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Toxins 2016, 8(10), 279; doi:10.3390/toxins8100279

Polyamines as Snake Toxins and Their Probable Pharmacological Functions in Envenomation

1
Division of Faculty Affairs, Okinawa Institute of Science and Technology Graduate University, 1919-1 Tancha, Onna-son, Kunigami-gun, Okinawa-ken 904-0495, Japan
2
Ecology and Evolution Unit, Okinawa Institute of Science and Technology Graduate University, 1919-1 Tancha, Onna-son, Kunigami-gun, Okinawa-ken 904-0495, Japan
3
Division of Research Support, Okinawa Institute of Science and Technology Graduate University, 1919-1 Tancha, Onna-son, Kunigami-gun, Okinawa-ken 904-0495, Japan
*
Author to whom correspondence should be addressed.
Academic Editor: R. Manjunatha Kini
Received: 13 July 2016 / Accepted: 5 September 2016 / Published: 26 September 2016
(This article belongs to the Section Animal Venoms)
View Full-Text   |   Download PDF [1069 KB, uploaded 26 September 2016]   |  

Abstract

While decades of research have focused on snake venom proteins, far less attention has been paid to small organic venom constituents. Using mostly pooled samples, we surveyed 31 venoms (six elapid, six viperid, and 19 crotalid) for spermine, spermidine, putrescine, and cadaverine. Most venoms contained all four polyamines, although some in essentially trace quantities. Spermine is a potentially significant component of many viperid and crotalid venoms (≤0.16% by mass, or 7.9 µmol/g); however, it is almost completely absent from elapid venoms assayed. All elapid venoms contained larger molar quantities of putrescine and cadaverine than spermine, but still at levels that are likely to be biologically insignificant. As with venom purines, polyamines impact numerous physiological targets in ways that are consistent with the objectives of prey envenomation, prey immobilization via hypotension and paralysis. Most venoms probably do not contain sufficient quantities of polyamines to induce systemic effects in prey; however, local effects seem probable. A review of the pharmacological literature suggests that spermine could contribute to prey hypotension and paralysis by interacting with N-methyl-d-aspartate (NMDA) and α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors, nicotinic and muscarinic acetylcholine receptors, γ-Aminobutyric acid (GABA) receptors, blood platelets, ryanodine receptors, and Ca2+-ATPase. It also blocks many types of cation-permeable channels by interacting with negatively charged amino acid residues in the channel mouths. The site of envenomation probably determines which physiological targets assume the greatest importance; however, venom-induced liberation of endogenous, intracellular stores of polyamines could potentially have systemic implications and may contribute significantly to envenomation sequelae. View Full-Text
Keywords: polyamines; snake venoms; spermine; spermidine; putrescine; cadaverine; titer; pharmacology; envenomation sequelae polyamines; snake venoms; spermine; spermidine; putrescine; cadaverine; titer; pharmacology; envenomation sequelae
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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MDPI and ACS Style

Aird, S.D.; Villar Briones, A.; Roy, M.C.; Mikheyev, A.S. Polyamines as Snake Toxins and Their Probable Pharmacological Functions in Envenomation. Toxins 2016, 8, 279.

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