Table 5.
Basal bioactivities of each toxin type
| Toxin type | Basal toxic activity |
|---|---|
| 3FTx | α-neurotoxicity, antagonistically binding to the nicotinic acetylcholine receptor. |
| Acetylcholinesterase | Rapid hydrolysis of choline released into the synapse, resulting in less neurotransmitter available for neuromuscular control. |
| ADAM | Tissue necrosis. |
| BNP | Potent induction of hypotension leading to loss of consciousness. |
| Cobra venom factor | Unregulated activation of the complement cascade, causing rapid and significant problems such as anaphylactic-type problems and/or tissue damage via hemolysis/cytolysis. |
| CNP-BPP | Potent induction of hypotension leading to loss of consciousness. |
| CRISP | Paralysis of peripheral smooth muscle and induction of hypothermia. |
| Crotamine | Myonecrosis. |
| Cystatin | Inhibition of body defensive enzymes. |
| Factor V | In Oxyuranus (Taipan) and Pseudonaja (Brown snake) venoms, combines with toxic form of factor X to potently convert prothrombin to thrombin. |
| Factor X | Potent conversion of prothrombin to thrombin in the presence of factor V, valcium and phospholipid. |
| Kallikrein | Increase of vascular permeability and production of hypotension in addition to stimulation of inflammation. |
| Kunitz | Inhibition of circulating serine proteinases. |
| L-amino oxidase | Apoptosis. |
| Lectin | Platelet aggregation mediated by galactose binding. |
| MIT | Potent constriction of intestinal smooth muscle, resulting in painful cramping, and induction of hyperalgesia. |
| NGF | Unknown. |
| PLA2 (IB) | Lipase activity resulting in inflammation and tissue destruction. |
| PLA2 (IIA) | Lipase activity resulting in inflammation and tissue destruction. |
| Sarafotoxin | Potent vasoconstriction resulting in acute hypertension. |
| SPRY | Induces hypolocomotion and hyperalgesia. Unknown which, if either, is basal activity. |
| VEGF | Increase of the permeability of the vascular bed and binding of heparin. Results in hypotension and shock. |
| Wagerlin | Presynaptically modulates γ-aminobutyric acid activated currents. Postsynaptically antagonistically binds to the ε form of the muscle nicotinic acetylcholine receptors. Presynaptic effect more potent than postsynaptic. Unknown which, if either, is basal activity. |
| Waprin | Bioactivities uncharacterized. |