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.