Environmental toxicants can cause acute adverse health outcomes and can predispose individuals to health issues that arise long after the exposure has terminated. In the Sadler lab, we use zebrafish as a tool to study the factors that cause liver disease. We are focused on how chronic exposure to low dosages of inorganic arsenic, a natural component of the Earth's crust, increases the risk of liver disease and interacts with other toxicants to cause toxicity. Work in the Sadler Lab lab has shown that early life exposure to low doses of arsenic sensitizes zebrafish to later exposure to ethanol, causing fatty liver disease (Bambino, Kathryn, Chi Zhang, Christine Austin, Chitra Amarasiriwardena, Manish Arora, Jaime Chu, and Kirsten C. Sadler. "Inorganic arsenic causes fatty liver and interacts with ethanol to cause alcoholic liver disease in zebrafish." Disease models & mechanisms 11, no. 2 (2018): dmm031575). A proposed mechanism of arsenic-induced hepatotoxicity is through induction of cell stress pathways, including oxidative stress and endoplasmic reticulum (ER) stress. Patrice is expanding this work to identify other toxicants that synergize with arsenic to cause disease and to determine the role of oxidative and ER stress in liver disease caused by arsenic.
Delaney, P., Nair, A.R., Palmer, C., Khan, N., and Sadler, K.C. (2020) Arsenic induced redox imbalance triggers the unfolded protein response in the liver of zebrafish. Toxicol Appl Pharmacol. 115307. PMID: 33147493.
Smith E.G., Hume B.C.C., Delaney P., Wiedenmann J., and Burt J.A. (2017) Genetic structure of coral-Symbiodinium symbioses on the world's warmest reefs. PLoS One. PMID: 28666005; PMCID: PMC5493405.