Abstract
This study looked at how toxic proteins in venoms of adult Australian eastern Brown snakes Pseudonaja textilis from South Australian and Queensland populations interact with physiological functions of the lab SD rat Rattus norvegicus. Circulatory collapse and incoagulable blood occurred instantly after injection of venom under the dorsal skin of anaesthetised and mechanically ventilated rats in an imitation of a P. textilis bite. Intravenous injection of purified P. textilis (Mackay, QLD) venom prothrombin activator proteins caused instant failure of circulation, testifying of high toxicity of these proteins and suggesting their role in rapid incapacitation of rodent prey. The hypothesis is further supported by circulatory collapse occurring instantly despite artificial respiration in envenomed rats and the finding of extremely high venom procoagulant potency in rat plasma. LC-MS and physiology assays revealed divergent venom composition and biological activity of South Australian (Barossa locality) and Queensland (Mackay locality) populations, which may be driven by selection for different prey. The Queensland venom of P. textilis was found to be more procoagulant and to exhibit predominately presynaptic neurotoxicity, while the South Australian venom contained diverse postsynaptic type II and III α-neurotoxins in addition to the presynaptic neurotoxins and caused significantly faster onset of neuromuscular blockade in the rat phrenic nerve-diaphragm preparation. LC-MS analysis found evidence of multiple coagulation factor X-like proteins in P. textilis venoms, including a match to P. textilis coagulation factor X isoform 2, previously known to be expressed only in the liver.
Highlights
Several studies have found a correlation between venom lethality and the type of prey consumed, supporting natural selection as one process driving snake venom evolution [1,2,3,4]
The difference in neurotoxic activity between the studied populations of P. textilis was larger than the difference between P. textilis and Australian coastal taipan Oxyuranus s. scutellatus, which abolished the diaphragm contractions by 95% in 60.063.5 min (n = 3)
Venoms from the South Australian and Queensland P. textilis populations injected in live rats were found to cause rapid collapse of the circulatory system
Summary
Several studies have found a correlation between venom lethality and the type of prey consumed, supporting natural selection as one process driving snake venom evolution [1,2,3,4]. The relevance of death as the cessation of all biological functions in prey acquisition is questionable because what determines whether or not the predator gets its meal is disablement of the physiological functions of the prey that would assist escape and or defence Another problem with lethality studies is that they are often done over an extended time period (e.g. 24 hours) which does not take into account the timeframe in which a particular physiological function is affected [5], and at different venom doses administered different toxins may cause death [6]. The aim of this study is to better understand pathologic processes that affect physiological functions of a rodent organism caused by the venoms of Australian eastern Brown snake Pseudonaja textilis populations This elapid is a prey generalist, feeding on a variety of rodents (including mice and rats ), birds, lizards and frogs [7]. Several of these proteins have been shown to be lethal when injected into the rodent bloodstream, including P. textilis venom prothrombin activator [11], pseudonajatoxin b [14] and short-chain neurotoxins [16]
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