Dopamine Oxidation and Parkinson’s Disease

• Caitlyn W. Barrett ^[1] ; Meghan L. Bucher ^[2] ; Teresa G. Hastings ^[1]
  1. [1] University of Pittsburgh

     University of Pittsburgh

     City of Pittsburgh, Estados Unidos

     
  2. [2] Pittsburgh Institute for Neurodegenerative Diseases, University of Pittsburgh Pittsburgh PA 15260 USA Department of Neuroscience, University of Pittsburgh Pittsburgh PA 15260 USA
• Localización: Oxidative stress and redox signalling in parkinson's disease / Rodrigo Franco (ed. lit.), Jonathan A. Doorn (ed. lit.), Jean-Christophe Rochet (ed. lit.), 2017, ISBN 9781782621881, págs. 116-143
• Idioma: español
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• Resumen

  • Parkinson’s disease (PD) is a neurodegenerative disease in which oxidative stress and mitochondrial dysfunction are thought to play substantial roles. The focus of this chapter is to link oxidative stress, mitochondrial health, and PD. These links will provide evidence for the selective loss of dopaminergic neurons of the substantia nigra (SN) pars compacta, a loss that is the primary pathological hallmark of PD. The principle neurotransmitter in dopaminergic neurons is the catecholamine dopamine (DA). Normal enzymatic catabolism of DA is capable of forming hydrogen peroxide, which increases basal reactive oxygen species (ROS) levels. Moreover, cytosolic DA is also capable of enzyme-catalyzed oxidation and auto-oxidation, which creates highly reactive dopamine quinone (DA-quinone). Due to the reactive nature of DA, nigral dopaminergic neurons are already vulnerable to damage, which can be exacerbated by oxidative stress, amplifying the detrimental effects of DA. This may establish a vicious cycle of ROS production and DA oxidation that plays a significant role in dopaminergic neuron degeneration in PD. This chapter will explore the DA oxidation pathways and the impact of DA oxidation on protein function, mitochondrial activity, and ultimately the health of the cell and organism.