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Mitochondrial Coenzyme Q
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Mitochondrial Coenzyme Q

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (30 November 2021) | Viewed by 27062

Special Issue Editor

Prof. Dr. Wieslawa Jarmuszkiewicz

E-Mail Website
Guest Editor
Department of Bioenergetics, Adam Mickiewicz University, 61-614 Poznan, Poland
Interests: mitochondrial ROS production; Coenzyme Q; Coenzyme Q deficiency; Coenzyme Q supplementation; mitochondrial Coenzyme Q in disorders; Coenzyme Q and mitochondrial function/dysfunction
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Coenzyme Q is a fat-soluble molecule present in all cell membranes, including the inner mitochondrial membrane. Coenzyme Q is not only an essential electron carrier in the mitochondrial respiratory chain, but also an important antioxidant in mitochondria and the entire cell. Ubichinol (reduced Coenzyme Q) by binding free radicals inhibits lipid peroxidation processes and prevents oxidative modifications of DNA, proteins and lipids. There is a growing interest in the use of Coenzyme Q10 and its related compounds in therapies of various diseases, including neurological and neurodegenerative diseases, in which oxidative damage to mitochondria occurs. On the other hand, mitochondrial Coenzyme Q participates in the production by respiratory chain of mitochondrial reactive oxygen species (ROS) that are formed as a byproduct of oxygen metabolism or under oxidative stress conditions. Disorders associated with mitochondrial Coenzyme Q deficiency are mainly associated with excessive mitochondrial ROS production and a decrease in ATP production, which may result in mitochondrial, cardiovascular, neurological or neurodegenerative diseases.

This Special Issue will cover all the molecular aspects of antioxidant and prooxidant properties of mitochondrial Coenzyme Q.

Prof. Dr. Wieslawa Jarmuszkiewicz
Guest Editor

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Keywords

  • Mitochondrial ROS production
  • Coenzyme Q
  • Coenzyme Q deficiency
  • Coenzyme Q supplementation
  • Mitochondrial Coenzyme Q in disorders
  • Coenzyme Q and mitochondrial function/dysfunction

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Published Papers (4 papers)

