COMPLEMENT ACTIVATION BY ANIMAL VENOMS

During activation of complement (C) system, C4b and C3b attach covalen tly to targets such as cell membranes. Deposited C4b serve both as the focus for the assembly of the C3 convertases and as ligands for C3b r eceptors or inactivators. C4a, C3a and C5a, mediators of the early eve nts of inflammation, are released into the fluid phase while C5b serve s to organize the cytolytical complex C5b-C9. Among the Arthropoda the venom from some spiders (Loxosceles) contain activators of the mammal ian C system, although the exact mechanism and point of the activation cascade in where they act were not yet elucidated. In the insect veno ms as honeybee, yellow jacket, yellow hornet, white-facet hornet, cate rpillars and wasp there are some components capable of reducing total haemolytic and serum levels. Interestingly, mellitin, a soluble haemol ytic peptide present in bee venom shares structural homology with huma n C9. Scorpion venom apparently are not active on the C system. Snakes , belonging to ELAPIDAE, CROTALIDAE and VIPERIDAE families produce ven oms containing components with a vast range of action on mammalian C s ystem,some acting by cleaving directly a particular component, white o thers interact with C components, the resulting complex being able as an amplificator, to activate part of the C cascade. Soluble mediators of inflammation, cell bound fragments of C components recognizable by specific receptors disposed on immune or inflammatory cells, or the fo rmation of multimolecular complex potentially capable of damage host c ells are the presumable consequences of C activation by animal venoms.