Benomyl, Aldehyde Dehydrogenase, DOPAL, and the Catecholaldehyde Hypothesis for the Pathogenesis of Parkinson’s Disease | Zendy

John E. Casida | Zendy; Breanna Ford | Zendy; Yunden Jinsmaa | Zendy; Patti Sullivan | Zendy; Adele Cooney | Zendy; David S. Goldstein | Zendy

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Benomyl, Aldehyde Dehydrogenase, DOPAL, and the Catecholaldehyde Hypothesis for the Pathogenesis of Parkinson’s Disease

Author(s) -

John E. Casida,

Breanna Ford,

Yunden Jinsmaa,

Patti Sullivan,

Adele Cooney,

David S. Goldstein

Publication year - 2014

Publication title -

chemical research in toxicology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.031

H-Index - 156

eISSN - 1520-5010

pISSN - 0893-228X

DOI - 10.1021/tx5002223

Subject(s) - aldehyde dehydrogenase , metabolite , dopamine , in vivo , biochemistry , benomyl , neurotoxicity , biology , 3,4 dihydroxyphenylacetic acid , pharmacology , chemistry , enzyme , neuroscience , toxicity , genetics , fungicide , homovanillic acid , receptor , organic chemistry , serotonin , botany

The dopamine metabolite 3,4-dihydroxyphenylacetaldehyde (DOPAL) is detoxified mainly by aldehyde dehydrogenase (ALDH). We find that the fungicide benomyl potently and rapidly inhibits ALDH and builds up DOPAL in vivo in mouse striatum and in vitro in PC12 cells and human cultured fibroblasts and glial cells. The in vivo results resemble those noted previously with knockouts of the genes encoding ALDH1A1 and 2, a mouse model of aging-related Parkinson's disease (PD). Exposure to pesticides that inhibit ALDH may therefore increase PD risk via DOPAL buildup. This study lends support to the "catecholaldehyde hypothesis" that the autotoxic dopamine metabolite DOPAL plays a pathogenic role in PD.

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