AccScience Publishing / GPD / Volume 2 / Issue 1 / DOI: 10.36922/gpd.227
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PERSPECTIVE ARTICLE

A hypothesis on the equilibrium between dopamine toxicity and detoxification: The roles of NQO2 and UDP-glucuronosyltransferases

Jean A. Boutin1,2* Gilles Ferry2 Karine Reybier3
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1 Laboratory of Neuroendocrine Endocrine and Germinal Differentiation and Communication (NorDiC), Univ Rouen Normandie, Inserm, UMR 1239, Rouen, France
2 Institut de Recherches Servier, 125 chemin de Ronde, Croissy-sur-Seine, France
3 Pharma-Dev UMR 152, Université de Toulouse, IRD, UPS, Toulouse, France
Submitted: 14 October 2022 | Accepted: 18 January 2023 | Published: 1 February 2023
© 2023 by the Author(s). This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution 4.0 International License ( https://creativecommons.org/licenses/by/4.0/ )
Abstract

NQO2 and tyrosine hydroxylase are co-expressed in dopaminergic neurons. These neurons produce dopamine, a diol, which, under aerobic conditions, can spontaneously revert to the more stable form, the o-quinone. O-quinones are preferred substrates of NQO2 over p-quinones. In ad hoc conditions, NQO2 reduces o-quinones into the original diols, leading to a futile cycle, the endpoint of which is a strong local production of reactive oxygen species that is deadly for the cells. This futile cycle can be interrupted by the conjugation of dopamine with UDP-glucuronic acid, leading to a glucuronide that cannot be part of the cycle because the glucuronide is not a substrate of NQO2. In this paper, we confer whether this futile cycle could be one of the causes of the specific death of dopaminergic neuronal population that is the signature of some degenerative diseases.

Keywords
Dopamine
Neurodegenerative diseases
Quinone reductase
Glucuronidation
Reactive oxygen species
Toxicity
Funding
None.
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Conflict of interest
The authors declare no conflict of interest.
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