You are here:
EXPOSURE OF CULTURED MYOCYTES TO ZINC RESULTS IN ALTERED BEAT RATE AND INTERCELLULAR COMMUNICATION.
Citation:
Graff, D., R B. Devlin, W. E. Cascio, J. Brackhan, B. MullerBorer, AND Bowman. Jill. EXPOSURE OF CULTURED MYOCYTES TO ZINC RESULTS IN ALTERED BEAT RATE AND INTERCELLULAR COMMUNICATION. Presented at Society of Toxiocology 42nd Annual Meeting, Salt Lake City, Utah, March 9-13, 2003.
Description:
Exposure of cultured myocytes to zinc results in altered beat rate and intercellular communication
Graff, Donald W, Devlin, Robert B, Brackhan, Joseph A, Muller-Borer, Barbara J, Bowman, Jill S, Cascio, Wayne E.
Exposure to ambient air pollution particulate matter (PM) is associated with increased morbidity and mortality. Recent toxicological studies have reported PM-induced changes in a number of cardiac parameters, including heart rate variability, arrhythmias, repolarization, and internal defibrillator discharges. The purpose of this study is to identify cellular processes that may contribute to cardiac dysfunction following PM exposure. Isolated neonatal rat ventricular myocytes were cultured for 11 days and then exposed to different concentrations of zinc (Zn), a soluble component found in many PM samples. Zn significantly decreased spontaneous myocytes beat rate by 15% 2hrs following exposure and 17% at 4 hrs compared to baseline. Since beat rate is influenced by intercellular communications, fluorescent recovery after photobleaching (FRAP) was then measured. FRAP rate, a physiological measure of cell-to-cell communication and gap junction permeability, was significantly decreased by 76% 4 hrs after exposure but not at 2 hrs. Changes were measured in gene expression of gap junction proteins which mediate communication between myocytes. Exposure of myocytes to Zn for 24 hrs resulted in a 76% increase in mRNA coding for connexin 43. These data suggest that soluble metals found in air pollution particles can affect the ability of cardiac myocytes to spontaneously beat, possibly by disruption of cell-to-cell communication. These effects potentially reflect disturbances in repolarization and impulse propagation which could contribute to PM-associated cardiac morbidity and mortality. This abstract does not necessarily reflect EPA policy.