Dermonecrotic toxins cleave the phosphodiester linkage between the phosphate and headgroup of certain phospholipids (sphingolipid and lysolipid substrates), forming an alcohol (often choline) and a cyclic phosphate. This toxin acts on sphingomyelin (SM) with high activity. It also acts on lysophosphatidylcholine (LPC), and lyso-platelet activating factor (LPAF, an alkyl-LPC) but not on phosphatidylcholine (PC). It may also act on ceramide phosphoethanolamine (CPE), lysophosphatidylcholine (LPC) and lysophosphatidylethanolamine (LPE), but not on lysophosphatidylserine (LPS), and lysophosphatidylglycerol (LPG). It acts by transphosphatidylation, releasing exclusively cyclic phosphate products as second products. In vivo, it induces dermonecrosis, vascular permeability, platelet aggregation, inflammatory response, edema and cytotoxicity against renal epithelial cells. It causes direct nephrotoxicity and is directly toxic to liver. It also induces hemolysis in a complement-dependent manner as well as in a complement-independent manner. The hemolysis provoked in a complement-independent manner is composed of several steps. The toxin binds to erythrocyte membranes, hydrolyzes membrane phospholipids (SM and LPC) thus generating metabolism products that cause hemolysis, probably by provoking an increase of calcium inside cells. The calcium influx is due to the opening of L-type calcium channels, since L-type calcium channel blockers inhibit calcium influx. In vivo, is lethal to mice when intraperitoneally injected.
