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An epigrammatic (abridged) recounting of the myriad tales of astonishing deeds and dire consequences pertaining to nitric oxide and reactive oxygen species in mitochondria with an ancillary missive concerning the origins of apoptosis.

Authors
Heck-DE; Kagan-VE; Shvedova-AA; Laskin-JD
Source
Toxicology 2005 Mar; 208(2):259-271
NIOSHTIC No.
20026206
Abstract
Mitochondria play a central role in the life and death of cells. These organelles serve as the major energy-producing powerhouse, whereby the generation of ATP is associated with the utilization of molecular oxygen. A significant fraction (2-3%) of molecular oxygen consumed by mitochondria may be reduced in a one-electron fashion to yield a series of reactive oxygen species (ROS) such as superoxide anion radical, hydrogen peroxide, and hydroxyl radical. ROS are capable of damaging components of the electron transport apparatus and can, in turn, disrupt mitochondrial functioning, limiting cellular ATP levels and ultimately resulting in cell death. ROS-induced disruption of electron transport can perpetuate production of deleterious ROS and propagate mitochondrial damage. Consequently, mitochondria are highly enriched with water-soluble and lipid-soluble antioxidants (glutathione, ascorbate, Vitamin E, and coenzyme Q) and antioxidant enzymes, such as superoxide dismutase, glutathione peroxidase, catalase, thioredoxins, and peroxiredoxin. Another important antioxidant acting as a very effective scavenger of reactive lipid (peroxyl, alkoxyl) radicals is nitric oxide (NO) generated by mitochondrial nitric oxide synthase. However, NO can also be very disruptive to mitochondria function, a process facilitated by its high reactivity with superoxide. This interaction results in the formation of peroxynitrite, an oxidant capable of causing oxidative/nitrosative stress, further aggravating mitochondrial dysfunction, causing ATP depletion and damage to cells. Thus, in the most general sense, the effects of NO in mitochondria may be either protective or deleterious depending on specific conditions of local redox environment (redox potential, ratio of oxidized to reduced glutathione, transition metals, and the presence of other oxygen- and nitrogen-centered radicals).
Keywords
Hydroxyl-groups; Enzymes; Cell-biology; Cell-function; Antioxidants; Antioxidation
CODEN
TXCYAC
CAS No.
10102-43-9
Publication Date
20050315
Document Type
Journal Article
Email Address
heck@eohsi.rutgers.edu
Fiscal Year
2005
NTIS Accession No.
NTIS Price
Issue of Publication
2
ISSN
0300-483X
NIOSH Division
HELD
Priority Area
Disease and Injury: Allergic and Irritant Dermatitis
Source Name
Toxicology
State
WV; PA; NJ
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