Special Issue "Oxidative Stress and Mitochondria"

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Toxicology".

Deadline for manuscript submissions: closed (31 July 2011)

Special Issue Editors

Guest Editor
Prof. Dr. Daret K. St. Clair
Graduate Center for Toxicology, 1095 V.A. Drive, 306 Health Sciences Research Building, Lexington, KY 40536-0305, USA
Website: http://www.mc.uky.edu/toxicology/faculty/stclair.asp
E-Mail: dstcl00@uky.edu
Phone: +1 859 257 3956
Fax: +1 859 323 1059

Guest Editor
Dr. Aaron K. Holley
Graduate Center for Toxicology, 1095 V.A. Drive, 448 Health Sciences Research Building, Lexington, KY 40536-0305, USA
E-Mail: aaron.holley@uky.edu

Special Issue Information

Dear Colleagues,

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
Guest Editor

Keywords

  • mitochondria
  • reactive oxygen species
  • antioxidant enzymes
  • redox regulation
  • oxidative stress
  • retrograde signaling
  • cell signaling

Published Papers (10 papers)

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
Show/Hide Abstract | Cited by 8 | PDF Full-text (320 KB) | HTML Full-text | XML Full-text
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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
Show/Hide Abstract | Cited by 7 | PDF Full-text (288 KB) | HTML Full-text | XML Full-text

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
Show/Hide Abstract | Cited by 29 | PDF Full-text (199 KB) | HTML Full-text | 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
Show/Hide Abstract | Cited by 7 | PDF Full-text (544 KB) | HTML Full-text | 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
Show/Hide Abstract | Cited by 29 | PDF Full-text (567 KB) | HTML Full-text | 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
Show/Hide Abstract | Cited by 15 | PDF Full-text (649 KB) | HTML Full-text | XML Full-text

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
Show/Hide Abstract | Cited by 8 | PDF Full-text (811 KB) | HTML Full-text | 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
Show/Hide Abstract | Cited by 11 | PDF Full-text (303 KB) | HTML Full-text | 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
Show/Hide Abstract | Cited by 4 | PDF Full-text (586 KB) | HTML Full-text | XML Full-text

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
Show/Hide Abstract | Cited by 15 | PDF Full-text (430 KB) | HTML Full-text | XML Full-text

Last update: 26 February 2014

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