title: Weak electromagnetic fields alter Ca(2+) handling and protect against hypoxia-mediated damage in primary newborn rat myotube cultures.
abstract: Weak electromagnetic fields (WEF) enhance Ca(2+) entry into cells via voltage-gated Ca(2+) channels and affect various aspects of metabolism, structure, and function. However, little information is available on the effect of WEF on skeletal muscle, which depends primarily on intracellular Ca(2+) stores for function and metabolism. Here, we examine the effects of 30 min exposure of rat primary myotube cultures to WEF (1.75 μT, 16 Hz) on Ca(2+) handling and creatine kinase (CK) release. Free myoplasmic Ca(2+) concentration ([Ca(2+) i]) was measured with the ratiometric dye indo-1. WEF did not affect basal [Ca(2+)]i but decreased the twitch [Ca(2+)]i transient in a time-dependent manner, and the twitch amplitude was decreased to ∼30 % after 30 min. WEF completely abolished the increase in [Ca(2+)]i induced by potassium chloride (∼60 mM) but had no effect on the increase induced by caffeine (∼6 mM). Hypoxia (2 h exposure to 100 % argon) resulted in a marked loss of CK into the medium (400 % of normoxic value), as well as a rapid (within 20 min) and sustained increase in basal [Ca(2+)]i (∼20 % above baseline). However, during exposure to WEF, basal [Ca(2+)]i remained constant during the initial 60 min of hypoxia and, thereafter, increased to levels similar to those observed in the absence of WEF. Finally, WEF blocked about 80 % of hypoxia-mediated CK release (P < 0.05). These data demonstrate that WEF inhibits increases in [Ca(2+)]i by interfering with muscle excitation and protects against muscle damage induced by hypoxia. Thus, WEF may have therapeutic/protective effects on skeletal muscle.
authors.affiliation: Department of Physical Therapy, School of Health Sciences, Ariel University, Ariel, 40700, Israel.
authors.forename: Dana
authors.initials: D
authors.lastname: Adler
authors.affiliation: School of Engineering and the Institute of Nanotechnology and Advanced Materials, Bar Ilan University, Ramat Gan, 52900, Israel.
authors.forename: Dror
authors.initials: D
authors.lastname: Fixler
authors.affiliation: Department of Biomedical Engineering, Tel-Aviv University, Ramat Aviv, 69978, Israel.
authors.forename: Mickey
authors.initials: M
authors.lastname: Scheinowitz
authors.affiliation: Faculty of Life Sciences, Bar Ilan University, Ramat Gan, 52900, Israel.
authors.forename: Asher
authors.initials: A
authors.lastname: Shainberg
authors.affiliation: Department of Physical Therapy, School of Health Sciences, Ariel University, Ariel, 40700, Israel. abramk@ariel.ac.il.
authors.forename: Abram
authors.initials: A
authors.lastname: Katz
mesh_terms: D000818:Animals; D002110:Caffeine / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism*; D020013:Calcium Signaling / Q000187:drug effects / Q000502:physiology; D003402:Creatine Kinase / Q000378:metabolism; D004574:Electromagnetic Fields; D000860:Hypoxia / Q000378:metabolism*; D007211:Indoles / Q000378:metabolism; D009119:Muscle Contraction / Q000187:drug effects / Q000502:physiology; D018485:Muscle Fibers, Skeletal / Q000187:drug effects / Q000378:metabolism*; D018482:Muscle, Skeletal / Q000187:drug effects / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D007211:Indoles; D002110:Caffeine; D003402:Creatine Kinase; C048960:indo-1; D002118:Calcium
keywords: Caffeine; Creatine kinase; Hypoxia; KCl; Muscle contraction; Myotubes