Phenanthrene exposure causes cardiac arrhythmia in embryonic zebrafish via perturbing calcium handling

被引：44

作者：

Zhang, Youyu ^{[1
]}

Huang, Lixing ^{[1
]}

Zuo, Zhenghong ^{[1
,2
]}

Chen, Yixin ^{[1
]}

Wang, Chonggang ^{[1
,2
]}

机构：

[1] Xiamen Univ, State Key Lab Cellular Stress Biol, Sch Life Sci, Xiamen, Peoples R China

[2] Xiamen Univ, State Key Lab Marine Environm Sci, Xiamen, Peoples R China

来源：

AQUATIC TOXICOLOGY | 2013年 / 142卷

基金：

中国国家自然科学基金;

关键词：

Phenanthrene; Zebrafish; Embryos; Cardiac arrhythmia; Calcium; POLYCYCLIC AROMATIC-HYDROCARBONS; HOLT-ORAM-SYNDROME; SALMON ONCORHYNCHUS-GORBUSCHA; SARCOPLASMIC-RETICULUM; HEART-FAILURE; CONDUCTION SYSTEM; CRUDE-OIL; TBX5; CONTRACTION; EXPRESSION;

D O I：

10.1016/j.aquatox.2013.07.014

中图分类号：

Q17 [水生生物学];

学科分类号：

071004 ;

摘要：

Phenanthrene (Phe) is one of the most abundant and ubiquitous polycyclic aromatic hydrocarbons in the aquatic environment. It is known that Phe has cardiotoxic effects, but knowledge concerning the mechanism of cardiac dysfunction caused by Phe is still limited. In this study, zebrafish embryos were exposed to environmentally relevant concentrations of Phe, and an increase of an irregular rhythm was observed in Phe treated embryos. Disordered calcium (Ca2+) handling characterized by impaired sarcoplasmic reticulum Ca2+ uptake, and obvious Ca2+ accumulation in the cytoplasm was observed in rat embryonic cardiac myoblasts (H9C2) exposed to Phe. The mRNA level as well as protein expression of the SERCA2a Ca2+ pump in zebrafish hearts or H9C2 cells was significantly decreased by Phe exposure. The activity of Ca2+-ATPase in H9C2 cells was inhibited by Phe. Both the mRNA and protein levels of TBX5, a direct regulator of SERCA2a, were significantly decreased by Phe exposure. These results suggested that exposure to Phe could lead to arrhythmia in zebrafish embryos via perturbing the calcium handling pathway. (C) 2013 Elsevier B.V. All rights reserved.

引用

页码：26 / 32

页数：7

共 46 条

[1]

[Anonymous], DEVELOPMENT

[2] Calcium cycling in heart failure: how the fast became too furious [J].

Armand, AS ;

De Windt, LJ .

CARDIOVASCULAR RESEARCH, 2004, 62 (03) :439-441

[3] TBX5 drives Scn5a expression to regulate cardiac conduction system function [J].

Arnolds, David E. ;

Liu, Fang ;

Fahrenbach, John P. ;

Kim, Gene H. ;

Schillinger, Kurt J. ;

Smemo, Scott ;

McNally, Elizabeth M. ;

Nobrega, Marcelo A. ;

Patel, Vickas V. ;

Moskowitz, Ivan P. .

JOURNAL OF CLINICAL INVESTIGATION, 2012, 122 (07) :2509-2518

[4] INTRACELLULAR CALCIUM HOMEOSTASIS IN CARDIAC MYOCYTES [J].

BARRY, WH ;

BRIDGE, JHB .

CIRCULATION, 1993, 87 (06) :1806-1815

[5] Cardiac Metabolism and Arrhythmias [J].

Barth, Andreas S. ;

Tomaselli, Gordon F. .

CIRCULATION-ARRHYTHMIA AND ELECTROPHYSIOLOGY, 2009, 2 (03) :327-335

[6] Different TBX5 interactions in heart and limb defined by Holt-Oram syndrome mutations [J].

Basson, CT ;

Huang, TS ;

Lin, RC ;

Bachinsky, DR ;

Weremowicz, S ;

Vaglio, A ;

Bruzzone, R ;

Quadrelli, R ;

Lerone, M ;

Romeo, G ;

Silengo, M ;

Pereira, A ;

Krieger, J ;

Mesquita, SF ;

Kamisago, M ;

Morton, CC ;

Pierpont, MEM ;

Müller, CW ;

Seidman, JG ;

Seidman, CE .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1999, 96 (06) :2919-2924

[7] Na-Ca exchange and Ca fluxes during contraction and relaxation in mammalian ventricular muscle [J].

Bers, DM ;

Bassani, JWM ;

Bassani, RA .

SODIUM-CALCIUM EXCHANGE: PROCEEDINGS OF THE THIRD INTERNATIONAL CONFERENCE, 1996, 779 :430-442

[8] Apoptotic and Necrotic Action Mechanisms of Trimethyltin in Human Hepatoma G2 (HepG2) Cells [J].

Cai, Jiali ;

Wang, Mengmeng ;

Li, Bowen ;

Wang, Chonggang ;

Chen, Yixin ;

Zuo, Zhenghong .

CHEMICAL RESEARCH IN TOXICOLOGY, 2009, 22 (09) :1582-1587

[9] Cytochrome P4501A induction in oil-exposed pink salmon Oncorhynchus gorbuscha embryos predicts reduced survival potential [J].

Carls, MG ;

Heintz, RA ;

Marty, GD ;

Rice, SD .

MARINE ECOLOGY PROGRESS SERIES, 2005, 301 :253-265

[10] Constitutive cardiac overexpression of sarcoplasmic/endoplasmic reticulum Ca2+-ATPase delays myocardial failure after myocardial infarction in rats at a cost of increased acute arrhythmias [J].

Chen, Y ;

Escoubet, B ;

Prunier, F ;

Amour, J ;

Simonides, WS ;

Vivien, B ;

Lenoir, C ;

Heimburger, M ;

Choqueux, C ;

Gellen, B ;

Riou, B ;

Michel, JB ;

Franz, WM ;

Mercadier, JJ .

CIRCULATION, 2004, 109 (15) :1898-1903

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