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Dr. Bill Hanneman- a blond haired man with a crew cut wearing a brown collared polo shirt

William Hanneman, Ph.D.
Associate Professor

Phone: (970) 491-8635
Fax: (970) 491-7569
Office: 132 Physiology Building

Dr. Hanneman is the Toxicology Section Head. He is a faculty member of the interdisciplinary program in Cell and Molecular Biology. His research interests are in chemical induction of neuroendocrine disruption and molecular regulation of gene and protein expression. Dr. Hanneman also supervises the toxicology section’s "Molecular and Analytical Laboratory" which offers "fee for service" analysis of toxicological samples.


Research Interests

Chemicals that cause nerve injury and neurological deficits are a structurally diverse group. For the vast majority of these chemicals the corresponding molecular mechanisms of action are not well understood. In other areas of toxicology (such as hepatotoxicity) it is well understood that oxidative metabolites known as electrophiles will react with cellular proteins by covalently binding nucleophilic amino acid residues. Cellular toxicity occurs when electrophilic adduct formation disrupts protein structure and/or function, which secondarily causes damage to organelles, metabolic pathways, and/or physiological processes. Since many neurotoxicants are also electrophiles, our laboratory has hypothesized that the corresponding pathophysiological mechanisms of neuroendocrine disruption involve protein adduction and dysfunction.

Currently Funded Research Projects
Chlorotriazine (Cl-TRI) compounds such as atrazine (ATRA) are the most commonly used herbicides in the United States, with more that 30,000 tons (60 million pounds) applied annually. Exposure to ATRA and other Cl-TRIs causes a spectrum of reproductive deficits in laboratory species that involve selective disruption of the hypothalamic-pituitary gonadal (HPG) axis. Our long-term goal is to better understand the role of environmental compounds (such and ATRA) in reproductive disorders in humans. At present the central hypothesis of our laboratory is that exposure to ATRA results in suppression of the LH surge by selective alteration in GnRH-dependent signaling pathways in the HPG axis. This hypothesis has been formulated upon published data from our laboratory demonstrating that the effects of ATRA on suppression of the LH surge are attributable to its metabolite, diaminochlorotriazine (McMullin et al., 2004, 2007) and that diaminochlorotriazine (DACT) directly effects the HPG axis via protein adduction (Dooley et al., 2006, 2007).

Selected Publications

  • Dooley GP, Reardon KF, Prenni JE, Tjalkens RB, Legare ME, Foradori CD, Tessari JE, and Hanneman WH. Proteomic Analysis of Diaminochlorotriazine Adducts in Wister Rat Pituitary Glands and LßT2 Rat Pituitary Cells Chem Res Toxico (In press).

  • Moreno JA, Sullivan KA, Carbone DL, Hanneman WH, and Tjalkens RB. Manganese potentiates NF-κB-dependent expression of nitric oxide synthase 2 in astrocytes by activating soluble guanylate cyclase and extracellular responsive kinase signaling pathways. J. Neurosci. Res. (In press).

  • McMullin TS, Hanneman WH, Cranmer BK, Tessari JD, Andersen ME. Oral absorption and oxidative metabolism of atrazine in rats evaluated by physiological modeling approaches. Toxicology. 2007 Oct 30;240(1-2):1-14.

  • Dooley GP, Hanneman WH, Carbone DL, Legare ME, Andersen ME, Tessari JD. Development of an immunochemical detection method for atrazine-induced albumin adducts. Chem Res Toxicol. 2007 Jul;20(7):1061-6.

  • Maier MS, Legare ME, Hanneman WH. The aryl hydrocarbon receptor agonist 3,3’,4,4’, 5-pentachlorobiphenyl induces distinct patterns of gene expression between hepatoma and glioma cells: chromatin remodeling as a mechanism for selective effects. Neurotoxicology. 2007 May;28(3):594-612.

  • McMullin TS, Andersen ME, Tessari JD, Cranmer B, Hanneman WH. Estimating constants for metabolism of atrazine in freshly isolated rat hepatocytes by kinetic modeling. Toxicol In Vitro. 2007 Apr;21(3):492-501.

