Louise M. Winn


Louise WinnContact Information

Phone: 613.533.6465
Email: winnl@queensu.ca

School of Environmental Studies, Department of Biomedical and Molecular Sciences


B.Sc. (University of Minnesota)
Ph.D. (University of Toronto)


Please direct inquiries to the contact information provided.Academic Training

Research Interests

My research focuses on the evidence suggesting that fetal toxicity may be mediated, at least in part, by the embryonic bioactivation of xenobiotics (i.e. pharmaceutical drugs and environmental chemicals) to free radical intermediates, which can lead to increased oxidative stress and ultimately teratogenesis. I am particularly interested in the effects of increased oxidative stress on embryonic signalling pathways and embryonic homologous DNA recombination. Currently my lab is focusing on several xenobiotics including benzene, TCDD, valproic acid and thalidomide as models of xenobiotic-initiated teratogenesis. Using both in vivo animal and cell culture models, we are evaluating the effects of these xenobiotics on embryonic signalling pathways involving several proteins including c-Myb, Pim-1, Ras and p53. Additionally, we are investigating mechanisms of xenobiotic-initiated homologous recombination and the role of oxidative stress in this process. Examples of the kinds of studies that my lab is interested in include: the evaluation of the molecular biological effects of in utero xenobiotic exposure on the offspring of exposed female mice, including alterations in cell signalling pathways; the evaluation of xenobiotic-initiated ROS production and embryonic oxidative damage; and the effects of xenobiotic exposure on homologous DNA recombination.

  • Singh, R. and Winn, L.M. (2008) The effects of 1,4-benzoquinone on c-Myb and topoisomerase II in K-562 cells. Mutat. Res. 645: 33-38.
  • Wan, J. and Winn, L.M. (2008) In utero exposure to benzene increases embryonic c-Myb and Pim-1 protein levels in CD-1 mice. Toxicol. Appl. Pharmacol. 228: 326-333.
  • Wan, J. and Winn, L.M. (2007) Benzene�s metabolites alter c-Myb signaling via reactive oxygen species in HD3 cells. Toxicol. Appl. Pharmacol. 222: 180-189.
  • Badham H.J. and Winn, L.M. (2007) Investigating the role of the aryl hydrocarbon in benzene-initiated toxicity: Benzene, hydroquinone and benzoquinone do not activate the AhR in vitro. Toxicology 229: 177-185.
  • Thadani, N.A., McNamee, J.P. and Winn, L.M. (2006) Thalidomide alters c-Myb and Pim-1 signaling in K-563 cells. Pharmacol. Res. 54: 91-96.
  • Defoort, E.N., Kim, P.M. and Winn, L.M. (2006) Valproic acid increases conservative homologous recombination frequency and reactive oxygen species formation: A potential mechanism for valproic acid-induced neural tube defects. Mol. Pharmacol. 69: 1304-1310.
  • Dawson, J.E., Raymond, A.M. and Winn, L.M. (2006) Folic acid and pantothenic acid protection against valproic-acid induced neural tube defects in CD-1 mice. Toxicol. Appl. Pharmacol. 211: 124-132.