Australian Tiger Snake Notechis Scutatus Research Articles

Myocardial Infarction as a Rare Consequence of a Snakebite

A healthy 28-year-old man with no history of cardiac disease and no cardiac risk factors presented to the hospital 2 hours after being bitten on his right hand by his pet snake. He was in anaphylactic shock and was rapidly resuscitated with fluids, inotropic support, intramuscular antitetanus serum, and intravenous infusion of Viper-FAB, an antidote. His vital signs normalized and he was admitted to intensive care for further observation. One hour after admission, the patient’s systolic blood pressure dropped to 40 mm Hg. Intravenous noradrenaline was started. Thirty minutes later, the patient lost consciousness in association with a rhythm change to torsade de pointes. He was defibrillated with 100 J (biphasic defibrillator) to sinus rhythm. Intravenous magnesium was started, and a repeat 12-lead ECG showed a prolonged corrected QT interval at 490 ms with no ST elevation (Figure 1). An urgent echocardiogram demonstrated normal-sized left ventricle with mild hypokinesis of the anterior wall and a global left ventricular fraction of 60%. Tissue Doppler images acquired by Vivid-7 (GE Medical) …

Immunological properties of notexin, a potent presynaptic and myotoxic component from venom of the Australian tiger snake Notechis scutatus scutatus

Neutralizing antibodies were raised in mice against notexin, the most toxic phospholipase A 2 (PLA 2) from Notechis scutatus scutatus venom, without the necessity of detoxifying the toxin prior to immunization. Using a sensitive radioimmunoassay we demonstrated that anti-notexin antibodies recognized (i) the parent antigen, (ii) closely related isoforms of notexin and (iii) venoms from Notechis genus snakes. In contrast, they failed to recognize other purified PLA 2 or PLA 2-containing venoms from other origins. Substitutions or chemical modifications occurring in the C-terminal part of the polypeptide chain of notexin altered the binding affinity for antibodies, implying that this region constitutes an antigenic domain of notexin.

Complete amino-acid sequence of a non-neurotoxic, non-enzymatic phospholipase A2 homolog from the venom of the Australian tiger snake Notechis scutatus scutatus.

The complete amino acid sequence of Notechis II-1, a non-neurotoxic, non-enzymatic phospholipase A2 homolog from the venom of the Australian tiger snake Notechis s. scutatus has been determined. The protein consists of a single chain of 119 amino acids. The main fragmentation of the reduced and S-carboxymethylated derivative was accomplished by cleavage with Staphylococcus aureus V8 protease. Tryptic peptides were used to align and complete the sequence, which was determined mainly by automated Edman degradation. Notechis II-1 contains all of the residues that appear to be invariant in elapid and pancreatic phospholipases A2 except at position 30 in the sesquence, where an otherwise invariant glycine is replaced by serine.

Amino acid sequence of a postsynaptic neurotoxin from the venom of the Australian tiger snake Notechis scutatus scutatus

Although 60 percent of the protein in tiger snake (Notechis scutatus scutatus) venom consists of the basic per-synaptically neurotoxic and myotoxic phospholipases notexin and Notechis II-5 and other phospholipase homologs such as Notechis II-1, several post-synaptic "curaremimetic" neurotoxins are present in small amounts. The major one of these is a typical "long" neurotoxin containing 73 amino acids in a single peptide chain cross-linked by five disulfide bridges. The formula weight calculated from the amino acid sequence is 8,051. The LD50 for intravenous injection into mice is 125 micrograms/kg.

Isolation and amino acid sequence of a neurotoxic phospholipase A from the venom of the Australian tiger snake Notechis scutatus scutatus.

The complete amino acid sequence of notechis 5, a neurotoxic phospholipase A from the venom of Notechis scutatus scutatus (Australian tiger snake), has been elucidated. The main fragmentation of the 119-residue peptide chain was accomplished by digesting the reduced and S-carboxymethylated derivative of the protein with a staphylococcal protease specific for glutamoyl bonds. Tryptic peptides were used to align and complete the sequence of the four staphylococcal protease peptides. The sequence was determined by Edman degradation by means of the direct phenylthiohydantoin method. Notechis 5 differs in seven positions from the recently elucidated sequence of the presynaptic neurotoxin notexin from the same venom. Notechis 5 has a 50% higher specific prospholipase A activity than notexin when assayed against egg yolk but is only one-third as toxic.

Isolation of A non-neurotoxic, non-enzymatic phospholipase a homologue from the venom of the australian tiger snake Notechis scutatus scutatus

Isolation of A non-neurotoxic, non-enzymatic phospholipase a homologue from the venom of the australian tiger snake Notechis scutatus scutatus

Purification of a presynaptic neurotoxin from the venom of the Australian tiger snake Notechis scutatus scutatus

The venom of the Australian tiger snake Notechis scutatus scutatus has been fractionated by ion-exchange chromatography on Bio-Rex 70 in an ammonium acetate gradient. The main neurotoxic component, the notexin, which constituted 6 per cent of the crude venom, was thereby obtained in a high degree of purity (⩾97 per cent) in one purification step. It is a basic protein of 119 amino acid residues in a single peptide chain cross-linked by seven disulfide bridges. The formula weight is 13,574. The LD 100 is 25 μg/kg mouse. The toxin causes dyspnea and paralysis of the hind legs and in the final stages before death, the mice lie immobilized. The death follows two to three days after the administration of a lethal dose. The notexin is a presynaptic toxin which inhibits the release of acetylcholine from motor nerves. The tiger snake venom also contained four other highly active toxins, three of which were submitted to a preliminary study. The first of these toxins has about 60 amino acid residues and an LD 100 of 100 μg/kg mouse, and the second has about 70 residues and an LD 100 of 150 μg. Both toxins have probably a postsynaptic mode of action, as they appear to have all characteristics in common with the postsynaptic cobra ( Naja naja) neurotoxins. The third toxin, which contains about 120 residues and has an LD 100 of 600 μg, causes respiratory distress characteristic for a postsynaptic neurotoxin. Sublethal doses can give rise to difficulty in breathing lasting for as long as 48 hr. It resembles the dimers formed during the freeze-drying of cobra neurotoxins. These dimers also cause dyspnea lasting for a long period, whereas the corresponding time for the monomeric cobra toxins is maximally 6 hr.

Purification of a presynaptic neurotoxin from the venom of the Australian tiger snake Notechis scutatus scutatus: Evert Karlsson, David Eaker and Lars Rydén, Toxicon, 1972, 10, 405 (Biokemiska Institutionen, Box 531, S-751 21 Uppsala 1, Sweden)

Purification of a presynaptic neurotoxin from the venom of the Australian tiger snake Notechis scutatus scutatus: Evert Karlsson, David Eaker and Lars Rydén, Toxicon, 1972, 10, 405 (Biokemiska Institutionen, Box 531, S-751 21 Uppsala 1, Sweden)