  • Bowers OJ, Sommersted KB, Sowell RT, Boling GE, Hanneman WH, Titus RG, Dekrey GK. 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) reduces Leishmania major burdens in C57BL/6 mice. Am J Trop Med Hyg. 2006 Oct;75(4):749-52.

  • Broccardo CJ, Billings RE, Andersen ME, Hanneman WH. Probing the control elements of the CYP1A1 switching module in H4IIE hepatoma cells. Toxicol Sci. 2005 Nov;88(1):82-94.

  • Chubb LS, Andersen ME, Broccardo CJ, Legare ME, Billings RE, Dean CE, Hanneman WH. Regional induction of CYP1A1 in rat liver following treatment with mixtures of PCB 126 and PCB 153. Toxicol Pathol. 2004 Jul-Aug;32(4):467-73.

  • Flint AF, U'Ren L, Legare ME, Withrow SJ, Dernell W, Hanneman WH. Overexpression of the erbB-2 proto-oncogene in canine osteosarcoma cell lines and tumors. Vet Pathol. 2004 May;41(3):291-6.

  • McMullin TS, Andersen ME, Nagahara A, Lund TD, Pak T, Handa RJ, Hanneman WH. Evidence that atrazine and diaminochlorotriazine inhibit the estrogen/progesterone induced surge of luteinizing hormone in female Sprague-Dawley rats without changing estrogen receptor action. Toxicol Sci. 2004 Jun;79(2):278-86.

  • French CT, Hanneman WH, Chubb LS, Billings RE, Andersen ME. Induction of CYP1A1 in primary rat hepatocytes by 3,3',4,4',5-pentachlorobiphenyl: evidence for a switch circuit element. Toxicol Sci. 2004 Apr;78(2):276-86.

  • Broccardo CJ, Billings RE, Chubb LS, Andersen ME, Hanneman WH. Single cell analysis of switch-like induction of CYP1A1 in liver cell lines. Toxicol Sci. 2004 Apr;78(2):287-94

  • Legare ME, Hanneman WH. Genetic, biochemical, and characterization of neurological mutant 3, a new mouse model for Parkinson's disease. Genet Mol Res. 2003 Sep 30;2(3):288-94.

  • Bae DS, Hanneman WH, Yang RS, Campain JA. Characterization of gene expression changes associated with MNNG, arsenic, or metal mixture treatment in human keratinocytes: application of cDNA microarray technology. Environ Health Perspect. 2002 Dec;110 Suppl 6:931-41.

  • Schimenti, K.J., Hanneman, W.H., and Schimenti, J.C. 1997. Evidence for Cyclophosphamide-induced Gene Conversion and Mutation in Mouse Germ Cells. Toxicology and Applied Pharmacology 147:343-350.

  • Legare, M.E., Hanneman, W.H., Barhoumi, R., and Tiffany-Castiglioni, E. 1997. The Effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin Exposure in Primary Rat Astroglia: Identification of Biochemical and Cellular Targets. Neurotoxicology 18(2):515-524.

  • Hanneman, W.H., Schimenti, K.J., and Schimenti, J.C. 1997. Molecular Analysis of Gene Conversion in Spermatids From Transgenic Mice. Gene 200:185-192.

  • Hanneman, W.H., Legare, M.E., Sweeney, S., and Schimenti, J.C. 1997. Cisplatin Increases Meiotic Crossing-over in Mice. Proceedings of the National Academy of Sciences 94:8681-8685.

  • Hanneman, W.H., Legare, M.E., Tiffany-Castiglioni, E., and Safe, S.H. 1996. The Need for Cellular, Biochemical and Mechanistic Studies in PCB Neurotoxicity. Neurotoxiology and Teratrology 18(3):247-250.
  • Department Contact Information:

    Environmental and Radiological Health Sciences
    1681Campus Delivery
    Fort Collins, CO 80523

    Phone: (970) 491-7038
    Fax: (970) 491-2940