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Abstract

Atrazine is a commonly used herbicide in the United States that is reported to contaminate drinking water sources. Studies indicate atrazine adversely impacts the neuroendocrine and reproductive systems, and that it may be a potential carcinogen. The current maximum contaminant level in drinking water is 3 parts per billion (ppb); however, levels higher than 3 ppb are often reported. Ongoing studies in our laboratory are investigating the immediate and latent adverse health outcomes associated with a developmental atrazine exposure and identifying the genetic and epigenetic mechanisms of toxicity using the zebrafish model system. MicroRNAs (miRNAs) are epigenetic regulators that posttranscriptionally control the translation of mRNA. A preliminary study indicated expression of miR-126, a miRNA associated with angiogenesis and tumorigenesis, to be altered following an embryonic atrazine exposure. To further investigate the developmental expression of miR-126 in zebrafish, quantitative PCR (qPCR) was used to profile expression throughout embryogenesis. Expression of miR- 126 was developmental time point specific with significant peaks in expression at 36, 60, and 72 hours postfertilization (hpf). The deregulation of miR-126 by atrazine was also tested using qPCR. Zebrafish embryos exposed to 0.3, 3, or 30 ppb of atrazine were compared to a control treatment at all six developmental time points. While a dose-response trend in upregulation at 36 hpf and in down-regulation at 48 hpf was observed, a significant increase in expression was only observed at 60 hpf in embryos exposed to 30 ppb atrazine. This study is providing a greater understanding of an epigenetic mechanism of atrazine toxicity.

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