Document Detail


Pathophysiological and pharmacological implications of mitochondria-targeted reactive oxygen species generation in astrocytes.
MedLine Citation:
PMID:  18692534     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Astrocytes, in addition to passively supporting neurons, have recently been shown to be actively involved in synaptic transmission and neurovascular coupling in the central nervous system (CNS). This review summarizes briefly our previous observations using fluorescent probes coupled with laser scanning digital imaging microscopy to visualize spatio-temporal alteration of mitochondrial reactive oxygen species (mROS) generation in intact astrocytes. mROS formation is enhanced by exogenous oxidants exposure, Ca2+ stress and endogenous pathological defect of mitochondrial respiratory complexes. In addition, mROS formation can be specifically stimulated by visible light or visible laser irradiation and can be augmented further by photodynamic coupling with photosensitizers, particularly with mitochondria-targeted photosensitizers. "Severe" oxidative insult often results in massive and homogeneous augmentation of mROS formation which causes cessation of mitochondrial movement, pathological fission and irreversible swelling of mitochondria and eventually apoptosis or necrosis of cells. Mitochondria-targeted antioxidants and protectors such as MitoQ, melatonin and nanoparticle C(60) effectively prevent "severe" mROS generation. Intriguingly, "minor" oxidative insults enhance heterogeneity of mROS and mitochondrial dynamics. "Minor" mROS formation-induced fission and fusion of mitochondria relocates mitochondrial network to form a mitochondria free gap, i.e., "firewall", which may play a crucial role in mROS-mediated protective "preconditioning" by preventing propagation of mROS during oxidative insults. These mROS-targeted strategies for either enhancement or prevention of mitochondrial oxidative stress in astrocytes may provide new insights for future development of therapeutic interventions in the treatment of cancer such as astrocytomas and gliomas and astrocyte-associated neurodegeneration, mitochondrial diseases and aging.
Authors:
Mei-Jie Jou
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Review     Date:  2008-07-05
Journal Detail:
Title:  Advanced drug delivery reviews     Volume:  60     ISSN:  1872-8294     ISO Abbreviation:  Adv. Drug Deliv. Rev.     Publication Date:    2008 Oct-Nov
Date Detail:
Created Date:  2008-09-15     Completed Date:  2008-12-29     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8710523     Medline TA:  Adv Drug Deliv Rev     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  1512-26     Citation Subset:  IM    
Affiliation:
Department of Physiology and Pharmacology, Chang Gung University, Tao-Yuan 333, Taiwan. mjjou@mail.cgu.edu.tw
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MeSH Terms
Descriptor/Qualifier:
Antioxidants / pharmacology*
Apoptosis
Astrocytes / drug effects,  metabolism*,  radiation effects
Fluorescent Dyes
Fullerenes / pharmacology
Humans
Lasers
Light
Melatonin / pharmacology
Mitochondria / drug effects,  metabolism*,  radiation effects
Nanoparticles
Necrosis
Organophosphorus Compounds / pharmacology
Oxidative Stress / physiology
Photosensitizing Agents / pharmacology*
Reactive Oxygen Species / metabolism*
Ubiquinone / analogs & derivatives,  pharmacology
Chemical
Reg. No./Substance:
0/10-(6'-ubiquinonyl)decyltriphenylphosphonium bromide; 0/Antioxidants; 0/Fluorescent Dyes; 0/Fullerenes; 0/Organophosphorus Compounds; 0/Photosensitizing Agents; 0/Reactive Oxygen Species; 1339-63-5/Ubiquinone; 73-31-4/Melatonin; 99685-96-8/fullerene C60

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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