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Biomolecules
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The Physiological and Pathological New Function of Mitochondrial ROS and...
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The Physiological and Pathological New Function of Mitochondrial ROS and Intraorganellar Cross-Talks Part II

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Structure and Dynamics".

Deadline for manuscript submissions: closed (3 June 2024) | Viewed by 6770

Special Issue Editors

Prof. Dr. Hideyuki J. Majima

E-Mail Website
Guest Editor
School of Allied Health Sciences, Walailak University, Nakhon Si Thammarat 80160, Thailand
Interests: mitochondria; oxidative stress; cell signaling; mitochondrial DNA; mitochondrial RNA; lipid peroxidation; hair; neuron; aging
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Ken Itoh

E-Mail Website
Guest Editor
Department of Stress Response Science, Center for Advanced Medical Sciences, Hirosaki University Graduate School of Medicine, 5 Zaifucho, Hirosaki 036-8562, Japan
Interests: Nrf2; ATF4; mito-nuclear communication; mitochondrial antioxidant; Keap1; anti-aging
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Thijsj G. Rttema described “Mitochondria in the second act”, citing Pittis and Gabaldón (page 101), who provide evidence that the host cell from which eukaryotes evolved was already genetically chimaeric before the mitochondrial symbiosis, suggesting that mitochondria evolved later in eukaryotic evolution than was previously presumed (https://www.nature.com/articles/nature16876; Nature volume 531, pages 39–40 (03 March 2016)). This means that when mitochondria are established, it is possible to commence cross-talk between mitochondria and other organelles. This is one of the newest topics causing a reconsidering of intracellular organelle cross-talk. Majima et al. were the first to report that reactive oxygen species (ROS) generated from mitochondria promote apoptosis (Majima et al., J Biol. Chem. 1998), while Itoh et al. described the function of the Nrf2-Keap1 intercellular signal for the first time (Itoh et al., Biochem. Biophys. Res. Commun. 1997, Itoh et al., Genes Dev. 1999). A recent study has described that ROS generated from mitochondria initiate cellular transduction in cytosol (Indo et al. Handb Exp Pharmacol. 2017). In this Special Issue, the further roles of mitochondria-generated ROS and the subsequent intraorganellar cross-talks, signal exchange, and protein import, important in retaining cellular networks and homeostasis, will be discussed. We aim to establish a new world of cellular functions.

Prof. Dr. Hideyuki J. Majima
Prof. Dr. Ken Itoh
Guest Editors

Manuscript Submission Information

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Keywords

  • mitochondrial ROS
  • cellular signaling
  •  intraorganellar cross-talks
  • mito-nuclear communication
  • mitochondrial antioxidant
  • aging

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Related Special Issue

Published Papers (2 papers)

