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The Journal of Neuroscience, January 1, 2000, 20(1):1-7
Mice Deficient in Cellular Glutathione Peroxidase Show Increased Vulnerability to Malonate, 3-Nitropropionic Acid, and 1-Methyl-4-Phenyl-1,2,5,6-Tetrahydropyridine
Peter Klivenyi1, Ole A. Andreassen1, Robert J. Ferrante2, Alpaslan Dedeoglu2, Gerald Mueller1, Eric Lancelot1, Mikhail Bogdanov1, Julie K. Andersen3, Dongmei Jiang3, and M. Flint Beal1, 4 1 Neurology Service, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, 2 Departments of Neurology, Pathology, and Psychiatry, Boston University School of Medicine, Boston, Massachusetts, and the Department of Veterans Affairs, Bedford, Massachusetts, 3 Department of Gerontology, University of Southern California, Los Angeles, California, and 4 Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York, New York 10021
Glutathione peroxidase (GSHPx) is a critical intracellular enzyme involved in detoxification of hydrogen peroxide (H2O2) to water. In the present study we examined the susceptibility of mice with a disruption of the glutathione peroxidase gene to the neurotoxic effects of malonate, 3-nitropropionic acid (3-NP), and 1-methyl-4-phenyl-1,2,5,6-tetrahydropyridine (MPTP). Glutathione peroxidase knock-out mice showed no evidence of neuropathological or behavioral abnormalities at 2-3 months of age. Intrastriatal injections of malonate resulted in a significant twofold increase in lesion volume in homozygote GSHPx knock-out mice as compared to both heterozygote GSHPx knock-out and wild-type control mice. Malonate-induced increases in conversion of salicylate to 2,3- and 2,5-dihydroxybenzoic acid, an index of hydroxyl radical generation, were greater in homozygote GSHPx knock-out mice as compared with both heterozygote GSHPx knock-out and wild-type control mice. Administration of MPTP resulted in significantly greater depletions of dopamine, 3,4-dihydroxybenzoic acid, and homovanillic acid in GSHPx knock-out mice than those seen in wild-type control mice. Striatal 3-nitrotyrosine (3-NT) concentrations after MPTP were significantly increased in GSHPx knock-out mice as compared with wild-type control mice. Systemic 3-NP administration resulted in significantly greater striatal damage and increases in 3-NT in GSHPx knock-out mice as compared to wild-type control mice. The present results indicate that a knock-out of GSHPx may be adequately compensated under nonstressed conditions, but that after administration of mitochondrial toxins GSHPx plays an important role in detoxifying increases in oxygen radicals.
Key words: MPTP; 3-nitropropionic acid; malonate; oxidative damage; free radicals; glutathione; Parkinson's; Huntington's
Copyright © 2000 Society for Neuroscience 0270-6474/0/2011-07$05.00/0
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