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Research

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16 pages, 3552 KiB  
Article
Effects of Endurance Training on the Coenzyme Q Redox State in Rat Heart, Liver, and Brain at the Tissue and Mitochondrial Levels: Implications for Reactive Oxygen Species Formation and Respiratory Chain Remodeling
by Karolina Dominiak, Lukasz Galganski, Adrianna Budzinska, Andrzej Woyda-Ploszczyca, Jerzy A. Zoladz and Wieslawa Jarmuszkiewicz
Int. J. Mol. Sci. 2022, 23(2), 896; https://doi.org/10.3390/ijms23020896 - 14 Jan 2022
Cited by 5 | Viewed by 3002
Abstract
Sixteen adult, 4-month-old male Wistar rats were randomly assigned to the training group (n = 8) or the control group (n = 8). We elucidated the effects of 8 weeks of endurance training on coenzyme Q (Q) content and the formation [...] Read more.
Sixteen adult, 4-month-old male Wistar rats were randomly assigned to the training group (n = 8) or the control group (n = 8). We elucidated the effects of 8 weeks of endurance training on coenzyme Q (Q) content and the formation of reactive oxygen species (ROS) at the tissue level and in isolated mitochondria of the rat heart, liver and brain. We demonstrated that endurance training enhanced mitochondrial biogenesis in all tested organs, while a significant increase in the Q redox state was observed in the heart and brain, indicating an elevated level of QH2 as an antioxidant. Moreover, endurance training increased the mQH2 antioxidant pool in the mitochondria of the heart and liver, but not in the brain. At the tissue and isolated mitochondria level, an increase in ROS formation was only observed in the heart. ROS formation observed in the mitochondria of individual rat tissues after training may be associated with changes in the activity/amount of individual components of the oxidative phosphorylation system and its molecular organization, as well as with the size of the oxidized pool of mitochondrial Q acting as an electron carrier in the respiratory chain. Our results indicate that tissue-dependent changes induced by endurance training in the cellular and mitochondrial QH2 pool acting as an antioxidant and in the mitochondrial Q pool serving the respiratory chain may serve important roles in energy metabolism, redox homeostasis and the level of oxidative stress. Full article
(This article belongs to the Special Issue Mitochondrial Coenzyme Q)
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16 pages, 1841 KiB  
Article
Biochemical Studies of Mitochondrial Malate: Quinone Oxidoreductase from Toxoplasma gondii
by Rajib Acharjee, Keith K. Talaam, Endah D. Hartuti, Yuichi Matsuo, Takaya Sakura, Bundutidi M. Gloria, Shinya Hidano, Yasutoshi Kido, Mihoko Mori, Kazuro Shiomi, Masakazu Sekijima, Tomoyoshi Nozaki, Kousuke Umeda, Yoshifumi Nishikawa, Shinjiro Hamano, Kiyoshi Kita and Daniel K. Inaoka
Int. J. Mol. Sci. 2021, 22(15), 7830; https://doi.org/10.3390/ijms22157830 - 22 Jul 2021
Cited by 7 | Viewed by 4124
Abstract
Toxoplasma gondii is a protozoan parasite that causes toxoplasmosis and infects almost one-third of the global human population. A lack of effective drugs and vaccines and the emergence of drug resistant parasites highlight the need for the development of new drugs. The mitochondrial [...] Read more.
Toxoplasma gondii is a protozoan parasite that causes toxoplasmosis and infects almost one-third of the global human population. A lack of effective drugs and vaccines and the emergence of drug resistant parasites highlight the need for the development of new drugs. The mitochondrial electron transport chain (ETC) is an essential pathway for energy metabolism and the survival of T. gondii. In apicomplexan parasites, malate:quinone oxidoreductase (MQO) is a monotopic membrane protein belonging to the ETC and a key member of the tricarboxylic acid cycle, and has recently been suggested to play a role in the fumarate cycle, which is required for the cytosolic purine salvage pathway. In T. gondii, a putative MQO (TgMQO) is expressed in tachyzoite and bradyzoite stages and is considered to be a potential drug target since its orthologue is not conserved in mammalian hosts. As a first step towards the evaluation of TgMQO as a drug target candidate, in this study, we developed a new expression system for TgMQO in FN102(DE3)TAO, a strain deficient in respiratory cytochromes and dependent on an alternative oxidase. This system allowed, for the first time, the expression and purification of a mitochondrial MQO family enzyme, which was used for steady-state kinetics and substrate specificity analyses. Ferulenol, the only known MQO inhibitor, also inhibited TgMQO at IC50 of 0.822 μM, and displayed different inhibition kinetics compared to Plasmodium falciparum MQO. Furthermore, our analysis indicated the presence of a third binding site for ferulenol that is distinct from the ubiquinone and malate sites. Full article
(This article belongs to the Special Issue Mitochondrial Coenzyme Q)
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15 pages, 1537 KiB  
Article
Identification of 3,4-Dihydro-2H,6H-pyrimido[1,2-c][1,3]benzothiazin-6-imine Derivatives as Novel Selective Inhibitors of Plasmodium falciparum Dihydroorotate Dehydrogenase
by Endah Dwi Hartuti, Takaya Sakura, Mohammed S. O. Tagod, Eri Yoshida, Xinying Wang, Kota Mochizuki, Rajib Acharjee, Yuichi Matsuo, Fuyuki Tokumasu, Mihoko Mori, Danang Waluyo, Kazuro Shiomi, Tomoyoshi Nozaki, Shinjiro Hamano, Tomoo Shiba, Kiyoshi Kita and Daniel Ken Inaoka
Int. J. Mol. Sci. 2021, 22(13), 7236; https://doi.org/10.3390/ijms22137236 - 5 Jul 2021
Cited by 12 | Viewed by 4456
Abstract
Plasmodium falciparum’s resistance to available antimalarial drugs highlights the need for the development of novel drugs. Pyrimidine de novo biosynthesis is a validated drug target for the prevention and treatment of malaria infection. P. falciparum dihydroorotate dehydrogenase (PfDHODH) catalyzes the oxidation of [...] Read more.
Plasmodium falciparum’s resistance to available antimalarial drugs highlights the need for the development of novel drugs. Pyrimidine de novo biosynthesis is a validated drug target for the prevention and treatment of malaria infection. P. falciparum dihydroorotate dehydrogenase (PfDHODH) catalyzes the oxidation of dihydroorotate to orotate and utilize ubiquinone as an electron acceptor in the fourth step of pyrimidine de novo biosynthesis. PfDHODH is targeted by the inhibitor DSM265, which binds to a hydrophobic pocket located at the N-terminus where ubiquinone binds, which is known to be structurally divergent from the mammalian orthologue. In this study, we screened 40,400 compounds from the Kyoto University chemical library against recombinant PfDHODH. These studies led to the identification of 3,4-dihydro-2H,6H-pyrimido[1,2-c][1,3]benzothiazin-6-imine and its derivatives as a new class of PfDHODH inhibitor. Moreover, the hit compounds identified in this study are selective for PfDHODH without inhibition of the human enzymes. Finally, this new scaffold of PfDHODH inhibitors showed growth inhibition activity against P. falciparum 3D7 with low toxicity to three human cell lines, providing a new starting point for antimalarial drug development. Full article
(This article belongs to the Special Issue Mitochondrial Coenzyme Q)
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Review

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13 pages, 1286 KiB  
Review
Does Coenzyme Q10 Supplementation Improve Human Oocyte Quality?
by Cristina Rodríguez-Varela and Elena Labarta
Int. J. Mol. Sci. 2021, 22(17), 9541; https://doi.org/10.3390/ijms22179541 - 2 Sep 2021
Cited by 22 | Viewed by 14592
Abstract
Acquiring oocyte competence requires optimal mitochondrial function and adequate ATP levels. In this context, CoQ10 supplementation may improve human oocyte quality and subsequent reproductive performance given its role in ATP synthesis and mitochondrial protection from ROS oxidative damage. In infertility treatments, CoQ10 therapy [...] Read more.
Acquiring oocyte competence requires optimal mitochondrial function and adequate ATP levels. In this context, CoQ10 supplementation may improve human oocyte quality and subsequent reproductive performance given its role in ATP synthesis and mitochondrial protection from ROS oxidative damage. In infertility treatments, CoQ10 therapy can be orally supplied to promote a more favorable environment for oocyte development in vivo or by its addition to culture media in an attempt to improve its quality in vitro. Human clinical studies evaluating the impact of CoQ10 on reproductive performance are summarized in this review, although the available data do not clearly prove its ability to improve human oocyte quality. The main objective is to provide readers with a complete overview of this topic’s current status as well as the keys for potential future research lines that may help to take this therapy to clinical practice. Indeed, further clinical trials are needed to confirm these results along with molecular studies to evaluate the impact of CoQ10 supplementation on oxidative stress status and mitochondrial function in human gametes. Full article
(This article belongs to the Special Issue Mitochondrial Coenzyme Q)
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