Upon downstream modification by cyclooxygenases or lipoxygenases, arachidonic acid is modified into active compounds called eicosanoids.

Due to the increased presence and activity of PLA2 resulting from a snake or insect bite, arachidonic acid is released from the phospholipid membrane disproportionately.

The extracellular forms of phospholipases A2 have been isolated from different venoms (snake,[5] bee, and wasp), and from virtually every studied mammalian tissue (including pancreas and kidney) as well as from bacteria.

It has been shown that in PLA2G12B null mice, VLDL levels were greatly reduced, suggesting it could have an effect in lipoprotein secretion.

[18] However, the role of Lp-PLA2 in atherosclerosis may depend on its carrier in plasma, and several lines of evidence suggest that HDL-associated Lp-PLA2 may substantially contribute to the HDL antiatherogenic activities.

The rate limiting state is characterized as the degradation of the tetrahedral intermediate composed of a calcium coordinated oxyanion.

When phosphorylation is coupled with an influx of calcium ions, cPLA2 becomes stimulated and can translocate to the membrane to begin catalysis.

[24] Phosphorylation of cPLA2 may be a result of ligand binding to receptors, including: In the case of an inflammation, the application of glucocorticoids up-regulate (mediated at the gene level) the production of the protein lipocortin which may inhibit cPLA2 and reduce the inflammatory response.

In normal brain cells, PLA2 regulation accounts for a balance between arachidonic acid's conversion into proinflammatory mediators and its reincorporation into the membrane.

Lysophospholipids are another class of molecules released from the membrane that are upstream predecessors of platelet activating factors (PAF).

An optimal enzyme inhibitor would specifically target PLA2 activity on neural cell membranes already under oxidative stress and potent inflammation.

[26] Increase in phospholipase A2 activity is an acute-phase reaction that rises during inflammation, which is also seen to be exponentially higher in low back disc herniations compared to rheumatoid arthritis.