Triclosan impairs excitation-contraction coupling and Ca~(2+) dynamics in striated muscle

Cherednichenko G.; Zhang R.; Bannister R.A.Timofeyev V.Li N.Fritsch E.B.Feng W.Barrientos G.C.Schebb N.H.Hammock B.D.Beam K.G.Chiamvimonvat N.Pessah I.N.

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Triclosan impairs excitation-contraction coupling and Ca~(2+) dynamics in striated muscle

机译：Triclosan impairs excitation-contraction coupling and Ca~(2+) dynamics in striated muscle

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Triclosan (TCS), a high-production-volume chemical used as a bactericide in personal care products, is a priority pollutant of growing concern to human and environmental health. TCS is capable of altering the activity of type 1 ryanodine receptor (RyR1), but its potential to influence physiological excitation-contraction coupling (ECC) and muscle function has not been investigated. Here, we report that TCS impairs ECC of both cardiac and skeletal muscle in vitro and in vivo. TCS acutely depresses hemodynamics and grip strength in mice at doses ≥12.5 mg/kg i.p., and a concentration ≥0.52 μM in water compromises swimming performance in larval fathead minnow. In isolated ventricular cardiomyocytes, skeletal myotubes, and adult flexor digitorum brevis fibers TCS depresses electrically evoked ECC within ～10-20 min. In myotubes, nanomolar to low micromolar TCS initially potentiates electrically evoked Ca2+ transients followed by complete failure of ECC, independent of Ca2+ store depletion or block of RyR1 channels. TCS also completely blocks excitation-coupled Ca2+ entry. Voltage clamp experiments showed that TCS partially inhibits L-type Ca2+ currents of cardiac and skeletal muscle, and 3HPN200 binding to skeletal membranes is noncompetitively inhibited by TCS in the same concentration range that enhances 3Hryanodine binding. TCS potently impairs orthograde and retrograde signaling between Ltype Ca2+ and RyR channels in skeletal muscle, and L-type Ca2+ entry in cardiac muscle, revealing a mechanism by which TCS weakens cardiac and skeletal muscle contractility in a manner that may negatively impact muscle health, especially in susceptible populations.

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《Proceedings of the National Academy of Sciences of the United States of America》 |2012年第35期|14158-14163|共6页
作者
Cherednichenko G.; Zhang R.; Bannister R.A.Timofeyev V.Li N.Fritsch E.B.Feng W.Barrientos G.C.Schebb N.H.Hammock B.D.Beam K.G.Chiamvimonvat N.Pessah I.N.;
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作者单位

Department of Molecular Biosciences, School of Veterinary Medicine, University of California, Davis, CA 95616, United States;

Cardiology Division, Department of Medicine, University of Colorado Denver-Anschutz Medical Campus, Aurora, CO 80045, United States;

Division of Cardiovascular Medicine, Department of Internal Medicine, University of California, Davis, CA 95616, United StatesDepartment of Entomology and Cancer Center, University of California, Davis, CA 95616, United StatesDepartment of Physiology and Biophysics, University of Colorado Denver-Anschutz Medical Campus, Aurora, CO 80045, United States;

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收录信息美国《科学引文索引》(SCI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
原文格式 PDF
正文语种英语
中图分类自然科学总论;
关键词
Cachexia; Calcium regulation; Heart failure; L-type current; Muscle contraction;

Triclosan impairs excitation-contraction coupling and Ca~(2+) dynamics in striated muscle

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