The Basic Biology of Aging at the University of Washington
Terrance J. Kavanagh, Ph.D.

Biosketch Information
Email: tjkav@u.washington.edu

Dr. Kavanagh participates in several multi-project grants to: research overexpression of antioxidant enzyme genes in transgenic mice, genes that lower DNA damage and cause less aging-associated pathology; and the effects of chemicals on glutathione biosynthesis, with the ultimate goal utilizing glutathione biosynthesis as an integrative, effects-related biomarker of toxic chemical exposure. He is PI for the Analytical Cytology Facility Core of the Center for Ecogenetics and Environmental Health: Biochemical and Molecular Mechanisms Underlying Human Variability in Response to Environmental Exposures. As co-investigator of the Flow Cytometry Core for the Seattle Gastrointestinal Program Project he is researching whether oxidative DNA damage and mutagenesis contribute to gastrointestinal cancers and whether dietary intervention with antioxidants and phytochemical supplementation can decrease these oxidative biomarkers.

Dr. Kavanagh is testing the hypothesis that homocysteine alters inflammatory cell function by generating oxidative stress, thus accelerating the progress of atherosclerotic lesions. The role of antioxidants and redox status as well genetic determinants of homocysteine metabolism will be evaluated.

Dr. Kavanagh is Associate Professor, Department of Environmental Health, and Director, Analytical Cytology Core, Center for Ecogenetics and Environmental Health. He holds Diplomate Certification of the American Board of Toxicology and served as president of the Pacific Northwest Association of Toxicologists in 1997-98.

Selected Relevant Publications
Reid LL, Botta D, Shao J, Hudson FN, Kavanagh TJ. Molecular cloning and sequencing of cDNA encoding mouse glutamate-cysteine ligase regulatory subunit. Biochim Biophys Acta 1353:107-110, 1997.

Thompson, SA, Roellich KL, Grossmann A, Gilbert SG, Kavanagh TJ. Alterations in immune parameters associated with low level methylmercury exposure in mice. Immunopharmacol Immunotoxicol 20:299-314, 1998.

Ou YC, Thompson SA, Ponce RA, Schroeder J, Kavanagh TJ, Faustman EM. Induction of the cell cycle regulatory gene p21 (Waf1, Cip1) following methylmercury exposure in vitro and in vivo. Toxicol Appl Pharmacol 157:203-212 1999.

Thompson SA, White CC, Krejsa CM, Diaz D, Woods JS, Eaton DL, Kavanagh TJ. Induction of glutamate- cysteine ligase (g-glutamylcysteine synthetase) in the brains of adult female mice sub-chronically exposed to methylmercury. Toxicol Lett 110:1-9, 1999.

Jarvinen K, Pietarinen-Runtti P, Linnainmaa K, Raivio KO, Krejsa CM, Kavanagh T, Kinnula VL. Antioxidant defense mechanisms of human mesothelioma and lung adenocarcinoma cells. Amer J Physiol Lung Cell Mol Physiol 278:L696-702, 2000.

Hudson FN, Kavanagh TJ. Cloning and characterization of the proximal promoter region of the mouse glutamate-L-cysteine ligase regulatory subunit gene. Biochim Biophys Acta 1492:447-451, 2000.

Pierce RH, Campbell JS, Stephenson AB, Franklin CC, Chaisson M, Poot M, Kavanagh TJ, Rabinovitch PS, Fausto N. Disruption of redox homeostasis in tumor necrosis factor-induced apoptosis in a murine hepatocyte cell line. Am J Pathol 157:221-236, 2000.

Diaz D, Krejsa CM, WhiteCC, Keener KL, Farin FM, Kavanagh TJ. Tissue specific changes in the expression of glutamate-cysteine ligase mRNAs in mice exposed to methylmercury. Toxicol Lett 122:119-129, 2001.

Diaz D, Krejsa CM, Kavanagh TJ. Localization of glutamate-cysteine ligase mRNA and protein in mouse kidney and induction with methylmercury. Toxicol Lett 123:33-41, 2001.

Diaz D, Krejsa CM, Kavanagh TJ. Expression of glutamate-cysteine ligase during mouse development. Mol Reprod Dev, in press.