IMR Press / JIN / Volume 21 / Issue 2 / DOI: 10.31083/j.jin2102071
Open Access Short Communication
Sal synthase induced cytotoxicity of PC12 cells through production of the dopamine metabolites salsolinol and N-methyl-salsolinol
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1 Beijing Key Laboratory of Environmental and Viral Oncology, Beijing International Science and Technology Cooperation Base for Antiviral Drugs, Faculty of Environment and Life, Beijing University of Technology, 100124 Beijing, China
2 Beijing Institute of Biological Products Company Limited, 100176 Beijing, China
3 School of Life Science, Beijing Institute of Technology, 100081 Beijing, China
*Correspondence: (Xuechai Chen)
These authors contributed equally.
Academic Editor: Rafael Franco
J. Integr. Neurosci. 2022, 21(2), 71;
Submitted: 15 January 2021 | Revised: 3 February 2021 | Accepted: 15 March 2021 | Published: 23 March 2022
Copyright: © 2022 The Author(s). Published by IMR Press.
This is an open access article under the CC BY 4.0 license.

As a catechol isoquinoline, salsolinol (Sal) is widely distributed in mammalian brains, and is increased in the cerebrospinal fluid (CSF) and urine of Parkinsonian patients. Sal can be metabolized to N-methyl-salsolinol (NM-Sal), an MPP+-like neurotoxin, and impairs the function of dopaminergic neurons, causing the clinical symptoms of Parkinson’s disease (PD). Sal synthase, which catalyzes the production of Sal from dopamine and acetaldehyde, may be the important enzyme in the metabolism of catechol isoquinolines (CTIQs). Previously, our work demonstrated the existence of Sal synthase in rat brain and identified its amino acid sequence. However, the biological function of Sal synthase has not been thoroughly explored, especially its role in dopaminergic neuronal degeneration. In this study, we tried to clarify the catalytic role of Sal synthase in the formation of CTIQs which are endogenous neurotoxins in the mammalian brain. Furthermore, the cytotoxicity of Sal synthase was also observed in dopaminergic PC12 cells. The results demonstrated that Sal synthase overexpression can increase the level of Sal and NM-Sal, and ultimately cause mitochondria damage and apoptosis.

Sal synthase
Parkinson's disease
PC12 cells
Mitochondrial membrane potential
Fig. 1.
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