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Bahie M. Abou-Donia

Bahie M. Abou-Donia

Duke University School of Medicine


Dr. Mohamed Abou-Donia is a Professor of Pharmacology and Cancer Biology at Duke University Medical Center. He also holds a secondary appointment as a Professor of Neurobiology. He has been the Director of the Neurotoxicology Laboratory at Duke University Medical Center (1975-present). He was the Deputy Director of the Toxicology Program at Duke University from 1981 to 1995. He obtained his Ph.D. from the University of California at Berkeley. He is a Certified Toxicologist by both the American Board of Toxicology since 1981 and the Academy of Toxicological Sciences since 1982. The overall research program in his laboratory is directed toward understanding the basic mechanism by which chemicals, e.g., pesticides, solvents, industrial chemicals, heavy metals, drugs, and nerve agents, adversely the nervous system. He has been investigating the mechanisms involved in the Persian Gulf War Veterans’ Illnesses and developing treatment for them. His research program has focused on the assessment of brain injury from chemicals and trauma and developing serum biomarkers for such injuries. (e.g. J. Toxicol. Environ Health 76:363-380.). His research program has been funded by private organizations, e.g., Rockefeller Foundation and World Health Organization and federal agencies including NIESH, NIOSH, EPA, USDA, and DOD. He has more than 300 peer reviewed publications, most of which are in the area of neurotoxicology and edited a book “Neurotoxicology”.

Research Interest

Organophosphorus compounds (Ops) induce neurodegenerative disorders. This action is related to their ability to phosphorylate target proteins. Ops have three distinct actions: 1) Cholinergic neurotoxicity resulting from inhibition of acetylcholinesterase (AChE), 2) Organophosphorus ester-Induced Delayed Neurotoxicity (OPIDN), and 3) Organophosphorus ester-Induced Chronic Neurotoxicity (OPICN). Our recent studies using gene expression of rat brain, 15 min and 3 months after exposure to sarin, elucidated the sarin-induced neurotoxicity. A lethal dose of sarin caused up-regulation of nicotinic, muscarinic, GABAnergic and glutamergic receptors, consistent with the activation of glutamate receptors leading to the release of l-glutamate amino acid and activation of NMDA receptor resulting in massive Ca2+ influx and neuronal cell death. Calcium calmodulin kinase II was up-regulated in brain regions that are sensitive to OPIDN. This enzyme that is involved with glutamate receptors in the process of learning and memory is activated by Ca2+ influx through NMDA receptors resulting in mitochondrial dysfunction and free radical formation, followed by caspase activation and apoptotic cell death.