Effect of DHA and CoenzymeQ10 Against A�- and Zinc-Induced Mitochondrial Dysfunction in Human Neuronal Cells
Author(s) -
Nadia Sadli,
Colin J. Barrow,
Sean L. McGee,
Cenk Suphioglu
Publication year - 2013
Publication title -
cellular physiology and biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.486
H-Index - 87
eISSN - 1421-9778
pISSN - 1015-8987
DOI - 10.1159/000354433
Subject(s) - coenzyme q10 , mitochondrion , neuroprotection , neurotoxicity , docosahexaenoic acid , microbiology and biotechnology , neurodegeneration , biology , pharmacology , oxidative stress , reactive oxygen species , autophagy , chemistry , biochemistry , apoptosis , toxicity , medicine , fatty acid , disease , polyunsaturated fatty acid
Beta-amyloid (Aβ) protein is a key factor in the pathogenesis of Alzheimer's disease (AD) and it has been reported that mitochondria is involved in the biochemical pathway by which Aβ can lead to neuronal dysfunction. Coenzyme Q10 (CoQ10) is an essential cofactor involved in the mitochondrial electron transport chain and has been suggested as a potential therapeutic agent in AD. Zinc toxicity also affects cellular energy production by decreasing oxygen consumption rate (OCR) and ATP turnover in human neuronal cells, which can be restored by the neuroprotective effect of docosahexaenoic acid (DHA).
Accelerating Research
Robert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom
Address
John Eccles HouseRobert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom