Research article Special Issues

Effects of Methylmercury exposure in 3T3-L1 Adipocytes

  • Received: 17 October 2016 Accepted: 03 February 2017 Published: 08 February 2017
  • 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 and accumulates in the tissues of piscivores, 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. 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 showed 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 on specific cell types and cell models.

    Citation: Theresa Vertigan, Kriya Dunlap, Arleigh Reynolds, Lawrence Duffy. Effects of Methylmercury exposure in 3T3-L1 Adipocytes[J]. AIMS Environmental Science, 2017, 4(1): 94-111. doi: 10.3934/environsci.2017.1.94

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  • 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 and accumulates in the tissues of piscivores, 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. 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 showed 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 on specific cell types and cell models.


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    [1] Arctic Monitoring and Assessment Programme (2011) AMAP Assessment 2011: Mercury in the Arctic. Arctic Pollution 2011.
    [2] Krabbenhoft DP, Sunderland EM (2013) Global change and mercury. Science 341: 1457-1458. doi: 10.1126/science.1242838
    [3] Fisher JA, Jacob DJ, Soerensen AL, et al. (2012) Riverine source of Arctic Ocean mercury inferred from atmospheric observations. Nat Geosci 5: 499-504. doi: 10.1038/ngeo1478
    [4] Stern GA, Macdonald RW, Outridge PM, et al. (2012). How does climate change influence Arctic mercury? Sci Total Environ 414: 22-42. doi: 10.1016/j.scitotenv.2011.10.039
    [5] Loring PA, Duffy LK (2011) Managing environmental risks: the benefits of a place-based approach. Rural and Remote Health 11: 1800-1808.
    [6] Lemire M, Kwan M, Laouan-Sidi AE, et al. (2015) Local country food sources of methylmercury, selenium and omega-3 fatty acids in Nunavik, Northern Quebec. Sci Total Environ 509: 248-259.
    [7] Mahaffey KR (1999) Methylmercury: A new look at the risks. Public Health Reports 114: 397-413. doi: 10.1093/phr/114.5.397
    [8] Kanda H, Shinkai Y, Kumagai Y (2014) S -Mercuration of cellular proteins by methylmercury and its toxicological implications. J Toxicol Sci 39: 687-700. doi: 10.2131/jts.39.687
    [9] Weiss B (2007) Why Methylmercury Remains a Conundrum 50 Years after Minamata. Toxicol Sci 97: 223-225. doi: 10.1093/toxsci/kfm047
    [10] Kerper LE, Ballatori N, Clarkson TW (1992) Methylmercury transport across the blood-brain barrier by an amino acid carrier. Am J Physiol-Reg I 262: 761-765.
    [11] Kumagai Y, Kanda H, Shinkai Y, et al. (2013) The Role of the Keap1/Nrf2 Pathway in the Cellular Response to Methylmercury. Oxid Med Cell Longev 2013.
    [12] Hirooka T, Yamamoto C, Yasutake A, et al. (2013) Expression of VEGF-related proteins in cultured human brain microvascular endothelial cells and pericytes after exposure to methylmercury. J Toxicol Sci 38: 837-845. doi: 10.2131/jts.38.837
    [13] He K, Xun P, Liu K, et al. (2013) Mercury exposure in young adulthood and incidence of diabetes later in life: the CARDIA Trace Element Study. Diabetes Care 36: 1584-1589. doi: 10.2337/dc12-1842
    [14] Futatsuka M, Kitano T, Wakamiya J (1996) An epidemiological study on diabetes mellitus in the population living in a methyl mercury polluted area. J Epidemiol 6: 204-208. doi: 10.2188/jea.6.204
    [15] Yamamoto M, Yanagisawa R, Motomura E, et al. (2013) Increased methylmercury toxicity related to obesity in diabetic KK-Ay mice. J Appl Toxicol 34: 914-923.
    [16] Barnes DM, Hanlon PR, Kircher EA (2003) Effects of inorganic HgCl2 on adipogenesis. Toxicol Sci 75: 368-377. doi: 10.1093/toxsci/kfg195
    [17] Barnes DM, Kircher EA (2005) Effects of mercuric chloride on glucose transport in 3T3-L1 adipocytes. Toxicol in Vitro  19: 207-214. doi: 10.1016/j.tiv.2004.08.005
    [18] Cao Y (2013) Angiogenesis and vascular functions in modulation of obesity, adipose metabolism, and insulin sensitivity. Cell Metab 18: 478-489. doi: 10.1016/j.cmet.2013.08.008
    [19] Elias I, Franckhauser S, Bosch F (2013) New insights into adipose tissue VEGF-A actions in the control of obesity and insulin resistance. Adipocyte 2: 109-112. doi: 10.4161/adip.22880
    [20] Sun K, Asterholm IW, Kusminski CM, et al. (2012) Dichotomous effects of VEGF-A on adipose tissue dysfunction. Proc Natl Acad Sci USA 109: 5874-5879. doi: 10.1073/pnas.1200447109
    [21] Trayhurn P, Bing C, Wood IS (2005) Adipose Tissue and Adipokines-Energy Regulation from the Inside Out. In The WALTHAM International Nutritional Sciences Symposium (pp. 1935–1939).
    [22] Williams MG (1997) Development of Insulin Resistance in 3T3-L1 Adipocytes. J Biol Chem 272: 7759-7764. doi: 10.1074/jbc.272.12.7759
    [23] Martini CN, Brandani JN, Gabrielli M, et al. (2014) Effect of hexavalent chromium on proliferation and differentiation to adipocytes of 3T3-L1 fibroblasts. Toxicol in Vitro  28: 700-706. doi: 10.1016/j.tiv.2014.02.003
    [24] American Type 25 Culture Collection (2011) Chemically-Induced Differentiation of ATCC CL-173 (3T3-L1) Using Single-component Commercially-available Reagents. Retrieved February 10, 2015, available from: http://www.atcc.org/~/media/6124AF1E4C2A47CF904435117909AC25.ashx
    [25] Hamade AK (2014) Fish Consumption Advice for Alaskans: A Risk Management Strategy to Optimize the Public's Health (pp. 1–78). Section of Epidemiology Division of Public Health Department of Health and Social Services State of Alaska
    [26] Elias I, Franckhauser S, Bosch F (2013) New insights into adipose tissue VEGF-A actions in the control of obesity and insulin resistance. Adipocyte 2: 109-112. doi: 10.4161/adip.22880
    [27] Sun K, Asterholm IW, Kusminski CM, et al. (2012) Dichotomous effects of VEGF-A on adipose tissue dysfunction. Proc Natl Acad Sci USA 109: 5874-5879. doi: 10.1073/pnas.1200447109
    [28] Gregoire FM, Smas CM, Sul HS (1998) Understanding Adipocyte Differentiation. Physiol Rev 78: 783-810.
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