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Oxidative stress, mitochondrial dysfunction and neurodegenerative diseases; a mechanistic insight.
Biomed Pharmacother. 2015 Aug; 74:101-10.BP

Abstract

Mitochondria is one of the main source of oxidative stress (ROS), as it utilizes the oxygen for the energy production. ROS and RNS are normally generated by tightly regulated enzymes. Excessive stimulation of NAD(P)H and electron transport chain leads to the overproduction of ROS, results in oxidative stress, which is a good mediator to injure the cell structures, lipids, proteins, and DNA. Various oxidative events implicated in many diseases due to oxidative stress include alteration in mitochondrial proteins, mitochondrial lipids and mitochondrial DNA, Which in turn leads to the damage to nerve cell as they are metabolically very active. ROS/RNS at moderate concentrations also play roles in normal physiology of many processes like signaling pathways, induction of mitogenic response and in defense against infectious pathogens. Oxidative stress has been considered to be the main cause in the etiology of many diseases, which includes Parkinson's and Alzheimer diseases. Several PD associated genes have been found to be involved in mitochondrial function, dynamics and morphology as well. This review includes source of free radical generation, chemistry and biochemistry of ROS/RNS and mitochondrial dysfunction and the mechanism involved in neurodegenerative diseases.

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Publisher Full Text (DOI)

Authors+Show Affiliations

Bhat AH
Department of Clinical Biochemistry, University of Kashmir, Srinagar 190006, India.
Dar KB
Department of Clinical Biochemistry, University of Kashmir, Srinagar 190006, India.
Anees S
Department of Clinical Biochemistry, University of Kashmir, Srinagar 190006, India.
Zargar MA
Department of Biochemistry, University of Kashmir, Srinagar 190006, India.
Masood A
Department of Biochemistry, University of Kashmir, Srinagar 190006, India.
Sofi MA
Department of Clinical Biochemistry, University of Kashmir, Srinagar 190006, India.
Ganie SA
Department of Clinical Biochemistry, University of Kashmir, Srinagar 190006, India. Electronic address: showkat_ganie786@yahoo.com.

MeSH

AnimalsFree RadicalsHumansLipid MetabolismMitochondriaNeurodegenerative DiseasesOxidative StressReactive Nitrogen SpeciesReactive Oxygen SpeciesSignal Transduction

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

26349970

Citation

Bhat, Aashiq Hussain, et al. "Oxidative Stress, Mitochondrial Dysfunction and Neurodegenerative Diseases; a Mechanistic Insight." Biomedicine & Pharmacotherapy = Biomedecine & Pharmacotherapie, vol. 74, 2015, pp. 101-10.
Bhat AH, Dar KB, Anees S, et al. Oxidative stress, mitochondrial dysfunction and neurodegenerative diseases; a mechanistic insight. Biomed Pharmacother. 2015;74:101-10.
Bhat, A. H., Dar, K. B., Anees, S., Zargar, M. A., Masood, A., Sofi, M. A., & Ganie, S. A. (2015). Oxidative stress, mitochondrial dysfunction and neurodegenerative diseases; a mechanistic insight. Biomedicine & Pharmacotherapy = Biomedecine & Pharmacotherapie, 74, 101-10. https://doi.org/10.1016/j.biopha.2015.07.025
Bhat AH, et al. Oxidative Stress, Mitochondrial Dysfunction and Neurodegenerative Diseases; a Mechanistic Insight. Biomed Pharmacother. 2015;74:101-10. PubMed PMID: 26349970.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Oxidative stress, mitochondrial dysfunction and neurodegenerative diseases; a mechanistic insight. AU - Bhat,Aashiq Hussain, AU - Dar,Khalid Bashir, AU - Anees,Suhail, AU - Zargar,Mohammad Afzal, AU - Masood,Akbar, AU - Sofi,Manzoor Ahmad, AU - Ganie,Showkat Ahmad, Y1 - 2015/08/07/ PY - 2015/04/10/received PY - 2015/07/26/accepted PY - 2015/9/10/entrez PY - 2015/9/10/pubmed PY - 2016/6/9/medline KW - Alzheimer’s diseases KW - Mitochondrial DNA KW - Mitochondrial dysfunction KW - Oxidative stress KW - Parkinson’s diseases SP - 101 EP - 10 JF - Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie JO - Biomed Pharmacother VL - 74 N2 - Mitochondria is one of the main source of oxidative stress (ROS), as it utilizes the oxygen for the energy production. ROS and RNS are normally generated by tightly regulated enzymes. Excessive stimulation of NAD(P)H and electron transport chain leads to the overproduction of ROS, results in oxidative stress, which is a good mediator to injure the cell structures, lipids, proteins, and DNA. Various oxidative events implicated in many diseases due to oxidative stress include alteration in mitochondrial proteins, mitochondrial lipids and mitochondrial DNA, Which in turn leads to the damage to nerve cell as they are metabolically very active. ROS/RNS at moderate concentrations also play roles in normal physiology of many processes like signaling pathways, induction of mitogenic response and in defense against infectious pathogens. Oxidative stress has been considered to be the main cause in the etiology of many diseases, which includes Parkinson's and Alzheimer diseases. Several PD associated genes have been found to be involved in mitochondrial function, dynamics and morphology as well. This review includes source of free radical generation, chemistry and biochemistry of ROS/RNS and mitochondrial dysfunction and the mechanism involved in neurodegenerative diseases. SN - 1950-6007 UR - https://www.unboundmedicine.com/medline/citation/26349970/Oxidative_stress_mitochondrial_dysfunction_and_neurodegenerative_diseases DB - PRIME DP - Unbound Medicine ER -