Abstract:
AIM:Till date, the mode of action of β-PEA on neurons is not well illustrated. We tested the hypothesis that β-PEA has the ability to cause oxidative stress by inhibiting the antioxidant enzyme DT-diaphorase and mitochondrial complexes (Complex-I and complex-III). METHODS:Using molecular docking as a tool, we here studied and compared the inhibitory capacity of β-PEA on DT-diaphorase and mitochondrial complexes. Three-dimensional structures of mitochondrial complexes and DT-diaphorase and their ligands were downloaded from the respective data banks, and free energy of binding (docking scores) were determined. RESULTS:The present finding demonstrated for the first time that β-PEA potentiates reactive oxygen species generation by inhibiting the antioxidant enzyme DT-diaphorase, in addition to the mitochondrial complex-I and complex-III. CONCLUSION:As lowering of cellular antioxidant molecules is evident in many neurodegenerative disorders, β-PEA-induced lowering of DT-diaphorase activity may have the capability to cause neurodegeneration, which may be potentiated by its ability to inhibit mitochondrial complexes. Thus, β-PEA-due to its cumulative actions-may be more potent in causing neurodegeneration as compared to other endogenous neurotoxins.
journal_name
CNS Neurosci Therjournal_title
CNS neuroscience & therapeuticsauthors
Mazumder MK,Paul R,Borah Adoi
10.1111/cns.12113subject
Has Abstractpub_date
2013-08-01 00:00:00pages
596-602issue
8eissn
1755-5930issn
1755-5949journal_volume
19pub_type
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