期刊
AQUATIC TOXICOLOGY
卷 186, 期 -, 页码 50-66出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.aquatox.2017.02.021
关键词
Apoptosis; BAPTA-AM; Chlamydomonas reinhardtii; Intracellular free calcium homeostasis; Oxidative stress; Triclosan
资金
- MINECO/FEDER EU [CTM2013-45775-C2-2-R, CGL2010-15675]
- MINECO/FEDER EU
- MECD
- Postdoctoral Fellowship Juan de la Cierva from MINECO
The present study was aimed at investigating the role of intracellular free calcium, [Ca2+](c), in the early cellular response of the green alga Chlamydomonas reinhardtii to the emergent pollutant Triclosan (13.8 mu M; 24 h of exposure). There is a growing concern about the persistence and toxicity of this antimicrobial in aquatic environments, where non-target organisms such as C. reinhardtii, a primary producer of ecological relevance, might be severely impacted. A mechanistic study was undertaken which combined flow cytometry protocols, physiological as well as gene expression analysis. As an early response, Triclosan strongly altered [Ca2+](c) homeostasis which could be prevented by prechelation with the intracellular calcium chelator BAPTA-AM. Triclosan induced ROS overproduction which ultimately leads to oxidative stress with loss of membrane integrity, membrane depolarization, photosynthesis inhibition and mitochondrial membrane depolarization; within this context, Triclosan also induced an increase in caspase 3/7 activity and altered the expression of metacaspase genes which are indicative of apoptosis. All these adverse outcomes were dependent on [Ca2+](c). Interestingly, an interconnection between [Ca2+](c) alterations and increased ROS formation by Triclosan was found. Taken altogether these results shed light on the mechanisms behind Triclosan toxicity in the green alga Chlamydomonas reinhardtii and demonstrate the role of [Ca2+](c), in mediating the observed toxicity. (C) 2017 Elsevier B.V. All rights reserved.
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