The biochemical basis of Parkinson's disease: The role of catecholamineo-quinones: A review-discussion
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This paper reviews the possible role of catecholamineo-quinones (OQs) in the genesis of Parkinson's disease (PD). This disease is characterized by damage caused to the pigmented catecholaminergic cells in various areas of the brain. The pigment involved is neuromelanin that is the end product of catecholamine oxidation by theo-quinone route. Evidence is presented regarding the overproduction in PD of these catecholamine OQs that damage the electron chain in the mitochondria leading to cell death. The roles of glutathione S-transferase and reactive oxygen species in this are also surveyed. A review of all known biochemical properties of theseo-quinones is included. The hypothesis is put forward that an important factor in the genesis of PD may be the overload by environmental toxins of enzymes such as glutathioneS-transferase that also detoxify catecholamine OQs.
Baez, S., Segura-Aguilar, J., Widersten, M., Johansson, A.S. and Mannervik, B. (1997) “Glutathione transferases catalyze the detoxification of oxidized metabolites (OQs) of catecholamines and may serve as an antioxidant system preventing degenerative cellular processes”Biochem. J. 324, 25–28.PubMed
Barzilai, A., Zilkha-Falb, R., Daily, D., Stern, N., Offen, D., Ziv, I., Melamed, E. and Shirvan, A. (2000) “The molecular mechanism of dopamine-induced apoptosis: identification and characterization of genes that mediate dopamine toxicity.”,J. Neural. Trans. Supp.,60, 59–76.
Basma, A.N., Morris, E.J., Nicklas, W.J. and Geller, H.M. (1995) “l-DOPA cytotoxicity to PC12 cells in culture is via its autooxidation”,J. Neurochem. 64, 825–832.PubMed
Ben-Schachar, D., Zuk, R. and Glinka, Y. (1995) “Dopamine neurotoxicity: inhibition of mitochondrial respiraton”,J. Neurochem. 64, 718–723.
Berman, S.D. and Hastings, T.G. (1997) “Inhibition of glutamate transport in synaptosomes by dopamine oxidation and reactive oxygen species”,J. Neurochem. 69, 1185–1195.PubMed
Cassarino, D.S., Parks, J.K., Parker, W.D.J. and Bennett, Jr, J.P. (1999) “The parkinsonian neurotoxin MPP+ opens the mitochondrial pore and releases cytochrome c in isolated mitochondria via an oxidative mechanism”,Biochem. Biophys. Acta 1453, 49–62.PubMed
De Iuliis, A., Burlina, A.P., Zanatta, L., Boschetto, R., Zambenedetti, P. and Galzigna, L. (2002) “Increased dopamine peroxidation in post-mortem Parkinsonian brains,” Submitted for publication.
Drukarch, B., Langeveld, C.H. and Stoof, J.C. (1999) “Glutathione homeostasis linked to the vesicular storage of dopamine in rat PC12 pheochromocytoma cells”,Exp. Neurol. 145, S39.
Fornstedt, B., Brun, A., Rosengren, E. and Carlsson, A. (1989) “The apparent autooxidation rate of catechols in dopamine-rich regions of human brains increases with the degree of depigmentation of substantia nigra”,J. Neural. Transm. 1, 279–295.CrossRef
Galzigna, L., Schiappelli, M.P., Rigo, A. and Scarpa, M. (1999) “A rat brain fraction and different purified peroxidases catalyzing the formation of dopaminochrome from dopamine”,Biochem. Biophys. Acta 1427, 329–336.PubMed
Hastings, T.G. (1995) “Enzymatic oxidation of dopamine: the role of prostaglandin H synthase”,J. Neurochem. 64, 919–924.PubMed
Jenner, P. and Olanow, C.W. (1998) “Understanding cell death in Parkinson's disease”,Ann. Neurol. 44(S1), S77-S84.
Jimenez del Rio, M., Pardo, C.V., Pinxteren, J., de Potter, W., Ebinger, G. and Vauquelin, G. (1994) “Interaction of serotonin-and dopamine-related neurotoxins with “serotonin binding proteins” in bovine frontal cortex”,Biochem. Pharmacol. 48, 253–258.PubMed
Kuhn, D.M. and Arthur, Jr, R. (1988) “Dopamine inactivates tryptophan hydroxylase and forms a redox-cycling quinoprotein: possible endogenous toxin to serotonin neurons”,J. Neurosci. 18, 7111–7117.
Lereugle, B., Faucheux, B.A., Bouras, C., Nillesse, N., Spik, G., Hirsch, E.C., Agid, Y. and Hof, P.R. (1996) “Cellular distribution of iron-binding protein lactotransferrin in the mesencephlon of Parkinson's disease cases”,Arch. Neuropathol. 91, 566–572.CrossRef
Luo, T., Hattori, A., Munoz, J., Qin, Z.-H. and Roth, G.S. (1995) “Intrastriatal dopamine injection induces apoptosis through oxidation-involved activation of transcription factors AP-1 and NF-κB in rats”,Mol. Pharmacol. 56, 254–264.
Skellerud, K., Marstein, S., Schrader, H., Brundelet, P.J. and Jellum, E. (1980) “The cerebral lesions in a patient with generalized glutathione deficiency and pyroglutamic aciduria (5-oxoprolinemia)”,Acta Neuropath. 52, 219–225.
Smythies, J. The Dynamic Neuron. Cambridge, MA. MIT Press (2002).
Spencer, J.P.E., Jenner, P., Daniel, S.E., Lees, A.J., Marsden, D.C. and Halliwell, B. (1998) “Conjugates of catecholamines with cysteine and GSH in Parkinson's disease; possible mechanisms of formation involving reactive oxygen species”,J. Neurochem. 71, 2112–2122.PubMed
- The biochemical basis of Parkinson's disease: The role of catecholamineo-quinones: A review-discussion
Volume 4, Issue 1 , pp 77-81
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- Parkinson's disease
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- Author Affiliations
- 1. Center for Brain and Cognition, Department of Psychology, University of California, San Diego, 92093-0109, La Jolla, CA, USA
- 2. Department of Neuropsychiatry, Institute of Neurology, Queen Square, London, UK
- 3. Department of Diagnostics, Medical School, University of Padova, Padova, Italy