Please use this identifier to cite or link to this item: http://hdl.handle.net/1959.13/43204
- An examination of the cardiovascular effects of an 'Irukandji' jellyfish, Alatina nr mordens
Winter, Kelly L.;
Isbister, Geoffrey K.;
Schneider, Jennifer J.;
Seymour, Jamie E.;
Hodgson, Wayne C.
- The University of Newcastle. Faculty of Health, School of Medicine and Public Health
- Irukandji syndrome is usually characterized by delayed severe abdominal, back and chest pain associated with autonomic effects including diaphoresis, hypertension and, in severe cases, myocardial injury and pulmonary oedema. It is most often associated with envenoming by the jellyfish Carukia barnesi, but a number of other jellyfish, including Alatina mordens, are now known to produce Irukandji syndrome. In the present study, nematocyst-derived venom from A. nr mordens (150-250 μg/kg, i.v.) produced a long-lasting pressor effect in anaesthetised rats. This pressor response (250μg/kg, i.v.) was significantly inhibited by prior administration of the α-adrenoceptor antagonist prazosin (200 μg/kg, i.v.) but not by CSL box jellyfish antivenom (300 U/kg, i.v.). A. nr mordens venom 250 μg/kg (i.v.) caused marked increases in plasma adrenaline and noradrenaline concentrations following administration in anaesthetised rats. The venom did not contain appreciable amounts of either adrenaline or noradrenaline. A. nr mordens venom (25 μg/ml) produced a contractile response in rat electrically stimulated vas deferens which was markedly reduced in tissues pre-treated with reserpine (0.1 mM) or guanethidine (0.1 mM). Sodium dodecyl sulphate (SDS)-PAGE analysis showed that A. nr mordens venom is comprised of multiple protein bands ranging from 10 to 200 kDa. Western blot analysis using CSL box jellyfish antivenom indicated several antigenic proteins in A. nr mordens venom, however, it did not detect all proteins present in the venom. This study characterizes the in vitro and in vivo effects of A. nr mordens venom and indicates that the cardiovascular effects are at least partially mediated by endogenous catecholamine release.
- Toxicology Letters Vol. 179, Issue 3, p. 118-123
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