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@ARTICLE{Mueller:1005262,
author = {Mueller, Nicolas Pierre Friedrich and Carloni, Paolo and
Alfonso-Prieto, Mercedes},
title = {{M}olecular determinants of acrylamide neurotoxicity
through covalent docking},
journal = {Frontiers in pharmacology},
volume = {14},
issn = {1663-9812},
address = {Lausanne},
publisher = {Frontiers Media},
reportid = {FZJ-2023-01389},
pages = {1125871},
year = {2023},
abstract = {Acrylamide (ACR) is formed during food processing by
Maillard reaction between sugars and proteins at high
temperatures. It is also used in many industries, from water
waste treatment to manufacture of paper, fabrics, dyes and
cosmetics. Unfortunately, cumulative exposure to acrylamide,
either from diet or at the workplace, may result in
neurotoxicity. Such adverse effects arise from covalent
adducts formed between acrylamide and cysteine residues of
several neuronal proteins via a Michael addition reaction.
The molecular determinants of acrylamide reactivity and its
impact on protein function are not completely understood.
Here we have compiled a list of acrylamide protein targets
reported so far in the literature in connection with
neurotoxicity and performed a systematic covalent docking
study. Our results indicate that acrylamide binding to
cysteine is favored in the presence of nearby positively
charged amino acids, such as lysines and arginines. For
proteins with more than one reactive Cys, docking scores
were able to discriminate between the primary ACR
modification site and secondary sites modified only at high
ACR concentrations. Therefore, docking scores emerge as a
potential filter to predict Cys reactivity against
acrylamide. Inspection of the ACR-protein complex structures
provides insights into the putative functional consequences
of ACR modification, especially for non-enzyme proteins.
Based on our study, covalent docking is a promising
computational tool to predict other potential protein
targets mediating acrylamide neurotoxicity.},
cin = {IAS-5 / INM-9},
ddc = {610},
cid = {I:(DE-Juel1)IAS-5-20120330 / I:(DE-Juel1)INM-9-20140121},
pnm = {5241 - Molecular Information Processing in Cellular Systems
(POF4-524) / 5252 - Brain Dysfunction and Plasticity
(POF4-525)},
pid = {G:(DE-HGF)POF4-5241 / G:(DE-HGF)POF4-5252},
typ = {PUB:(DE-HGF)16},
pubmed = {36937867},
UT = {WOS:000952528800001},
doi = {10.3389/fphar.2023.1125871},
url = {https://juser.fz-juelich.de/record/1005262},
}