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Research

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14 pages, 684 KiB  
Article
Mitochondria Play Essential Roles in Intracellular Protection against Oxidative Stress—Which Molecules among the ROS Generated in the Mitochondria Can Escape the Mitochondria and Contribute to Signal Activation in Cytosol?
by Daisuke Masuda, Ikuo Nakanishi, Kei Ohkubo, Hiromu Ito, Ken-ichiro Matsumoto, Hiroshi Ichikawa, Moragot Chatatikun, Wiyada Kwanhian Klangbud, Manas Kotepui, Motoki Imai, Fumitaka Kawakami, Makoto Kubo, Hirofumi Matsui, Jitbanjong Tangpong, Takafumi Ichikawa, Toshihiko Ozawa, Hsiu-Chuan Yen, Daret K. St Clair, Hiroko P. Indo and Hideyuki J. Majima
Biomolecules 2024, 14(1), 128; https://doi.org/10.3390/biom14010128 - 19 Jan 2024
Cited by 7 | Viewed by 2751
Abstract
Questions about which reactive oxygen species (ROS) or reactive nitrogen species (RNS) can escape from the mitochondria and activate signals must be addressed. In this study, two parameters, the calculated dipole moment (debye, D) and permeability coefficient (Pm) (cm s−1), are [...] Read more.
Questions about which reactive oxygen species (ROS) or reactive nitrogen species (RNS) can escape from the mitochondria and activate signals must be addressed. In this study, two parameters, the calculated dipole moment (debye, D) and permeability coefficient (Pm) (cm s−1), are listed for hydrogen peroxide (H2O2), hydroxyl radical (•OH), superoxide (O2•−), hydroperoxyl radical (HO2•), nitric oxide (•NO), nitrogen dioxide (•NO2), peroxynitrite (ONOO−), and peroxynitrous acid (ONOOH) in comparison to those for water (H2O). O2•− is generated from the mitochondrial electron transport chain (ETC), and several other ROS and RNS can be generated subsequently. The candidates which pass through the mitochondrial membrane include ROS with a small number of dipoles, i.e., H2O2, HO2•, ONOOH, •OH, and •NO. The results show that the dipole moment of •NO2 is 0.35 D, indicating permeability; however, •NO2 can be eliminated quickly. The dipole moments of •OH (1.67 D) and ONOOH (1.77 D) indicate that they might be permeable. This study also suggests that the mitochondria play a central role in protecting against further oxidative stress in cells. The amounts, the long half-life, the diffusion distance, the Pm, the one-electron reduction potential, the pKa, and the rate constants for the reaction with ascorbate and glutathione are listed for various ROS/RNS, •OH, singlet oxygen (1O2), H2O2, O2•−, HO2•, •NO, •NO2, ONOO−, and ONOOH, and compared with those for H2O and oxygen (O2). Molecules with negative electrical charges cannot directly diffuse through the phospholipid bilayer of the mitochondrial membranes. Short-lived molecules, such as •OH, would be difficult to contribute to intracellular signaling. Finally, HO2• and ONOOH were selected as candidates for the ROS/RNS that pass through the mitochondrial membrane. Full article
(This article belongs to the Special Issue The Physiological and Pathological New Function of Mitochondrial ROS and Intraorganellar Cross-Talks Part II)
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Review

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16 pages, 1361 KiB  
Review
Mitochondrial Reactive Oxygen Species, Insulin Resistance, and Nrf2-Mediated Oxidative Stress Response—Toward an Actionable Strategy for Anti-Aging
by Shuya Kasai, Daichi Kokubu, Hiroki Mizukami and Ken Itoh
Biomolecules 2023, 13(10), 1544; https://doi.org/10.3390/biom13101544 - 19 Oct 2023
Cited by 10 | Viewed by 3646
Abstract
Reactive oxygen species (ROS) are produced mainly by mitochondrial respiration and function as signaling molecules in the physiological range. However, ROS production is also associated with the pathogenesis of various diseases, including insulin resistance (IR) and type 2 diabetes (T2D). This review focuses [...] Read more.
Reactive oxygen species (ROS) are produced mainly by mitochondrial respiration and function as signaling molecules in the physiological range. However, ROS production is also associated with the pathogenesis of various diseases, including insulin resistance (IR) and type 2 diabetes (T2D). This review focuses on the etiology of IR and early events, especially mitochondrial ROS (mtROS) production in insulin-sensitive tissues. Importantly, IR and/or defective adipogenesis in the white adipose tissues (WAT) is thought to increase free fatty acid and ectopic lipid deposition to develop into systemic IR. Fatty acid and ceramide accumulation mediate coenzyme Q reduction and mtROS production in IR in the skeletal muscle, while coenzyme Q synthesis downregulation is also involved in mtROS production in the WAT. Obesity-related IR is associated with the downregulation of mitochondrial catabolism of branched-chain amino acids (BCAAs) in the WAT, and the accumulation of BCAA and its metabolites as biomarkers in the blood could reliably indicate future T2D. Transcription factor NF-E2-related factor 2 (Nrf2), which regulates antioxidant enzyme expression in response to oxidative stress, is downregulated in insulin-resistant tissues. However, Nrf2 inducers, such as sulforaphane, could restore Nrf2 and target gene expression and attenuate IR in multiple tissues, including the WAT. Full article
(This article belongs to the Special Issue The Physiological and Pathological New Function of Mitochondrial ROS and Intraorganellar Cross-Talks Part II)
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