Presenter: Connor Fitch
Mentor: William Cresko
Poster: 15
Major: Biology
Perchlorate is a water contaminant that has been detected in drinking water across the U.S. Severe health effects result from exposure to high levels of perchlorate. Our lab has shown that perchlorate causes several abnormalities
in fish, including increased thyroid proliferation in stickleback and zebrafish. We aim to determine the molecular basis of perchlorate’s effects on thyroid development and cell proliferation. Two hypotheses for increased cell proliferation include activation of Wnt signaling pathways, and perchlorate reduced expression of miR-16, miR-24, and miR-195, a group of microRNAs that suppress cell proliferation. We hypothesize that perchlorate causes direct damage by increasing oxidative stress in threespine stickleback, subsequently activating Wnt pathways and leading to cell proliferation. In order to test for the presence of oxidative stress, we performed an assay to calorimetrically quantify the presence of malondialdehyde (MDA)—a known oxidative stress biomarker. Forty stickleback embryos (20 control, 20 chronically exposed to 100ppm perchlorate) between 100-150 days post fertilization were analyzed for MDA. Perchlorate significantly increased the presence of MDA by 0.34μM in the treated group, correlating to a 13% increase of MDA over the control group. This supports our hypothesis that perchlorate causes oxidative stress in fish. Perchlorate causes a multitude of abnormalities during development and our data demonstrate that oxidative stress may be one contributing factor. Currently we are performing qPCR analysis to determine the involvement of SOD, tp53, and axin2a/b in oxidative stress from perchlorate. In addition, we are using qPCR to examine if perchlorate decreases expression of miR-16, miR-24, and miR-195. These data will help us to determine a molecular connection between perchlorate and oxygen radicals on interruption of normal thyroid function.