A mitochondrial superoxide theory for oxidative stress diseases and aging

Indo, Hiroko P.; Yen, Hsiu-Chuan; Nakanishi, Ikuo; Matsumoto, Ken‐ichiro; Tamura, Masato; Nagano, Yumiko; Matsui, Hirofumi; Gusev, Oleg; Cornette, Richard; Okuda, Takashi; Minamiyama, Yukiko; Ichikawa, Hiroshi; Suenaga, Shigeaki; Oki, Misato; Sato, Tsuyoshi; Ozawa, Toshihiko; Clair, Daret K. St.; Majima, Hideyuki J.

doi:10.3164/jcbn.14-42

Cited by 283 publications

(207 citation statements)

References 90 publications

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“…Furthermore, Mn-SOD influences the activity of transcription factors (such as HIF-1α, AP-1, NF-κB and p53) and affects DNA stability [35]. A critical role of Mn-SOD under physiological and pathological conditions has recently been reviewed in details and the following findings of Mn-SOD confirm the critical role of Mn-SOD in the survival of aerobic life [36][37][38][39]:…”

Section: Superoxide Dismutase In Biological Systemsmentioning

confidence: 82%

Antioxidant Systems in Poultry Biology: Superoxide Dismutase

Surai¹

2016

J Anim Res Nutr

168

135

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Commercial poultry production is associated with various stresses responsible for decreasing productive and reproductive performance of growing chicks, breeders and commercial layers. A growing body of evidence shows that most of stresses in poultry production at the cellular level are associated with oxidative stress. Recently, a concept of the cellular antioxidant defense has been revised with special attention paid to cellular redox status maintenance and cell signaling. In fact, antioxidant systems of the living cell are based on three major levels of defense and superoxide dismutase (SOD) is shown to belong to the first level of the antioxidant defense network. Cellular antioxidant defenses are shown to include several options and vitagene activation in stress conditions is considered as a fundamental adaptive mechanism. The vitagene family includes various genes regulating synthesis of protective molecules including thioredoxins, sirtuins, heat shock proteins and SOD. However, by the time of writing no comprehensive review on the roles and effects of SOD in poultry biology has appeared. Therefore, the aim of this review is a critical analysis of the role of SOD in poultry biology with specific emphasis to its functions as an essential part of the vitagene network. From the analysis of the recent data related to SOD in poultry physiology and adaptation to stresses it is possible to conclude that: a) SOD as important vitagene is the main driving force in cell/body adaptation to various stress conditions. Indeed, in stress conditions additional synthesis of SOD is an adaptive mechanism to decrease ROS formation; b) If the stress is too high SOD activity is decreased and apoptosis is activated; c) there are tissue-specific differences in SOD expression which also depends on the strength of such stress-factors as heat, heavy metals, mycotoxins and other stressors; d) SOD is shown to provide an effective protection against lipid peroxidation in chicken embryonic tissues and semen; e) SOD is shown to be protective in heat and cold stress, toxicity stress as well as in other oxidative-stress related conditions in poultry production; f) there are complex interactions inside the antioxidant network of the cell/body to ensure an effective maintenance of homeostasis in stress conditions. Indeed, in many cases, nutritional antioxidants (vitamin E, selenium, carotenoids, phytochemicals, etc.) in the feed can increase SOD expression; g) nutritional means of SOD upregulation in stress conditions of poultry production and physiological and commercial consequences await further investigation; h) vitagene upregulation in stress conditions is emerging as an effective means for stress management.

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Section: Superoxide Dismutase In Biological Systemsmentioning

confidence: 82%

Antioxidant Systems in Poultry Biology: Superoxide Dismutase

Surai¹

2016

J Anim Res Nutr

168

135

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“…Due to the indispensable function in the processes of oxidative phosphorylation, Coenzyme Q-10 (CoQ-10) and its derivatives are the most prominent members in the family of Q/HQ [4][5][6][7]. Although the number of studies related to the chemical and redox features of CoQ family members has increased tremendously in the last three decades [8][9][10][11][12][13][14][15][16][17][18], many key features are still not well understood. In our last two publications we have shown that Coenzyme Q-1 (CoQ-1) and CoQ-10 undergo structural changes in strong alkaline environment or in the presence of Cytochrome P450 enzymes [19,20].…”

Section: Introductionmentioning

confidence: 99%

New insights into the chemistry of Coenzyme Q-0: A voltammetric and spectroscopic study

