Neurotoxicity of dipiperidinoethane due to in vivo conversion to a selective cholinesterase inhibitor.

Abstract:

:Dipiperidinoethane (DPE) administration produces seizures and CNS lesions. Here we elucidate the cholinergic origin of DPE toxicity. DPE is both an acetylcholinesterase (AChE) inhibitor and a muscarinic antagonist. This dual action negates most of the toxic effects of the compound in vivo. The neurotoxicity is believed to arise from oxidative conversion to DPE-N-oxide, which selectively inhibits AChE. Cytotoxicity does not involve muscarinic neurons, since binding parameters were unchanged following in vivo exposure.

journal_name

Brain Res

journal_title

Brain research

authors

Baron BM,Kashman Y,Sokolovsky M

doi

10.1016/0006-8993(85)90728-0

subject

Has Abstract

pub_date

1985-04-01 00:00:00

pages

164-7

issue

1

eissn

0006-8993

issn

1872-6240

pii

0006-8993(85)90728-0

journal_volume

331

pub_type

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