Professional Summary
Dr. Harris current interests include the role of oxidative stress and glutathione in mechanisms of developmental toxicology, redox-regulation of transcription factor activation, developmental gene expression, proliferation and differentiation, mechanisms of chemical toxicity in the developing limb and neural crest. He also teaches courses in developmental toxicology and biochemical and molecular toxicology. ', 'Mammalian developmental toxicology and biochemical mechanisms of teratogenesis; the role of biochemical defenses in developing rat conceptus that might influence the incidence and severity of dysmorphogenesis.
Courses Taught
EHS612: Biochemical and Molecular Toxicology
EHS622: Mechanisms of Developmental Toxicology
Education
Ph.D., Toxicology, University of North Carolina, 1985
M.S., Zoology, Brigham Young University, 1980
B.S., Zoology, Brigham Young University, 1978
Research Interest & Projects
Current research is focused on mammalian developmental toxicology and attempts to elucidate biochemical mechanisms of teratogenesis. Particular emphasis is placed on investigations of how alterations in intracellular glutathione redox status produced by exposure to teratogenic chemicals misreguate transcription factor function and growth factor activity to produce dysmorphogenesis. Rodent and rabbit whole embryo culture systems and cell cultures are used for evaluation of the mechanisms of important embryotoxins/teratogens such as thalidomide, ethanol and PCBs.
Development of the next generation of rat whole embryo culture (WEC) prediction model for the identification of development of developmental toxicants
Principal Investigator: Harris, C.
Sponsor: Pfizer
Selected Publications
Harris, C. and Hansen, J.M. (2006). In vitro methods for the study of Mechanisms of developmental toxicity. In RD Hood (Ed.) Developmental and Reproductive Toxicology: A Practical Approach (2nd Edition) (647-695). Taylor Francis.
Caruso, R.L., Upham, B.L. Harris, C. and Trosko, J.L. (2005). Divergent roles for glutathione in lindane-induced acute and delayed-onset inhibition of rat myometrial gap junctions Toxicological Sciences, 1, 694-702.
Caruso, R.L., Upham, B.L. , Harris,C. and Trosko, J.L. (2005). Biphasic lindane-induced oxidation of glutathione and inhibition of gap junctions in myometrial cells. Toxicological Sciences, 2, 417-426.
Hansen, J.M., Lee, E. and Harris, C. (2004). Spatial activities and induction of glutamatecysteine ligase in the organogenesis-stage rat embryo and isceral yolk sac. Toxicologic Sciences, In Press.
Harris, C., Dixon, M. and Hansen, J.M. (2004). Glutathione modulates methanol, formaldehyde and formate toxicity in cultured rat conceptuses. Cell Biology and Toxicology, In press.
Hansen, J.M.and Harris, C. (2004). A novel hypothesis for thalidomide-induced limb teratogenesis: redox misregulation of the NF-kB Pathway. Antioxidants and Redox Signaling, 6, 1-14.
Harris, C., Wang, S.W., Lauchu, J.J. and Hansen, J.M. (2003). Methanol metabolism and embryotoxicity in rat and mouse cnceptuses: comparisons of alcohol dehydrogenase (ADH1), formaldehyde dehydrogenase (ADH3) and catalase. Reprod Toxicol, 17, 349-357.
Mudge, B.R., Harris, C., Gilmont, R.R., Adamson, B.S. and Rees, R.S. (2002). Role of glutathione redox dysfunction in diabetic wounds. Wound Rep Reg, 10, 52-58.
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