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.