Gulaboski

Bogeski

Kokoškarova

et al. 2016

Bioelectrochemistry

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Coenzyme Q-0 (CoQ-0) is the only Coenzyme Q lacking an isoprenoid group on the quinoid ring, a feature important for its physico-chemical properties. Here, the redox behavior of CoQ-0 in buffered and non-buffered aqueous media was examined. In buffered aqueous media CoQ-0 redox chemistry can be described by a 2-electron-2-proton redox scheme, characteristic for all benzoquinones. In non-buffered media the number of electrons involved in the electrode reaction of CoQ-0 is still 2; however, the number of protons involved varies between 0 and 2. This results in two additional voltammetric signals, attributed to 2-electrons-1H + and 2-electrons-0H + redox processes, in which mono-and di-anionic compounds of CoQ-0 are formed. In addition, CoQ-0 exhibits a complex chemistry in strong alkaline environment. The reaction of CoQ-0 and OH − anions generates several hydroxyl derivatives as products. Their structures were identified with HPLC/MS. The prevailing radical reaction mechanism was analyzed by electron paramagnetic resonance spectroscopy. The hydroxyl derivatives of CoQ-0 have a strong antioxidative potential and form stable complexes with Ca 2+ ions. In summary, our results allow mechanistic insights into the redox properties of CoQ-0 and its hydroxylated derivatives and provide hints on possible applications.

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“…If the increase in free radicals is greater than the ability to neutralize them, ROS will attack cellular structures located near the sites where ROS are generated [30,44,48]. Functional imbalance between ROS levels and antioxidant concentrations can be caused by various disease states such as cancer, cardiovascular diseases, brain dysfunction, inflammatory diseases, neurodegenerative diseases, ischemiareperfusion injury, and aging [43,48,50,51].…”

Section: International Journal Of Physical Medicine and Rehabilitationmentioning

confidence: 99%

“…Under normal physiological conditions, this mitochondrial antioxidant defense system can adequately handles the potentially detrimental effects of ROS derived from energy metabolism, this cellular free-radical scavenging enzymes neutralize excess ROS and repair the enzymes that reverse ROSmediated damage [36,48]. However, when these enzymes cannot convert ROS such as the superoxide radical to H 2 O fast enough, oxidative damage occurs and accumulates in the mitochondria [29,30,49].…”

Section: International Journal Of Physical Medicine and Rehabilitationmentioning

confidence: 99%

“…The cell possesses antioxidant defense systems to counteract damaging ROS these are enzymatic antioxidants such as catalase, superoxide dismutase (SOD), glutathione peroxidase, and nonenzymatic antioxidants such as ascorbic acid (vitamin C), α-tocopherol (vitamin E) and β-carotene [30,43,48]. Under normal physiological conditions, this mitochondrial antioxidant defense system can adequately handles the potentially detrimental effects of ROS derived from energy metabolism, this cellular free-radical scavenging enzymes neutralize excess ROS and repair the enzymes that reverse ROSmediated damage [36,48].…”

Section: International Journal Of Physical Medicine and Rehabilitationmentioning

confidence: 99%

See 1 more Smart Citation

Mechanism of Mitochondrial Dysfunction during Chronic Fatigue

Muluye¹,

Bian²

2017

Int J Phys Med Rehabil

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A clinically defined condition characterized by persistent, severe, disabling fatigue lasting more than six months that is not reversed by sleep is regarded as chronic fatigue (CF). Fatigue is a complex phenomenon determined by several factors, including psychological health but at the biochemical level fatigue is related to the metabolic energy available to tissues and cells, mainly through mitochondrial respiration. Fatigue is the most common symptom of poorly functioning mitochondria. therefore dysfunction of these organelles may be the cause of the fatigue seen in CF. There is a great progress in the molecular understanding of mitochondrial disorder but the relation of mitochondrial dysfunction with CF and the underlying mechanism is not identified well in addition treatment of fatigue is still inadequate. In this review we try to summarize the relation between CF with mitochondrial dysfunction and determine the underline mechanism.

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A mitochondrial superoxide theory for oxidative stress diseases and aging

Cited by 283 publications

References 90 publications

Antioxidant Systems in Poultry Biology: Superoxide Dismutase

Antioxidant Systems in Poultry Biology: Superoxide Dismutase

New insights into the chemistry of Coenzyme Q-0: A voltammetric and spectroscopic study

Mechanism of Mitochondrial Dysfunction during Chronic Fatigue

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