Debbie Mustacich

Dr. Debbie Mustacich
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Senior Research Assistant Professor
Pharmacology/Nutrition/Toxicology

431 Linus Pauling Science Center
Linus Pauling Institute
541-737-8730 (voice mail)
541-737-5077 (fax)
debbie.mustacich@oregonstate.edu

Linus Pauling Institute

Education and Professional Training: 

B.A., Biology/Chemistry, Central Washington University
Teaching Certification, University of Puget Sound
Ph.D., Biochemistry/Biophysics, Oregon State University, 1998
Postdoctoral Fellow to Research Assistant Professor, Dept. of Pathology/Arizona Cancer Center, 1998-2003
Senior Scientist to Manager of Assay Development, Ventana Medical Systems, Inc., 2003-04
Research Faculty, Linus Pauling Institute, Oregon State University, 2004-08
Assistant Professor, Sr. Res., Department of Biomedical Sciences and Linus Pauling Institute, Oregon State University, Corvallis, OR, 2008-present

Professional Organizations: 

Society for Free Radical Biology and Medicine
International Society for Free Radical Research
Society of Toxicology
Pacific Northwest Association of Toxicologists
American Society for Biochemistry and Molecular Biology

Professional Awards: 
  • 1978 Dean's Scholar and Phi Kappa Phi Honor Society, Central Washington University
  • 1991-92 Molecular and Cellular Biology Research Fellowship, Oregon State University
  • 1991-92 Graduate School Fellowship, Oregon State University
  • 1995-97 Oregon Sports Lottery Scholarship, Oregon State University (2 awards)
  • 1996 Society of Toxicology Travel Award
  • 1996 Sigma Xi Honorable Mention, Oregon State University Graduate Conference
  • 1998-99 Cancer Biology Postdoctoral Fellowship, University of Arizona
  • 1999-2002 NIH Individual National Research Service Award (NRSA), University of Arizona
  • 2000-01 Caldwell Fellowship, University of Arizona
  • 2002-03 Cancer Prevention and Control Award, University of Arizona
Professional and Research Interests: 

One key focus of our research is to determine the ability of vitamins and other bioactive food components to modulate Xenobiotic enzymes and transporters and thereby alter the metabolism and/or elimination of environmental/occupational toxicants. Environmental toxins, as well as vitamins, herbs and other bioactive food components, are metabolized and excreted from the body by a complex network of enzymes and transport proteins, referred to as Xenobiotic pathways.
Our recent data suggests that high dose vitamin E supplementation provides protection from polycyclic aromatic hydrocarbons (PAHs) by increasing their conversion to non-DNA-reactive metabolites and increasing their elimination from the body. High-level occupational exposure to PAHs has been shown to increase cancer incidence in exposed workers and environmental exposures are associated with increased disease susceptibilities, i.e., asthma, infectious and chronic diseases, .  Defining the mechanism by which vitamin E provides protection from PAH exposures will not only increase our ability to protect PAH-exposed workers but also provide future research directions for determining the efficacy of vitamin E in environmental exposure situations to improve and extend human healthy life spans.
A second research focus is determining the mechanism by which platinum-based chemotherapeutic drugs cause neuropathy and the ability of vitamin E, alone or in combination with other antioxidants, to prevent these neuropathies. Although platinum-based chemotherapeutics are highly effective anti-cancer agents, platinum-induced neuropathies often leave patients and their families to choose between quality of life vs. life span. Determining the underlying mechanism by which these neuropathies develop will enable us to better provide cancer patients with the life extending benefits of these highly effective anti-cancer agents without the debilitating side effects that reduce quality of life for both patient and family.
A new research focus for our group is to determine the mechanism of secondary tissue damage following spinal cord injury (SCI) and develop treatment regimens for improved rehabilitation. Following the primary mechanical injury, SCI-initiated biochemical processes damage the surrounding tissue leading to secondary injury and further loss of neurological function. The etiology of this secondary injury is unknown; as is the role of oxidant/antioxidant status in the functional outcome following SCI injury. Our goal is to develope neuroprotective treatment regimens to reduce secondary injury and improve neurological outcomes for SCI patients.

Selected Publications: 

Mustacich D.J., Bruno R.S., and Traber M.G. (2007). Vitamin E. Vitam Horm 76, 1-21. (Invited Chapter)

 

 

Publications

2012
2011
2010
2009
2007