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Neurotoxicity Research

, Volume 36, Issue 4, pp 746–755 | Cite as

Superoxide Dismutases SOD1 and SOD2 Rescue the Toxic Effect of Dopamine-Derived Products in Human SH-SY5Y Neuroblastoma Cells

  • Alice Biosa
  • Federica De Lazzari
  • Anna Masato
  • Roberta Filograna
  • Nicoletta Plotegher
  • Mariano Beltramini
  • Luigi Bubacco
  • Marco BisagliaEmail author
Original Article

Abstract

The preferential loss of dopaminergic neurons in the substantia nigra pars compacta is one of the pathological hallmarks characterizing Parkinson’s disease. Although the pathogenesis of this disorder is not fully understood, oxidative stress plays a central role in the onset and/or progression of Parkinson’s disease and dopamine itself has been suggested to participate in the preferential neuronal degeneration through the induction of oxidative conditions. In fact, the accumulation of dopamine into the cytosol can lead to the formation of reactive oxygen species as well as highly reactive dopamine-quinones. In the present work, we first analyzed the cellular damage induced by the addition of dopamine (DA) in the culture medium of SH-SY5Y cells, discriminating whether the harmful effects were related to the generation of reactive oxygen species or to the toxicity associated to dopamine-derived quinones. Then, we tested and demonstrated the capability of the antioxidant enzymes SOD1 and SOD2 to protect cells from the noxious effects induced by DA treatment. Our results support further exploration of superoxide dismutating molecules as a therapeutic strategy against Parkinson’s disease.

Keywords

Dopamine Dopamine quinones Oxidative stress Parkinson’s disease Superoxide dismutation 

Notes

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© Springer Science+Business Media, LLC, part of Springer Nature 2019

Authors and Affiliations

  1. 1.Molecular Physiology and Biophysics Unit, Department of BiologyUniversity of PadovaPadovaItaly
  2. 2.Department of Medical Biochemistry and BiophysicsKarolinska InstitutetStockholmSweden

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