image: This shows an Australian box jellyfish. Yanagihara AA, Shohet RV (2012) Cubozoan Venom-Induced Cardiovascular Collapse Is Caused by Hyperkalemia and Prevented by Zinc Gluconate in Mice. PLoS ONE 7(12): e51368. doi:10.1371/journal.pone.0051368 view more
Credit: Robert Hartwick
Box jellyfish of the Chironex species are among the most venomous animals in the world, capable of killing humans with their sting. Their venom, though, which kills by rapidly punching holes in human red blood cells, can be slowed down by administering zinc, according to research published December 12 in the open access journal PLOS ONE by Angel Yanagihara from the University of Hawaii and colleagues.
The researchers developed ways to extract venom from the jellyfish, and tested it on human blood and on mice. They found that the venom created pores in human red blood cells, making them leak large amounts of potassium, which causes cardiac arrest and death.
As Yanagihara elaborates, "For over 60 years researchers have sought to understand the horrifying speed and potency of the venom of the Australian box jellyfish, arguably the most venomous animal in the world. We have found that a previously disregarded hemolysin can cause an avalanche of reactions in cells. This includes an almost instantaneous, massive release of potassium that can cause acute cardiovascular collapse and death."
The authors treated the cells with a zinc compound which inhibits this process, and found that the treatment could slow the pore-forming process in cells, and increased survival times in the mice treated with the compound, zinc gluconate. The research suggests that the venom's capacity to increase potassium levels is what makes it so dangerous, and that rapid administration of zinc may be a potential life-saver in human sting victims.
Citation: Yanagihara AA, Shohet RV (2012) Cubozoan Venom-Induced Cardiovascular Collapse Is Caused by Hyperkalemia and Prevented by Zinc Gluconate in Mice. PLoS ONE 7(12): e51368. doi:10.1371/journal.pone.0051368
Financial Disclosure: This work was supported in part by grants 958935, 991879, 20001741, 20011908, 20061497, 20071368, and 47031 from the Hawaii Community Foundation, as well as grants U54NS039406 from the Institute of Neurological Disorders and Stroke, UH1HL073449 from the National Heart Lung and Blood Institute, P20RR016453 and G12RR003061 from the National Center for Research Resources, and grant R21DA024444 from the National Institute on Drug Abuse, National Institutes of Health. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
Competing Interest Statement: AAY has a provisional patent for treatment of syndromes associated with pore-forming toxins, U.S. Patent Office #61245238. RVS is listed as a contributing party to this document. The filing of a provisional patent application for treatment of syndromes associated with pore-forming toxins, U.S. Patent Office #61245238 by the University of Hawaii Office of Technology Transfer and Economic Development with RVS is listed as a contributing party does not alter the adherence of the authors (AAY and RVS) to all the PLOS ONE policies on sharing data and materials.
PLEASE LINK TO THE SCIENTIFIC ARTICLE IN ONLINE VERSIONS OF YOUR REPORT (URL goes live after the embargo ends): http://dx.plos.org/10.1371/journal.pone.0051368
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