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Effects of the marine toxin palytoxin on human skin keratinocytes: role of ionic imbalance

PELIN, MARCO
•
ZANETTE, CATERINA
•
DE BORTOLI, MARCO
altro
FLORIO, CHIARA
2011
  • journal article

Periodico
TOXICOLOGY
Abstract
Palytoxin (PLTX), a marine toxin identified in Palythoa zoanthid corals and Ostreopsis dinoflagellates, represents an increasing hazard for human health. Recently, dermatological problems have been associated to cutaneous exposure to PLTX during Ostreopsis blooms arising the need for experimental data characterizing PLTX effects on the skin. This study highlights in vitro the cytotoxic effects of PLTX on human keratinocytes (HaCaT cell line). A short time exposure (4 h) to PLTX reduced mitochondrial activity (MTT assay), cell mass (SRB assay) and plasma membrane integrity (LDH leakage) with different potencies: EC50 values of 6.1±1.3×10−11, 4.7±0.9×10−10M and 1.8±0.1×10−8 M, respectively. PLTX effect on mitochondrial activity was ouabain- and Na+-sensitive, but only partially sensitive to removal of Ca2+ ions. One hour exposure to the toxin also induced a Na+-dependent and Ca2+-independent superoxide anion production. These results indicate that among the chain of intracellular events following the interaction of PLTX with the Na+/K+-ATPase the first and crucial step is the increased intracellular Na+ concentration that triggers a sequence of cell dysfunction involving mitochondrial affection and oxidative stress, leading to an irreversible cell death. The PLTX concentrations inducing cytotoxicty seem to be lower than those of potential cutaneous human exposure during Ostreopsis ovata blooms, indicating the harmful potential of the toxin.
DOI
10.1016/j.tox.2011.01.010
WOS
WOS:000288578900004
Archivio
http://hdl.handle.net/11368/2309592
info:eu-repo/semantics/altIdentifier/scopus/2-s2.0-79951575702
Diritti
metadata only access
Soggetti
  • Palytoxin

  • human HaCaT keratinoc...

  • cytotoxicity

  • ROS

  • mitochondrial dysfunc...

  • cutaneous toxicity

Web of Science© citazioni
31
Data di acquisizione
Jan 19, 2024
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