You are here:
An Automated Heart Rate Detection Platform in Wild-Type Zebrafish for Cardiotoxicity Screening of Fine Particulate Matter Air Pollution
Martin, W., A. Tennant, R. Conolly, J. Stevens, D. DeMarini, Ian Gilmour, W. Cascio, M. Hays, B. Martin, L. Thompson, M. Hazari, S. Padilla, AND A. Farraj. An Automated Heart Rate Detection Platform in Wild-Type Zebrafish for Cardiotoxicity Screening of Fine Particulate Matter Air Pollution. Society of Toxicology Annual Meeting, San Antonio, Texas, March 11 - 16, 2018.
This work may help expedite cardiotoxicity determinations of fine PM from multiple air pollution sources as well as identify PM sources linked to the most toxic components. This may in turn facilitate risk assessment efforts.
Exposure to air pollution-derived particulate matter (PM) causes adverse cardiovascular health outcomes, with increasing evidence implicating soluble components of PM; however, the enormous number of unique PM samples from different air sheds far exceeds the capacity of conventional in vivo approaches to characterize potential health impacts. The zebrafish (Danio rerio) is a vertebrate model widely used to evaluate heart function in vivo given the high degree of functional conservation with humans. The purpose of this study was to develop a rapid cardiotoxicity screen for PM. Here, we present an assay that relies on measurement of a simple health metric, i.e. heart rate (HR), acquired quickly from hundreds of zebrafish embryos without the use of drug anesthetics, restraint, fluorescent labeling or confocal microscopy. Short video recordings acquired using bright-field imaging of 2-day old wild-type zebrafish were processed using an original algorithm and scripts that derived HR from heart contraction patterns. To examine the utility of this approach in the cardiotoxicity testing of PM, we compared the effects of treatment (5.5 h) with organic extracts of PM collected from compressor generated diesel exhaust (C-DEP), low sulfur diesel (B0), soy biodiesel (B100), and a 1:1 blend of B0 and B100 (B50). Epinephrine, a drug known to increase HR, caused dose-dependent increases in HR (peak increase = 14%, 177 beats per minute, or bpm, vs. vehicle control (155 bpm); whereas clonidine, a drug known to decrease HR, and all PM extracts caused decreases in HR (peak decreases of 10% for clonidine (120 bpm), 20% for C-DEP and B0 (125 bpm), and 8% for B100 (143 bpm), vs. vehicle (155 bpm, p B100. Analysis of B50 is in progress. Taken together, this approach may help expedite determinations of the relative cardiotoxicity of PM, drug candidates, and other chemicals [This abstract does not reflect USEPA policy.]