期刊
AQUATIC TOXICOLOGY
卷 78, 期 1, 页码 66-73出版社
ELSEVIER
DOI: 10.1016/j.aquatox.2006.02.007
关键词
caspase; cellular stress; hydrogen peroxide; Microcystis aeruginosa; microcystins; programmed cell death
An unprecedented bloom of the cyanobacterium, Microcystis aeruginosa Katz. occurred in the St. Lucie Estuary, FL in the summer of 2005. Samples were analyzed for toxicity by ELISA and by use of the polymerase chain reaction (PCR) with specific oligonucleotide primers for the mcyB gene that has previously been correlated with the biosynthesis of toxic microcystins. Despite the fact that secreted toxin levels were relatively low in dense natural assemblages (3.5 mu g l(-1)), detectable toxin levels increased by 90% when M. aeruginosa was stressed by an increase in salinity, physical injury, application of the chemical herbicide paraquat, or UV irradiation. The application of the same stressors caused a three-fold increase in the production of H2O2 when compared to non-stressed cells. The application of micromolar concentrations of H2O2 induced programmed cell death (PCD) as measured by a caspase protease assay. Catalase was capable of inhibiting PCD, implicating H2O2 as the inducing oxidative species. Our results indicate that physical stressors induce oxidative stress, which results in PCD and a concomitant release of toxin into the surrounding media. Remediation strategies that induce cellular stress should be approached with caution since these protocols are capable of releasing elevated levels of microcystins into the environment. (c) 2006 Elsevier B.V. All rights reserved.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据