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Your Environment. Your Health.

Michael E. Wyde, Ph.D., D.A.B.T

Systems Toxicology Group

Michael E. Wyde, Ph.D., D.A.B.T
Michael Wyde, Ph.D.
Tel 984-287-3210
Fax 919-541-4255
P.O. Box 12233
Mail Drop K2-12
Durham, N.C. 27709

Michael E. Wyde, Ph.D., D.A.B.T., manages and participates in multidisciplinary teams of NIEHS/NTP scientists to develop research programs to address a broad array of toxicological study needs for chemicals selected for study by the National Toxicology Program. This includes the design, analysis, interpretation, and integration of carcinogenicity, reproductive and developmental, genetic, and general toxicology studies. These research programs serve to identify hazards associated with chemical exposure and increase our understanding of the interaction between chemical exposure and the development of disease. These studies are published as NTP Technical Reports and peer-reviewed research papers in scientific journals and provide critical data for use in risk assessment for human exposure.

Wyde serves as the project leader for several chemicals including compounds that are used in consumer products, as food additives, as chemical intermediates, and environmental contaminants. He has a particular interest in chemical mixtures and herbal products, as well the application of dose-response modeling to NTP data for use in risk assessment, such as the determination of Benchmark Doses for carcinogenic and non-carcinogenic responses.

Wyde received a B.S. in biochemistry from North Carolina State University, Raleigh, North Carolina and a Ph.D. in toxicology from the University of North Carolina at Chapel Hill. He completed postdoctoral work at CIIT Centers For Health Research in Research Triangle Park, North Carolina.

Selected Publications

  1. Yoshizawa K, Walker NJ, Nyska A, Kissling GE, Jokinen MP, Brix AE, Sells DM, Wyde ME. (2010) Thyroid follicular lesions induced by oral treatment for two years with 2,3,7,8-tetrachlorodibenzo-p-dioxin and dioxin-like compounds in female Harlan Sprague-Dawley rats. Toxicologic pathology. 38(7): 1037-1050. [Abstract]
  2. Wyde ME, Kirwan S, Zhang F, Laughter A, Hoffman HB, Bartolucci-Page E, Gaido KW, Yan B, You L. (2005) Di-n-butyl phthalate activates constitutive androstane receptor and pregnane X receptor and enhances the expression of steroid-metabolizing enzymes in the liver of rat fetuses. Toxicol Sci. 86:281-90. [Abstract]
  3. Nyska A, Yoshizawa K, Jokinen MP, Brix AE, Sells DM, Wyde ME, Orzech DP, Kissling GE, Walker NJ. (2005) Olfactory epithelial metaplasia and hyperplasia in female Harlan Sprague-Dawley rats following chronic treatment with polychlorinated biphenyls. Toxicol Pathol. 33: 371-377. [Abstract]
  4. Walker NJ, Crockett PW, Nyska A, Brix AE, Jokinen MP, Sells DM, Hailey JR, Easterling M, Haseman JK, Yin M, Wyde ME, Bucher JR, Portier CJ. (2005) Dose-additive carcinogenicity of a defined mixture of "dioxin-like compounds." Environ Health Perspect. 113: 43-48. [Abstract]
  5. Yoshizawa K, Walker NJ, Jokinen MP, Brix AE, Sells DM, Marsh T, Wyde ME, Orzech D, Haseman JK, Nyska A. (2005) Gingival carcinogenicity in female Harlan Sprague-Dawley rats following two-year oral treatment with 2,3,7,8-tetrachlorodibenzo-p-dioxin and dioxin-like compounds. Toxicol Sci. 83:64-77. [Abstract]
  6. Wyde ME, Braen AP, Hejtmancik M, Johnson JD, Toft JD, Blake JC, Cooper SD, Mahler J, Vallant M, Bucher JR, Walker NJ. (2004) Oral and dermal exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) induces cutaneous papillomas and squamous cell carcinomas in female hemizygous Tg.AC transgenic mice. Toxicol Sci. 82:34-45. [Abstract]
  7. Nyska, A, Jokinen, MP, Brix, AE, Sells, DM, Wyde, ME, Haseman, JK, Flake, G, and Walker, NJ. (2004) Exocrine pancreatic pathology in female Sprague-Dawley rats following chronic treatment with 2,3,7,8-tetrachlorodibenzo-p-dioxin and dioxin-like compounds. Environ Health Perspect. 112: 903-909. [Abstract]
  8. Wyde, ME, Bartolucci, E, Ueda, A, Zhang, H, Yan, B, Negishi, M, and You, L. (2003) The environmental pollutant 1,1-dichloro-2,2-bis(p-chlorophenyl)ethylene (DDE) induces rat hepatic cytochrome P450 2B and 3A expression through the constitutive androstane receptor and pregnane X receptor. Mol. Pharmacol. 64:1-8. [Abstract]
  9. Wyde, ME, Eldridge, SR, Cambre, TE, Lebetkin, MS, Lucier, GW, and Walker, NJ. (2002) Promotion of altered hepatic foci by 2,3,7,8-tetrachlorodibenzo-p-dioxin and 17 ß-estradiol in male Sprague-Dawley rats. Toxicol. Sci. 68: 295-303. [Abstract]
  10. Wyde, ME, Wong, V, Kim, AH, Lucier, GW, and Walker, NJ. (2001) Induction of hepatic 8-oxo-deoxyguanosine adducts by 2,3,7,8-tetrachlorodibenzo-p-dioxin in Sprague-Dawley rats is female-specific and estrogen-dependent, Chem. Res. Toxicol., 14: 849-855. [Abstract]
  11. Wyde, ME, Lucier, GW, and Walker, NJ. (2001) Regulation of 2,3,7,8-tetrachlorodibenzo-p-dioxin-induced tumor promotion by 17 ß-estradiol in female Sprague-Dawley rats, Toxicol. Appl. Pharmacol., 173:7-17. [Abstract]
  12. Wyde, ME, Lucier, GW, Seely, J, and Walker, NJ. (2000) Toxicity of chronic exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin in diethylnitrosamine-initiated ovariectomized rats implanted with subcutaneous 17 ß-estradiol pellets, Toxicol. Sci. 54:493-499. [Abstract]
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