Abstract:
:Production of hydrogen peroxide as a by-product of the breakdown of catecholamines by the enzyme monoamine oxidase (MAO) has been hypothesized to contribute to the increased proclivity of dopaminergic neurons for oxidative injury. We established clonal dopaminergic PC12 cell lines which have elevated MAO activity levels resulting from transgenic expression of the B isoform of the enzyme. Both MAO-A and MAO-B have relatively equivalent affinities for dopamine, and since PC12 primarily express the A and not the B form of the enzyme, this allowed us to distinguish the transgenic MAO activity in these cells from endogenous using the MAO-B specific substrate PEA. Elevation of MAO activity levels in the MAO-B+ cells resulted in higher levels of both free radicals and free radical damage compared with controls. In addition, increased MAO-B levels within PC12 cells caused a dose-dependent increase in sensitivity to the toxin MPTP. Our data suggests that oxidation of catecholamines by MAO can contribute to free radical damage in catecholaminergic neurons and that the low MAO-B activity levels found endogenously in these cells likely accounts for their relative resistance to MPTP toxicity.
journal_name
J Neurosci Resjournal_title
Journal of neuroscience researchauthors
Wei Q,Yeung M,Jurma OP,Andersen JKdoi
10.1002/(SICI)1097-4547(19961215)46:6<666::AID-JNRsubject
Has Abstractpub_date
1996-12-15 00:00:00pages
666-73issue
6eissn
0360-4012issn
1097-4547pii
10.1002/(SICI)1097-4547(19961215)46:6<666::AID-JNRjournal_volume
46pub_type
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