Faculty Profile

Craig Harris

Craig Harris, PhD

  • Dow Professor Emeritus of Toxicology
  • Professor Emeritus, Toxicology
  • Professor Emeritus, Nutritional Sciences

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.

  • PhD in Toxicology, University of North Carolina, 1985
  • MS in Zoology, Brigham Young University, 1980
  • BS in Zoology, Brigham Young University, 1978

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

Neier, K., E.M. Marchlewicz, L.D. Bedrosian, D.C. Dolinoy and C. Harris (2019). Characterization of the mouse white adipose tissue redox environment and associations with perinatal environmental exposures to bisphenol A and high-fat diets. J Nutr Biochem 66: 86-97.

Harris, C. (2019) Rat Whole Embryo Culture In: Developmental Toxicology: Methods and Protocols (2nd ed.). Methods in Molecular Biology vol. 1965, J.M. Hansen and Louise M. Winn (eds) Springer Science+Business Media, LLC, New York, NY. Pp 195-217.

Harris, C. (2019) Assessment of Histiotrophic Nutrition using Fluorescent Probes. In: Developmental Toxicology: Methods and Protocols Protocols (2nd ed.). Methods in Molecular Biology vol. 1965, J.M. Hansen and Louise M. Winn (eds) Springer Science+Business Media, LLC, New York, NY. pp. 261-279.

Hansen, J.M., Jones, D.P. and Harris, C. (2019) The Redox Theory of Development. Antiox Redox Signal (under revision).

Rocco, S.A., L. Koneva, L.Y. Middleton, T. Thong, S. Solanki, S. Karram, K. Nambunmee, C. Harris, L.S. Rozek, M.A. Satror, Y. Shah, J.A. Colacino. (2018) Cadmium exposure inhibits branching morphogenesis and causes alterations consistent with HIF-1a inhibition in human primary breast organoids. Toxciol. Sci. 164(2): 592-602.

Veltman, K., C. Harris, Y. Ahmad and O. Jolliet (2018). A mechanistic model for thiol redox dynamics in the organogenesis stage rat conceptus. Reprod Toxicol 82: 38-49.

Veltman, K., Y. Ahmad, C. Harris, O. Jolliet (2017). Characterizing thiol redox dynamics in the organogenesis stage rat embryo. Free Rad Biol Med. 113:97-108.

Hansen, J. and C. Harris (2015). Glutathione During Embryonic Development. Biochim Biophys Acta. 1850(8): 1527-1542.

Jilek, J.L., K.E. Sant, K.H. Cho, M.S. Reed, J. Pohl, J.M. Hansen, C. Harris (2015) Ethanol Alters Histiotrophic Nutrition Pathways, the Redox Environment, and the Thiol Proteome during Rat Organogenesis. Toxicol. Sci.; 147(2): 475-489

Harris, C., J.L. Jilek, K.E. Sant, J. Pohl, M. Reed, J. M. Hansen (2015) Amino Acid Starvation Produced by Protease Inhibition Produces Differential Alterations in Redox Status and the Thiol Proteome in Organogenesis-Stage Rat Embryos and Visceral Yolk Sacs. J. Nutr. Biochem. 26(12) 1589-1598.

Email: charris@umich.edu 
Phone: 734-936-3397
Fax: 734-763-8095

Address: M6017 SPH II
1415 Washington Heights
Ann Arbor, Michigan 48109-2029