Special Issue "Oxidative Stress and Mitochondria"
Deadline for manuscript submissions: closed (31 July 2011)
Prof. Dr. Daret K. St. Clair
Graduate Center for Toxicology, 1095 V.A. Drive, 306 Health Sciences Research Building, Lexington, KY 40536-0305, USA
Phone: +1 859 257 3956
Fax: +1 859 323 1059
Dr. Aaron K. Holley
Graduate Center for Toxicology, 1095 V.A. Drive, 448 Health Sciences Research Building, Lexington, KY 40536-0305, USA
Mitochondria are important sites for a variety of cellular processes, including amino acid and fatty acid metabolism, the citric acid cycle, nitrogen metabolism, and oxidative phosphorylation to produce ATP. Mitochondria are also an important source of reactive oxygen species (ROS). Myriad enzyme systems within mitochondria contribute to ROS production. Superoxide radicals can be produced by complexes I and III of the electron transport chain, the cytochrome P450 family of enzymes localized to mitochondria, and the release of free iron cations from the catalytic centers of iron-sulfur centers of various enzymes, such as aconitase, which, are susceptible to attack by superoxide radicals. Through these processes, mitochondria also produce hydrogen peroxide from superoxide radical dismutation, the hydroxyl radical through the iron-catalyzed Haber-Weiss reaction, and the highly reactive peroxynitrite molecule (ONOO-) from the interaction between superoxide radicals with nitric oxide, an uncharged radical synthesized by nitric oxide synthase (NOS).
Under normal conditions ROS are important for regulation of various cellular processes including metabolic cell signaling. Mitochondria communicate with other organelles of the cell, such as the nucleus, through a process called retrograde signaling to maintain cellular homeostasis and adapt to changing metabolic requirements of the cell. It is well documented that ROS contribute significantly to the regulation of the activity of various signal transduction pathways and transcription factors. For example, various members of the MAP kinase pathway are activated by ROS. ROS play a role in growth factor receptor activation through oxidative deactivation of protein tyrosine phosphatases that maintain the growth factor receptors in an inactive state. Multiple transcription factors, including NF-κB, AP-1, HIF-1, and p53, are sensitive to ROS. Altered activation of these signaling pathways and transcription factors results in changes in gene expression and initiation of different cellular events, including cell proliferation, senescence, apoptosis, angiogenesis, and autophagy.
While ROS are important for normal cellular activities, aberrant production of ROS, or diminished capacity to scavenge excessive ROS, leads to an imbalance in the redox environment of the cell. Myriad ROS-scavenging enzyme systems are in place to detoxify mitochondrial ROS. Manganese superoxide dismutase (MnSOD) is the major ROS scavenger of the cell, catalyzing the dismutation of superoxide radicals to hydrogen peroxide and molecular oxygen. Hydrogen peroxide, a non-radical ROS, is detoxified by multiple enzymes in mitochondria, including glutathione peroxidase, peroxiredoxin, as well as glutathione and protein thiols. The presence of these molecules in regulation of mitochondria-centered signaling has yet to be fully investigated. The disparity from normal ROS levels can cause damage of lipids, proteins, and DNA, all of which contribute to the development of various pathologies, including age-related ailments, neurological disorders, cardiovascular diseases, diabetes, and cancer.
Because of the omnipresence of ROS in cells and contribution of mitochondria in the production and removal of cellular ROS, a greater understanding of oxidative stress in mitochondria, under both normal and disease-causing conditions, and the involvement of mitochondrial ROS in global regulation of gene expression can illuminate the contribution of mitochondria in the development of disease and may lead to the advancement of new and novel therapeutic modalities that exploit mitochondria in treating many maladies.
Daret K. St. Clair
Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. Papers will be published continuously (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.
Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are refereed through a peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed Open Access monthly journal published by MDPI.
- reactive oxygen species
- antioxidant enzymes
- redox regulation
- oxidative stress
- retrograde signaling
- cell signaling
Article: Impaired Mitochondrial Respiratory Functions and Oxidative Stress in Streptozotocin-Induced Diabetic Rats
Int. J. Mol. Sci. 2011, 12(5), 3133-3147; doi:10.3390/ijms12053133
Received: 14 March 2011; in revised form: 11 April 2011 / Accepted: 29 April 2011 / Published: 13 May 2011| Download PDF Full-text (430 KB) | Download XML Full-text
Int. J. Mol. Sci. 2011, 12(8), 5373-5389; doi:10.3390/ijms12085373
Received: 6 July 2011; in revised form: 2 August 2011 / Accepted: 15 August 2011 / Published: 22 August 2011| Download PDF Full-text (586 KB) | Download XML Full-text
Int. J. Mol. Sci. 2011, 12(9), 6226-6239; doi:10.3390/ijms12096226
Received: 21 July 2011; in revised form: 14 September 2011 / Accepted: 20 September 2011 / Published: 23 September 2011| Download PDF Full-text (303 KB) | Download XML Full-text
Review: Metabolomics of Oxidative Stress in Recent Studies of Endogenous and Exogenously Administered Intermediate Metabolites
Int. J. Mol. Sci. 2011, 12(10), 6469-6501; doi:10.3390/ijms12106469
Received: 18 August 2011; in revised form: 13 September 2011 / Accepted: 21 September 2011 / Published: 28 September 2011| Download PDF Full-text (811 KB) | Download XML Full-text
Int. J. Mol. Sci. 2011, 12(10), 6894-6918; doi:10.3390/ijms12106894
Received: 26 July 2011; in revised form: 26 September 2011 / Accepted: 5 October 2011 / Published: 18 October 2011| Download PDF Full-text (649 KB) | Download XML Full-text
Int. J. Mol. Sci. 2011, 12(10), 7114-7162; doi:10.3390/ijms12107114
Received: 8 August 2011; in revised form: 28 September 2011 / Accepted: 8 October 2011 / Published: 21 October 2011| Download PDF Full-text (567 KB) | Download XML Full-text
Int. J. Mol. Sci. 2011, 12(10), 7163-7185; doi:10.3390/ijms12107163
Received: 29 July 2011; in revised form: 30 September 2011 / Accepted: 20 October 2011 / Published: 21 October 2011| Download PDF Full-text (544 KB) | Download XML Full-text
Review: Roles of Oxidative Stress, Apoptosis, PGC-1α and Mitochondrial Biogenesis in Cerebral Ischemia
Int. J. Mol. Sci. 2011, 12(10), 7199-7215; doi:10.3390/ijms12107199
Received: 1 August 2011; in revised form: 12 October 2011 / Accepted: 19 October 2011 / Published: 21 October 2011| Download PDF Full-text (199 KB) | Download XML Full-text
Review: Effect of Polyphenols on Oxidative Stress and Mitochondrial Dysfunction in Neuronal Death and Brain Edema in Cerebral Ischemia
Int. J. Mol. Sci. 2011, 12(11), 8181-8207; doi:10.3390/ijms12118181
Received: 19 September 2011; in revised form: 18 October 2011 / Accepted: 14 November 2011 / Published: 18 November 2011| Download PDF Full-text (288 KB) | Download XML Full-text
Int. J. Mol. Sci. 2012, 13(2), 2368-2386; doi:10.3390/ijms13022368
Received: 17 November 2011; in revised form: 18 February 2012 / Accepted: 20 February 2012 / Published: 22 February 2012| Download PDF Full-text (320 KB) | Download XML Full-text
Last update: 26 September 2012