Low Molecular Weight Chitosan (∼20 kDa) protects acrylamide induced oxidative stress in D. melanogaster by restoring dopamine and KIF5B levels

[Display omitted] •Acrylamide (AA) induces oxidative stress related motor dysfunction in D. melanogaster.•Low Molecular Weight Chitosan (∼20 kDa) restores the induced AA toxicity stress.•Dopamine and KIF5B expression will be hampered in AA induced flies and LMWC repairs. Acrylamide (AA) presence and...

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Veröffentlicht in:Carbohydrate polymers 2019-10, Vol.222, p.115005, Article 115005
Hauptverfasser: Kumar, P. Pramod, K. V., Harish Prashanth
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Sprache:eng
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Zusammenfassung:[Display omitted] •Acrylamide (AA) induces oxidative stress related motor dysfunction in D. melanogaster.•Low Molecular Weight Chitosan (∼20 kDa) restores the induced AA toxicity stress.•Dopamine and KIF5B expression will be hampered in AA induced flies and LMWC repairs. Acrylamide (AA) presence and formation are predominant in fried, baked and heat-processed foods. Using Drosophila model, we have investigated the dietary AA-arbitrate oxidative stress induced neurotoxicity and the effect of soluble Low Molecular Weight Chitosan (LMWC) supplementation. We assessed the neurodegenerative and behavioural effect of AA (0–10 mM) exposure in Drosophila (adult males). As a result, the exposed flies showed distinctive locomotor impairments and incident of mortality [51% in 5 mM AA (sub-toxic level) for 7 days] and higher mortality with increased concentration of acrylamide. Further, exposure of AA toxicity was also correlated with changing levels of oxidative markers, ETC complexes and cholinergic function of flies. Decreased dopamine (25 μg/mg) and kinesin motor protein levels were confirmed by HPLC and Immunoblotting studies, respectively. Interestingly, the co-exposure of LMWC alongside AA ameliorates respective biochemical changes with restoring dopamine (30 μg/mg, control groups 32 μg/mg) and kinesin motor protein (KIF5B) levels. These results indicated that supplementation of biocompatible LMWC may be promising candidate for complete protection against AA induced oxidative stress.
ISSN:0144-8617
1879-1344
DOI:10.1016/j.carbpol.2019.115005