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Anion Channel Inhibitor NPPB-Inhibited Fluoride Accumulation in Tea Plant (Camellia sinensis) Is Related to the Regulation of Ca(2+), CaM and Depolarization of Plasma Membrane Potential

Tea plant is known to be a hyper-accumulator of fluoride (F). Over-intake of F has been shown to have adverse effects on human health, e.g., dental fluorosis. Thus, understanding the mechanisms fluoride accumulation and developing potential approaches to decrease F uptake in tea plants might be bene...

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Autores principales: Zhang, Xian-Chen, Gao, Hong-Jian, Yang, Tian-Yuan, Wu, Hong-Hong, Wang, Yu-Mei, Zhang, Zheng-Zhu, Wan, Xiao-Chun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4730302/
https://www.ncbi.nlm.nih.gov/pubmed/26742036
http://dx.doi.org/10.3390/ijms17010057
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author Zhang, Xian-Chen
Gao, Hong-Jian
Yang, Tian-Yuan
Wu, Hong-Hong
Wang, Yu-Mei
Zhang, Zheng-Zhu
Wan, Xiao-Chun
author_facet Zhang, Xian-Chen
Gao, Hong-Jian
Yang, Tian-Yuan
Wu, Hong-Hong
Wang, Yu-Mei
Zhang, Zheng-Zhu
Wan, Xiao-Chun
author_sort Zhang, Xian-Chen
collection PubMed
description Tea plant is known to be a hyper-accumulator of fluoride (F). Over-intake of F has been shown to have adverse effects on human health, e.g., dental fluorosis. Thus, understanding the mechanisms fluoride accumulation and developing potential approaches to decrease F uptake in tea plants might be beneficial for human health. In the present study, we found that pretreatment with the anion channel inhibitor NPPB reduced F accumulation in tea plants. Simultaneously, we observed that NPPB triggered Ca(2+) efflux from mature zone of tea root and significantly increased relative CaM in tea roots. Besides, pretreatment with the Ca(2+) chelator (EGTA) and CaM antagonists (CPZ and TFP) suppressed NPPB-elevated cytosolic Ca(2+) fluorescence intensity and CaM concentration in tea roots, respectively. Interestingly, NPPB-inhibited F accumulation was found to be significantly alleviated in tea plants pretreated with either Ca(2+) chelator (EGTA) or CaM antagonists (CPZ and TFP). In addition, NPPB significantly depolarized membrane potential transiently and we argue that the net Ca(2+) and H(+) efflux across the plasma membrane contributed to the restoration of membrane potential. Overall, our results suggest that regulation of Ca(2+)-CaM and plasma membrane potential depolarization are involved in NPPB-inhibited F accumulation in tea plants.
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spelling pubmed-47303022016-02-11 Anion Channel Inhibitor NPPB-Inhibited Fluoride Accumulation in Tea Plant (Camellia sinensis) Is Related to the Regulation of Ca(2+), CaM and Depolarization of Plasma Membrane Potential Zhang, Xian-Chen Gao, Hong-Jian Yang, Tian-Yuan Wu, Hong-Hong Wang, Yu-Mei Zhang, Zheng-Zhu Wan, Xiao-Chun Int J Mol Sci Article Tea plant is known to be a hyper-accumulator of fluoride (F). Over-intake of F has been shown to have adverse effects on human health, e.g., dental fluorosis. Thus, understanding the mechanisms fluoride accumulation and developing potential approaches to decrease F uptake in tea plants might be beneficial for human health. In the present study, we found that pretreatment with the anion channel inhibitor NPPB reduced F accumulation in tea plants. Simultaneously, we observed that NPPB triggered Ca(2+) efflux from mature zone of tea root and significantly increased relative CaM in tea roots. Besides, pretreatment with the Ca(2+) chelator (EGTA) and CaM antagonists (CPZ and TFP) suppressed NPPB-elevated cytosolic Ca(2+) fluorescence intensity and CaM concentration in tea roots, respectively. Interestingly, NPPB-inhibited F accumulation was found to be significantly alleviated in tea plants pretreated with either Ca(2+) chelator (EGTA) or CaM antagonists (CPZ and TFP). In addition, NPPB significantly depolarized membrane potential transiently and we argue that the net Ca(2+) and H(+) efflux across the plasma membrane contributed to the restoration of membrane potential. Overall, our results suggest that regulation of Ca(2+)-CaM and plasma membrane potential depolarization are involved in NPPB-inhibited F accumulation in tea plants. MDPI 2016-01-05 /pmc/articles/PMC4730302/ /pubmed/26742036 http://dx.doi.org/10.3390/ijms17010057 Text en © 2016 by the authors; licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons by Attribution (CC-BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Zhang, Xian-Chen
Gao, Hong-Jian
Yang, Tian-Yuan
Wu, Hong-Hong
Wang, Yu-Mei
Zhang, Zheng-Zhu
Wan, Xiao-Chun
Anion Channel Inhibitor NPPB-Inhibited Fluoride Accumulation in Tea Plant (Camellia sinensis) Is Related to the Regulation of Ca(2+), CaM and Depolarization of Plasma Membrane Potential
title Anion Channel Inhibitor NPPB-Inhibited Fluoride Accumulation in Tea Plant (Camellia sinensis) Is Related to the Regulation of Ca(2+), CaM and Depolarization of Plasma Membrane Potential
title_full Anion Channel Inhibitor NPPB-Inhibited Fluoride Accumulation in Tea Plant (Camellia sinensis) Is Related to the Regulation of Ca(2+), CaM and Depolarization of Plasma Membrane Potential
title_fullStr Anion Channel Inhibitor NPPB-Inhibited Fluoride Accumulation in Tea Plant (Camellia sinensis) Is Related to the Regulation of Ca(2+), CaM and Depolarization of Plasma Membrane Potential
title_full_unstemmed Anion Channel Inhibitor NPPB-Inhibited Fluoride Accumulation in Tea Plant (Camellia sinensis) Is Related to the Regulation of Ca(2+), CaM and Depolarization of Plasma Membrane Potential
title_short Anion Channel Inhibitor NPPB-Inhibited Fluoride Accumulation in Tea Plant (Camellia sinensis) Is Related to the Regulation of Ca(2+), CaM and Depolarization of Plasma Membrane Potential
title_sort anion channel inhibitor nppb-inhibited fluoride accumulation in tea plant (camellia sinensis) is related to the regulation of ca(2+), cam and depolarization of plasma membrane potential
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4730302/
https://www.ncbi.nlm.nih.gov/pubmed/26742036
http://dx.doi.org/10.3390/ijms17010057
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