卡尔顿毒素 2（KmTx2）对卡尔多利毒素（Dinophyceae）的细胞毒性机制。
The cytotoxic mechanism of karlotoxin 2 (KmTx 2) from Karlodinium veneficum (Dinophyceae).
机构信息
University of Maryland Center for Environmental Science, Institute of Marine and Environmental Technology, 701 East Pratt Street, Suite 236, Baltimore, MD 21202, USA.
University of Maryland, Baltimore, Center for Biomedical Engineering and Technology and Department of Physiology, University of Maryland School of Medicine, Baltimore, MD 21201, USA.
出版信息
Aquat Toxicol. 2015 Feb;159:148-55. doi: 10.1016/j.aquatox.2014.11.028. Epub 2014 Dec 15.
Abstract
This study demonstrates that the polyketide toxin karlotoxin 2 (KmTx 2) produced by Karlodinium veneficum, a dinoflagellate associated with fish kills in temperate estuaries world-wide, alters vertebrate cell membrane permeability. Microfluorimetric and electrophysiological measurements were used to determine that vertebrate cellular toxicity occurs through non-selective permeabilization of plasma membranes, leading to osmotic cell lysis. Previous studies showed that KmTx 2 is lethal to fish at naturally-occurring concentrations measured during fish kills, while sub-lethal doses severely damage gill epithelia. This study provides a mechanistic explanation for the association between K. veneficum blooms and fish kills that has long been observed in temperate estuaries worldwide.
摘要
本研究表明，由中肋骨条藻引起的多酮毒素卡尔多毒素 2（KmTx2）改变了脊椎动物细胞膜的通透性。微荧光和电生理测量表明，脊椎动物细胞毒性是通过对质膜的非选择性渗透，导致细胞渗透溶解。先前的研究表明，KmTx2 在鱼类死亡期间自然存在的浓度下对鱼类是致命的，而亚致死剂量则严重损害了鱼类的鳃上皮。这项研究为中肋骨条藻水华与世界范围内温带河口长期观察到的鱼类死亡之间的关联提供了一种机制解释。
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