Effects of methylmercury exposure on 3T3-L1 adipocytes

• Main Author: Vertigan, Theresa
• Other Authors: Duffy, Lawrence, Drew, Kelly, Dunlap, Kriya
• Format: Thesis
• Language: English
• Published: 2015
• Subjects: Arctic; Fairbanks; Climate change; Human health; Alaska
• Online Access: http://hdl.handle.net/11122/5765

Thesis (M.S.) University of Alaska Fairbanks, 2015 Mercury-containing compounds are environmental pollutants that have become increasingly consequential in the Arctic regions of North America due to processes of climate change increasing their release and availability at northern latitudes. Currently, the form of mercury known to be most detrimental to human health is methylmercury, CH₃Hg⁺, which is found in the environment primarily accumulated in the tissues of predatory fish, including those consumed by Alaska Natives through subsistence gathering. Much is known about the neurotoxicity of methylmercury after exposure to high concentrations, but little is known about toxicity to other tissues and cell types, particularly for long-term exposure and the lower concentrations that would occur through fish consumption. This study aims to investigate the potential effects of methylmercury exposure on adipocytes, the main cellular components of adipose (fat) tissue, and explore possible consequences of exposure on metabolic disorders such as obesity and diabetes. Effects of methylmercury exposure on 3T3-L1 adipocytes in culture were assessed using assays for cytotoxicity and an ELISA assay for vascular endothelial growth factor (VEGF), a signaling molecule shown to be important for maintaining metabolic status in adipose tissue. Results showed that exposure to methylmercury leads to significant toxicity in adipocytes at exposures of 100 ng/mL during later stages of differentiation, but lower methylmercury concentrations produced little to no toxicity. Results also indicate that VEGF secretion is elevated in adipocytes exposed to methylmercury after the process of differentiating into mature, fat-storing cells. These results provide a basis for further exploration into metabolic consequences of methylmercury exposure.