| The main objective in the laboratory
is in understanding the cellular mechanisms underlying cell death
in neurodegenerative processes, with a particular emphasis in Parkinson's
disease. Areas of investigation include: excitatory amino acid (i.e.
glutamate, aspartate) mediated excitotoxicity, oxidative stress,
2nd messenger signaling and metabolism; glycolytic and oxidative
metabolism in the central nervous system and elucidation of mechanisms
associated with cell death due to perturbations of metabolism from
endogenous or environmental sources. Current interest is in understanding
the biochemistry and cellular consequences of protein glutathionylation,
a mechanism by which proteins have glutathione covalently attached
to cysteine residues. Biochemical, cell culture, molecular biology
and proteomic approaches are used to address the issue.
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| For complete list: PubMed
Gluck, M., Ehrhart,
J., Jayatilleke, E. and Zeevalk, G.D. (2002) Inhibition
of brain mitochondrial respiration by dopamine: involvement of H2O2
and hydroxyl radicals but not glutathione-protein mixed disulfides.
J. Neurochem. 82:66-74.
Ehrhart, J., Gluck, M. and Zeevalk, G.D., (2002) Functional
glutaredoxin (thioltransferase activity in brain and liver mitochondria.
Parkinsonism and Related Disorders 8: 395-400.
Ehrhart, J. and Zeevalk, G.D. (2003) Cooperative
interaction between ascorbate and glutathione during mitochondrial
impairment in mesencephalic cultures.J. Neurochem. 86 (6): 1487-1497.
Zeevalk, G.D., Bernard, L.P. and Ehrhart,
J. (2003) Glutathione and ascorbate: Role in protein- glutathione-mixed
disulfide formation during oxidative stress and potential relevance
to Parkinson's disease. Ann. N.Y. Acad. Sci. 991: 342-345.
Alfinito, P.D., Wang, S-P., Manzino,L.,
Zeevalk, G.D., and Sonsalla, P.K.. (2003) Adenosine A1
and A2a Receptor-Mediated protection of dopaminergic and GABAergic
neurons against mitochondrial inhibition. J. Neurosci. 23: 10982-10987.
Gluck, M.R. and Zeevalk, G.D. (2004)
Inhibition of brain mitochondrial respiration by dopamine and its
metabolites: implications for Parkinson’s disease and catechalamine-associated
diseases. J. Neurochem.. 91: 788-795.
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