William Hanneman, Ph.D.
Associate Professor

Phone: (970) 491-8635
Fax: (970) 491-7569
Email: William.Hanneman@colostate.edu
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.

Degrees

• Ph.D., Toxicology, Texas A & M University
• M.S., Physiology, California State Polytechnic University
• B.S., Animal Science, University of California, Davis

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