Massey, Thomas E - Queen's University - Department of Biomedical and Molecular Sciences

个人简介

Pulmonary Molecular Toxicology: The respiratory system is unique because of its very large surface area which is constantly exposed to the environment through inhalation of air. The increasing incidence of lung disease associated with environmental factors and chemicals can therefore be caused by agents present in the air, or carried to the lungs by the bloodstream. Molecular Basis of Pulmonary Susceptibility to Carcinogens: We are examining the pulmonary enzyme systems responsible for the toxification (i.e. metabolic activation) and detoxification of cancer-causing chemicals, as well as the molecular consequences (i.e. protooncogene activation, tumour suppressor gene inactivation) of reactive metabolite binding to cellular DNA and the ability of chemicals to alter DNA repair processes. Biochemical Basis for Drug-Induced Pulmonary Fibrosis: Treatment of patients with the antidysrhythmic drug, amiodarone, can result in life-threatening pulmonary fibrosis (i.e. accumulation of connective tissue in the lungs). We are studying which cellular processes are disrupted by amiodarone, leading to cell death and subsequent fibrosis.

研究领域

Pulmonary Biochemical Toxicology The respiratory system is unique because of its very large surface area which is constantly exposed to the environment through inhalation of air. The increasing incidence of lung disease associated with environmental factors and chemicals can therefore be caused by agents present in the air, or carried to the lungs by the bloodstream. Biochemical and Molecular Basis of Pulmonary Susceptibility to Carcinogens We are examining the balance of pulmonary enzyme systems in the toxification (i.e. metabolic activation) and detoxification of cancer-causing chemicals, as well as the molecular consequences (i.e. protooncogene activation, tumour suppressor gene inactivation) of reactive metabolite binding to cellular DNA. Emphasis is placed on the roles different lung cell types play in these processes. Biochemical Basis for Drug-Induced Pulmonary Fibrosis Treatment of patients with the antidysrhythmic drug, amiodarone, can result in life-threatening pulmonary fibrosis (i.e. accumulation of connective tissue in the lungs). We are studying which cellular processes are disrupted by amiodarone, leading to cell death and subsequent fibrosis.

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J.E. Mulder, J.F. Brien, W.J. Racz, T. Takahashi, and T.E. Massey. Mechanism of cytotoxicity of amiodarone and desethylamiodarone in non-transformed human peripheral lung epithelial cells. J. Pharmacol. Exp. Ther., 336: 551-559, 2011. V. Ho, T.E. Massey, and W.D. King. Thymidylate synthase gene polymorphisms and markers of DNA methylation capacity. Molec. Genet. Metab., 102: 481-487, 2011. W.D. King, V. Ho, L. Dodds, S. Perkins, I. Casson , and T.E. Massey. Relationships among biomarkers of one-carbon metabolism. Mol. Biol. Rep., 39: 7805-7812, 2012. L.C. Kobayashi, H. Limburg, Q. Miao, C. Woolcott, L.L. Bedard, T.E. Massey, and K.J. Aronson. Folate intake, alcohol consumption, and the methylenetetrahydrofolate reductase (MTHFR) C677T gene polymorphism: influence on prostate cancer risk and interactions. Front. Oncol., 2:100. doi: 10.3389/fonc.2012.00100, 2012 (8 pages), 2012. F.C. Roth, J.E. Mulder, J.F. Brien, T. Takahashi and T.E. Massey. Cytotoxic interaction between amiodarone and desethylamiodarone in human peripheral lung epithelial cells. Chemico-Biol. Interact., 204: 135-139, 2013. V. Ho, T.E. Massey, and W.D. King. Effects of methionine synthase and methylenetetrahydrofolate reductase gene polymorphisms on markers of one-carbon metabolism. Genes & Nutrition, 8: 571-80, 2013. N. Gupta, R.M. Curtis, J.E. Mulder, and T.E. Massey. Acute in vivo treatment with 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone does not alter genomic 8-hydroxydeoxyguanosine levels or base excision repair activities in murine lung and liver. DNA Repair, 12: 1031-1036, 2013. J. E. Mulder, R. Mehta, G.S. Bondy and T.E. Massey. Up-regulation of nucleotide excision repair in mouse lung and liver following chronic exposure to aflatoxin B1 and its dependence on p53 genotype. Toxicol. Appl. Pharmacol., 275: 96-103, 2014. K.A. Guindon-Kezis, J.E. Mulder and T.E. Massey. In vivo treatment with aflatoxin B1 increases DNA oxidation, base excision repair activity and 8-oxoguanine DNA glycosylase 1 levels in mouse lung. Toxicology, 321: 21-26, 2014.