- B.A., Wheaton College, 2001
- Ph.D., Brown University, 2006
- General Biology
- Cell Biology
Office Hours (Fall 2012)
Monday 11:30-1 and Tuesday/Thursday 9-10 am
or by appointment.
Chronic exposure to metal compounds, such as nickel, cobalt, and cadmium, has long been known to increase cancer incidence among affected individuals. Unlike organic waste, metals are not degraded by living organisms and may accumulate up to harmful levels. The mechanisms of cancer induction by these compounds are not well understood, but recent research shows a multifaceted pattern of metal interactions with cellular macromolecules and genetic processes. My primary research interest is focused on understanding the molecular mechanisms of cytotoxicity and genotoxicity following coexposure to heavy metals. In order to understand these processes, we use molecular and genetic approaches in a human cell culture model. Altogether, our improved understanding of the mechanisms of DNA damage and toxicity will enhance our knowledge in the development of cancer.
I have had numerous students involved in this project, both during the summer and academic year. The opportunity to work in the laboratory has enabled the students to experience the frustrations and excitement of research. Additionally, many students who have worked in my lab have gone on to pursue advanced degrees and obtain research internships at prestigious institutions. Each year students from my lab present their results at the annual Society of Toxicology Meeting as well as at various Washington College events
In addition to the human cell culture model to examine the cytotoxicity and genotoxicity of heavy metals we are also using a zebrafish model to examine developmental defects following exposure. Zebrafish has long been considered a powerful alternative animal model because of its tractable genetics and embryology. More specifically, it has proven to be particularly important in ecotoxicology for studies examining the effects of heavy metals in water and soil samples. In my research, adult zebrafish and larvae are exposed to various concentrations of heavy metals and developmental abnormalities are monitored.
- Reynolds, M., Armknecht, S., Johnston, T., Zhitkovich, A. Undetectable role of oxidative damage in cell cycle, cytotoxic, and clastogenic effects of Cr(VI) in human lung cells with restored ascorbate levels. Mutagenesis 2012 (in press).
- Patel, E., Lynch, C., Ruff, V., Reynolds, M. Co-exposure to nickel and cobalt enhances cytotoxicity and oxidative stress in human lung epithelial cells. Toxicology and Applied Pharmacology (2012) http://www.sciencedirect.com/science/article/pii/S0041008X11004558
- Zecevic A, Hagan E, Reynolds M, Poage G, Johnston T, Zhitkovich A. XPA impacts formation but not proteasome-sensitive repair of DNA-protein crosslinks. Mutagenesis. 2010. 25 (4) 381-8.
- Reynolds, M. Understanding the Effects of Exposure to Environmental Contaminant on Normal Zebrafish Development. Labstracts 2009 31 (1).
- Reynolds M, Peterson-Roth EC, Baspalov IA, Johnston A, Gurel V, Menard H, Zhitkovich A. Rapid DNA double strand breaks resulting from processing of Cr-DNA crosslinks by both MutS dimers. Cancer Res. 2009 Feb 1;69(3):1071-9.
- Reynolds M, Zhitkovich A. Cellular vitamin C increases chromate toxicity via a death program requiring mismatch repair but not p53. Carcinogenesis. 2007 Jul;28(7):1613-20.
- Reynolds M, Stoddard L, Bespalov I, Zhitkovich A. Ascorbate acts as a highly potent inducer of chromate mutagenesis and clastogenesis: linkage to DNA breaks in G2 phase by mismatch repair. Nucleic Acids Res. 2007; 35(2):465-76.
- Messer J, Reynolds M, Stoddard L, Zhitkovich A. Causes of DNA single-strand breaks during reduction of chromate by glutathione in vitro and in cells. Free Radic Biol Med. 2006 Jun 1;40(11):1981-92. Epub 2006 Feb 20.
- Karaczyn A, Ivan S, Reynolds M, Zhitkovich A, Kasprzak KS, Salnikow K. Ascorbate depletion mediates up-regulation of hypoxia-associated proteins by cell density and nickel. J Cell Biochem. 2006 Apr 1;97(5):1025-35.
- Peterson-Roth E, Reynolds M, Quievryn G, Zhitkovich A. Mismatch repair proteins are activators of toxic responses to chromium-DNA damage. Mol Cell Biol. 2005 May;25(9):3596-607.
- Reynolds M, Peterson E, Quievryn G, Zhitkovich A. Human nucleotide excision repair efficiently removes chromium-DNA phosphate adducts and protects cells against chromate toxicity. J Biol Chem. 2004 Jul 16;279(29):30419-24. Epub 2004 Apr 15.
Recent And Upcoming Poster Presentations
- Chowdhury, K. and Reynolds, M Cytotoxic and Genotoxic Effects of Coexposure to Nickel and Cadmium. Annual Society of Toxicology Meeting, Salt Lake City, UT (2010).
- Lynch, C. and Reynolds, M Toxicological Effects of Coexposure to Nickel and Cobalt in Human Lung Epithelial Cells. Annual Society of Toxicology Meeting, Salt Lake City, UT (2010)
- Lynch, C. and Reynolds, M Mechanisms of Cellular Toxicity for Dual Exposure to NiCl2 and CoCl2 in H460 Human Lung Epithelial Cells. 2010 Sigma Xi Annual Meeting & International Research Conference Raleigh, NC (2010).
- Longwell, B. and Reynolds, M Characterization of the Molecular Mechanism of Cadmium and Nickel-Induced Toxicity. Annual Society of Toxicology Meeting, Washington DC, DC (2011).
- Lynch, C. and Reynolds, M Mechanisms of Cellular Toxicity for Dual Exposure to NiCl2 and CoCl2 in H460 Human Lung Epithelial Cells. Annual Society of Toxicology Meeting, Washington DC, DC (2011).
- Patel, E., Ruff, V., Reynolds, M. Co-exposure to nickel and cobalt increases cytotoxicity and genotoxicity of H460 human lung epithelial cells. Family Fall Weekend, Washington College (2011).
- Reynolds, M. Collection of Web Resources for the Teaching of Toxicology. Annual Society of Toxicology Meeting. San Francisco, CA (2012).
- Patel, E., Lynch, C., Ruff, V., Reynolds, M. Co-exposure to nickel and cobalt chloride enhances cytotoxicity and oxidative stress in human lung epithelial cells. Annual Society of Toxicology Meeting. San Francisco, CA (2012).