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Mitochondrial dysfunction and cell death in neurodegenerative diseases through nitroxidative stress.
Brain Res. 2016 Apr 15; 1637:34-55.BR

Abstract

Mitochondria are important for providing cellular energy ATP through the oxidative phosphorylation pathway. They are also critical in regulating many cellular functions including the fatty acid oxidation, the metabolism of glutamate and urea, the anti-oxidant defense, and the apoptosis pathway. Mitochondria are an important source of reactive oxygen species leaked from the electron transport chain while they are susceptible to oxidative damage, leading to mitochondrial dysfunction and tissue injury. In fact, impaired mitochondrial function is commonly observed in many types of neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease, Huntington's disease, alcoholic dementia, brain ischemia-reperfusion related injury, and others, although many of these neurological disorders have unique etiological factors. Mitochondrial dysfunction under many pathological conditions is likely to be promoted by increased nitroxidative stress, which can stimulate post-translational modifications (PTMs) of mitochondrial proteins and/or oxidative damage to mitochondrial DNA and lipids. Furthermore, recent studies have demonstrated that various antioxidants, including naturally occurring flavonoids and polyphenols as well as synthetic compounds, can block the formation of reactive oxygen and/or nitrogen species, and thus ultimately prevent the PTMs of many proteins with improved disease conditions. Therefore, the present review is aimed to describe the recent research developments in the molecular mechanisms for mitochondrial dysfunction and tissue injury in neurodegenerative diseases and discuss translational research opportunities.

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Authors+Show Affiliations

Akbar M
Section of Molecular Pharmacology and Toxicology, Laboratory of Membrane Biochemistry and Biophysics, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD, USA.
Essa MM
Department of Food Science and Nutrition, College of Agriculture and Marine Sciences, Sultan Qaboos University, Oman; Ageing and Dementia Research Group, Sultan Qaboos University, Oman.
Daradkeh G
Department of Food Science and Nutrition, College of Agriculture and Marine Sciences, Sultan Qaboos University, Oman.
Abdelmegeed MA
Section of Molecular Pharmacology and Toxicology, Laboratory of Membrane Biochemistry and Biophysics, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD, USA.
Choi Y
Section of Molecular Pharmacology and Toxicology, Laboratory of Membrane Biochemistry and Biophysics, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD, USA.
Mahmood L
Department of Nutritional Sciences, Qatar University, Qatar.
Song BJ
Section of Molecular Pharmacology and Toxicology, Laboratory of Membrane Biochemistry and Biophysics, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD, USA.

MeSH

Age FactorsAntioxidantsApoptosisDNA, MitochondrialGlutamic AcidHumansLipid MetabolismMitochondriaMitochondrial ProteinsNeurodegenerative DiseasesOxidation-ReductionOxidative StressReactive Oxygen Species

Pub Type(s)

Journal Article
Research Support, N.I.H., Intramural
Research Support, Non-U.S. Gov't
Review

Language

eng

PubMed ID

26883165

Citation

Akbar, Mohammed, et al. "Mitochondrial Dysfunction and Cell Death in Neurodegenerative Diseases Through Nitroxidative Stress." Brain Research, vol. 1637, 2016, pp. 34-55.
Akbar M, Essa MM, Daradkeh G, et al. Mitochondrial dysfunction and cell death in neurodegenerative diseases through nitroxidative stress. Brain Res. 2016;1637:34-55.
Akbar, M., Essa, M. M., Daradkeh, G., Abdelmegeed, M. A., Choi, Y., Mahmood, L., & Song, B. J. (2016). Mitochondrial dysfunction and cell death in neurodegenerative diseases through nitroxidative stress. Brain Research, 1637, 34-55. https://doi.org/10.1016/j.brainres.2016.02.016
Akbar M, et al. Mitochondrial Dysfunction and Cell Death in Neurodegenerative Diseases Through Nitroxidative Stress. Brain Res. 2016 Apr 15;1637:34-55. PubMed PMID: 26883165.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Mitochondrial dysfunction and cell death in neurodegenerative diseases through nitroxidative stress. AU - Akbar,Mohammed, AU - Essa,Musthafa Mohamed, AU - Daradkeh,Ghazi, AU - Abdelmegeed,Mohamed A, AU - Choi,Youngshim, AU - Mahmood,Lubna, AU - Song,Byoung-Joon, Y1 - 2016/02/13/ PY - 2015/07/16/received PY - 2016/02/02/revised PY - 2016/02/05/accepted PY - 2016/2/18/entrez PY - 2016/2/18/pubmed PY - 2017/1/25/medline KW - Antioxidants KW - Mitochondrial dysfunction KW - Neurodegenerative diseases KW - Neuronal cell death KW - Oxidative stress KW - Post-translational protein modifications KW - Translational research SP - 34 EP - 55 JF - Brain research JO - Brain Res VL - 1637 N2 - Mitochondria are important for providing cellular energy ATP through the oxidative phosphorylation pathway. They are also critical in regulating many cellular functions including the fatty acid oxidation, the metabolism of glutamate and urea, the anti-oxidant defense, and the apoptosis pathway. Mitochondria are an important source of reactive oxygen species leaked from the electron transport chain while they are susceptible to oxidative damage, leading to mitochondrial dysfunction and tissue injury. In fact, impaired mitochondrial function is commonly observed in many types of neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease, Huntington's disease, alcoholic dementia, brain ischemia-reperfusion related injury, and others, although many of these neurological disorders have unique etiological factors. Mitochondrial dysfunction under many pathological conditions is likely to be promoted by increased nitroxidative stress, which can stimulate post-translational modifications (PTMs) of mitochondrial proteins and/or oxidative damage to mitochondrial DNA and lipids. Furthermore, recent studies have demonstrated that various antioxidants, including naturally occurring flavonoids and polyphenols as well as synthetic compounds, can block the formation of reactive oxygen and/or nitrogen species, and thus ultimately prevent the PTMs of many proteins with improved disease conditions. Therefore, the present review is aimed to describe the recent research developments in the molecular mechanisms for mitochondrial dysfunction and tissue injury in neurodegenerative diseases and discuss translational research opportunities. SN - 1872-6240 UR - https://www.unboundmedicine.com/medline/citation/26883165/Mitochondrial_dysfunction_and_cell_death_in_neurodegenerative_diseases_through_nitroxidative_stress_ DB - PRIME DP - Unbound Medicine ER -