Pathophysiological and pharmacological implications of mitochondria-targeted reactive oxygen species generation in astrocytes.

Pathophysiological and pharmacological implications of mitochondria-targeted reactive oxygen species generation in astrocytes. Research Abstract Details 

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Pathophysiological and pharmacological implications of mitochondria-targeted reactive oxygen species generation in astrocytes. Abstract Text:

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, Ca(2+) 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.

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PUBMED ID PMID:

MEDLINE DATE: 2008 Oct-Nov

Pathophysiological and pharmacological implications of mitochondria-targeted reactive oxygen species generation in astrocytes. Journal Published:

PUBLICATION TYPE: Journal Article

Journal: Advanced drug delivery reviews

VOLUME: 60

Page Numbers: 1512-26

Journal Abbreviation: Adv. Drug Deliv. Rev.

ISSN: 0169-409X

DAY: 5

MONTH: 07

YEAR: 2008

Pathophysiological and pharmacological implications of mitochondria-targeted reactive oxygen species generation in astrocytes. Information

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LANGUAGE: eng

NlmUniqueID: 8710523

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Grant and Affiliation Information for Pathophysiological and pharmacological implications of mitochondria-targeted reactive oxygen species generation in astrocytes.

AFFILIATION: Department of Physiology and Pharmacology, Chang Gung University, Tao-Yuan, 333, Taiwan.

Country: Netherlands

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MEDLINETA: Adv Drug Deliv Rev

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