow. The optical density (OD) is measured spectrophotometrically at a wavelength of 450 nm ± 2 nm. The concentration of Universal AA in tested samples can be calculated by comparing the OD of the samples to the standard curve.

Arachidonic acid (AA, eicosatetraenoic acid) is a polyunsaturated omega-6 fatty acid with the formula C20H32O2 whose twenty-carbon chain carries four cis double bonds, and it is liquid at room temperature. It occurs widely in the phospholipids of animal cell membranes and in animal neutral fats. Although it can be derived from linoleic acid, it is regarded as an essential fatty acid obtained partly from dietary sources such as meat, eggs and fish. Arachidonic acid is the key precursor of eicosanoids. Upon cell stimulation it is liberated from membrane phospholipids by phospholipase A2 and rapidly converted through cyclooxygenase, lipoxygenase and cytochrome P450 pathways into prostaglandins, thromboxanes and leukotrienes, which collectively govern inflammation, vascular tone, platelet aggregation and immune responses. Profiling arachidonic acid and its metabolites is important in inflammation, lipid metabolism and cardiovascular research, where disturbed eicosanoid signaling contributes to atherosclerosis and cancer. Quantitation in plasma, serum and tissue assesses essential fatty acid status, characterizes the source pool of inflammatory mediators and supports evaluation of cyclooxygenase- or lipoxygenase-directed drugs as well as dietary interventions that modify omega-6 intake.