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Alice M. Hudder, Ph.D. |
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Wayne State University |
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Tel. |
(313) 964-1976 |
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Fax. |
(313) 577-0082 |
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Institute for Environmental Health Sciences
Wayne State University |
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| Research Interests: | ||
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Our laboratory is interested in the intersection between genetics and the environment and how this relates to complex human diseases. Chronic exposure to environmental stressors, even at low doses, can lead to altered cell signaling and changes in gene expression. Sustained alterations in signaling and gene expression can lead to the initiation and progression of complex diseases, such as breast cancer and liver disease. These pathological processes develop slowly over time, are heterogeneous in nature, and vary in degree of aggressiveness. One common feature of complex human diseases is the increase in inflammatory responses and a likely role of chronic oxidative stress. A low level of oxidative stress may be present in tissues exposed to environmental agents without any acute symptoms present. And yet such low level exposures can cause fundamental changes in basic physiology through alterations in patterns of gene expression, which can lead to increased risk of disease. A better understanding of the effects of altered gene expression on key cellular pathways is necessary for evaluating the impact of environmental toxins on human health. Naturally occurring environmental toxins from cyanobacteria blooms, such as the microcystins, are an emerging issue in the United States. Microcystins are a family of cyclic heptapeptide hepatoxins produced by several different species of cyanobacteria. Epidemiological studies have indicated that one of the risk factors for the high occurrence of primary hepatocellular carcinoma is consumption of microcystins in drinking water. In our laboratory, we use toxicogenomics to study the effects of microcystins and other toxins on pathophysiology in mouse and tissue culture model systems. |
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| Select Publications: | ||
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Hudder, A. and Novak, R.F. (2008) miRNAs: effectors of environmental influences on gene expression and disease. Tox Sci, in press. Overton, L.L., Hudder, A. and Novak, R.F. (2008) The CYP2E1 subfamily. In: Cytochromes P450 Role in the Metabolism and Toxicity of Drugs and Other Xenobiotics. C. Ioannides (Ed) Royal Soc Chem (Publisher), in press. Hudder, A., Song, W., O’Shea, K.E., and Walsh, P.J. (2007) Toxicogenomic evaluation of microcystins treated with ultrasonic irradiation. Toxicol Appl Pharmacol 220(3): 357-364. Idrisi, N., Barimo, J.F., Hudder, A., Capo, T., and Walsh, P.J. (2005) Rates of Nitrogen Excretion and Oxygen Consumption in the California Sea Hare, Aplysia californica, Bull. Mar. Sci., 79 (1): 231-237. Hudder, A., Nathanson, L., and Deutscher, M. P. (2003) Organization of Mammalian Cytoplasm. Mol. Cell. Biol. 23 (24): 9318-9326. Hudder, A. and Werner, R. (2000) Analysis of a Charcot-Marie-Tooth disease mutation reveals an essential IRES element in the connexin32 gene. J. Biol. Chem. 275: 34586-34591. Werner, R., and Hudder, A. (2000) Gap Junctions. Methods 20: 127-128. Hudder, A. (1999) Letter in Science 286: 15. Schiavi, A. Hudder, A. and Werner, R. (1999) Connexin43 mRNA contains a functional internal ribosome entry site. FEBS Letters 464: 118-122. Zhou, X-W., Pfahnl, A., Werner, R., Hudder, A., Llanes, A., Luebke, A., and Dahl, G. (1997) Identification of a pore lining segment in gap junction hemichannels. Biophysical J. 72: 1946-1953. |
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