Carolyn Kapron
Associate Professor

On Sabatical Leave Fall 2009 and Winter 2010.

B.Sc. (Waterloo) M.Sc., Ph.D. (McGill) Office: ESC A211 Phone: 705-748-1011 ext 7641 Email: ckapron@trentu.ca Lab: ext 7731 Webpage:

Research:
Developmental biology and toxicology. The cellular and molecular basis of abnormal embryonic development. Stress-activated signal transduction pathways. Cell adhesion molecules in development.

Teaching:
Cell Biology, Developmental Biology and Immunology.

Coordinator:
Internship in Health Sciences.

Biology 1030H: Current Issues in Biology II (Molecular and Cell Biology section)
Biology 2070H: Cell Biology
Biology 4080H: Developmental Biology
Biology 4160H: Immunology
Biology 4450: Internship in Health Sciences (course coordinator)

Between 3 and 7 per cent of newborn infants have a developmental malformation. While in some cases the cause of the malformation can be traced to a particular environmental agent or a particular mutated gene, in the vast majority of cases no particular cause can be pinpointed. It is thought that in many cases the cause is a multifactorial one. In other words, several elements have brought about the malformation, and in the end a malformation occurred because of a combination of genetic and environmental factors. While only a few environmental factors have been positively identified as ones that cause birth defects, many chemicals and drugs are suspected of doing so. In almost all cases, it is not known how the particular environmental factor has damaged the embryo's cells to lead to a malformation. Neither is it known why some embryos are susceptible and others are not. Using mice as a model system, my research attempts to identify the damage that is done at the level of the embryonic cells and to determine whether there are means by which the embryo naturally protects itself from harm. At the same time as having a practical application of possibly reducing the risk of birth defects in susceptible individuals, a more theoretical aspect of biology can also be explored--that is the ways in which an embryo can respond to a changing environment at the level of its cells.

Journal Articles:
Kapron, C.M. and D.G. Trasler. 1997. Genetic determinants of abnormal development in mouse and rat embryos in vitro. Int. J. Dev. Biol. 41: 37-344.

Sylvester, L., C.M. Kapron and C. Smith. 2000. In utero ethanol exposure decreases rapid eye movement sleep in female Sprague-Dawley rat offspring. Neuroscience Letters. 289: 13-16.

Warren, S., Patel, S. and C.M. Kapron. 2000. The effect of vitamin E exposure on cadmium toxicity in mouse embryo cells in vitro. Toxicology 142: 119-126.

Doyle, D. and C.M. Kapron. 2002. Manganese-induced toxicity in micromass cultures of mouse embryo limb bud cells. Toxicology In Vitro 16:101-6.

Kapron C. 2002 Identification of the mouse Loop-tail gene: a model for human craniorachischisis? Bioessays. 24:580-3.

Haberstroh, K., and C.M. Kapron. 2003. Induction of the JNK
signaling pathway by cadmium in mouse midbrain cells in micromass culture. In preparation.

Lu, J., and C.M. Kapron. 2003. Differential induction of stress signaling pathways by cadmium in primary cultures of mouse embryo limb bud and midbrain cells. In preparation.

MacKinnon, Y., and C. M. Kapron. 2003. Glutathione protects cultured murine embryonic cells from cadmium-induced inhibition of proliferation and differentiation and prevents the activation of c-Jun N-terminal kinase. In preparation.

Abstracts of Meeting Presentations
Haberstroh, K.M.W., and C.M. Kapron. 1998. Cellular mechanisms of cadmium embryonic toxicity. Teratology 57: 228.

Haberstroh, K.M.W., and C.M. Kapron. 1999. Cadmium-induced stress signaling pathways in mouse midbrain cells in micromass culture. Teratology 59: 451.

Lu, J., and C.M. Kapron. 2000. Toxicant-induced stress signaling pathways in primary cultures of mouse embryo limbbud and midbrain cells. Presented at the Annual Meeting of the Canadian Federation of Biological Societies, Ottawa.

MacKinnon, Y.M.W., and C.M. Kapron. 2001. Indirect evidence for the involvement of reactive oxygen species in the toxicity of cadmium in mouse embryo limb bud cell culture. Teratology 63: 294.

Associated Organizations:
The Teratology Society
The Society of Toxicology of Canada
The Canadian Society for Biochemistry and Molecular and Cellular Biology

Graduate Student Projects Related to Health:

• Charbonneau, M. (M.Sc. expected 2005) Inhibition of the Immune Response by Pesticide Exposure in Frogs
  
• Cheng, L. (M.Sc. expected 2004) The Role of c-jun in Cadmium Induced Embryotoxicity
  
• MacKinnon, Y. (M.Sc. 2002) The Role of Oxidative Stress in Cadmium Toxicity and the Cadmium-Induced Activation of the Stress-Activated Protein Kinase (SAPK) in Primary Cultures of Mouse Embryo Limb Bud Cells
  
• Liu, J., (M.Sc. 2001) Cadmium-Induced Activation of Mitogen-Activated Protein Kinase Pathways and Cytotoxicity Effects in Primary Cultures of Mouse Embryonic Cells.
  
• Haberstroh, K. (M.Sc. 1999) Cadmium-Induced Cell Toxicity and Stress-Activated Protein Kinase Induction in the Midbrain Cells of Two Strains of Mice.

Research Projects and Grants:

1998-2002 Cellular mechanisms of cadmium-induced embryotoxicity. (NSERC Operating)
2000-2001 Oxidative stress and cell signaling pathways in teratogenesis (Trent NSERC Committee)
2001 Centrifuge (with S. Rafferty (lead) and J.Yee) (NSERC equipment)
2002-2004 Stress signal transduction pathways and embryotoxicity (NSERC Operating)