Toxicon : official journal of the International Society on Toxinology
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The seas and oceans around Australia harbour numerous venomous jellyfish. Chironex fleckeri, the box jellyfish, is the most lethal causing rapid cardiorespiratory depression and although its venom has been characterised, its toxins remain to be identified. A moderately effective antivenom exists which is also partially effective against another chirodropid, Chiropsalmus sp. ⋯ The venom contains a sodium channel modulator. Two species of Physalia are present and although one is potentially lethal, has not caused death in Australian waters. Other significant genera of jellyfish include Tamoya, Pelagia, Cyanea, Aurelia and Chyrosaora.
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Biography Historical Article
The pioneers of venom production for Australian antivenoms.
Before the introduction of the first Australian antivenom was the era of the self-styled 'snakemen' and their diverse snakebite remedies. Many received multiple bites from highly dangerous snakes, some of which were deliberately taken to either prove a certain treatment or liven up their show. ⋯ Collecting venoms in the development and early production of antivenoms was carried out by a number of professional herpetologists often with little or no reward and in some instances at the ultimate cost of their lives. This paper reviews the most important of those late nineteenth and twentieth century snakemen and their contributions to venom research, antivenom production and current toxinological knowledge.
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Bothrops jararaca venom (Bjv) is known to induce local inflammation and severe pain. Since, mast cells are able to secrete mediators involved in algesic processes, in this study we examined the putative role of these cells in the hyperalgesia triggered by Bjv in the rat paw. We noted that treatment with mast cell stabilizer sodium cromoglicate as well as with histamine and 5-hydroxytriptamine receptor antagonists meclizine and methysergide, respectively, inhibited the Bjv-induced hyperalgesia. ⋯ Bjv-induced histamine secretion was clearly sensitive to treatment with sodium cromoglicate and sodium nedocromil. We further observed that metalloproteinase inhibitors 1,10-phenantroline and DM43 inhibited mast cell degranulation in vitro, under conditions where inhibitors of phospholipase A(2) as well as of serine- and cysteine-proteinases were inactive. Altogether, our findings indicate that mast cells seem to contribute to the hyperalgesia caused by Bjv in the rat paw, and also provide evidence that this response might be dependent on the ability of the Bjv to activate directly mast cells.
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Mu-conotoxin SIIIA, a novel blocker of tetrodotoxin-resistant (TTX-R) voltage-gated sodium channels (VGSCs) has been identified from the fish-hunting cone snail, Conus striatus. The deduced sequence consists of a 20-residue signal peptide, a 31-residue pro-peptide, and a 20-residue mature toxin with its N-terminal Gln cyclized and C-terminus amidated. Mu-SIIIA shares the common cysteine arrangement with other mu-conotoxins. ⋯ Similarly, one crucial basic residue (Arg12 in mu-PIIIA) is replaced by serine in the latter two toxins. Such differences might endow them with the capacity to selectively inhibit TTX-S or TTX-R VGSCs. Considering that TTX-R VGSCs predominantly expressed in DRG neurons play pivotal roles in the nociceptive information transmission and that their specific antagonists are still lacking, mu-SIIIA might provide a useful tool for functional studies of these channels, and potentially be developed as an efficient pain killer.
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Comparative Study
Characterization of the acute pancreatitis induced by secretory phospholipases A2 in rats.
Acute pancreatitis (AP) is an inflammatory disease of the pancreas characterized by local inflammation and extrapancreatic effects such as lung injury. Secretory phospholipases A(2) (PLA(2)s) have been implicated in triggering AP, but their exact role to evoke AP is largely unknown. Therefore, we have tested the ability of sPLA(2)s to induce AP in rats, using venom sPLA(2)s with residual or high enzymatic activity (bothropstoxin-II and Naja mocambique mocambique venom PLA(2), respectively), as well as sPLA(2) devoid of catalytic activity (piratoxin-I). ⋯ The lung myeloperoxidase and serum amylase were also increased for all groups, although the Naja mocambique mocambique venom PLA(2) induced higher lung myeloperoxidase and serum amylase values, compared with piratoxin-I and/or bothropstoxin-II. Histopathology of pancreas and lungs in piratoxin-I-injected rats showed interstitial oedema in both tissues, and neutrophil infiltration with acinar cell necrosis in pancreas. In conclusion, sPLA(2)s induce AP in rats and the catalytic activity is not essential to induce the local effects in pancreas, although it appears to contribute partly to the remote lung injury.