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Demin, Oleg; Kholodenko, Boris N.; Скулачев, В.П.

doi:10.1023/a:1006849920918

Cited by 96 publications

(34 citation statements)

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“…Some insight can be obtained from a kinetic model of mitochondrial respiration published elsewhere [31,32]. This model implements all available kinetic knowledge concerning the individual enzymes and non-enzymic steps of the mitochondrial oxidative phosphorylation machinery.…”

Section: Discussionmentioning

confidence: 99%

Kinetics and control of oxidative phosphorylation in rat liver mitochondria after chronic ethanol feeding

Marcinkeviciute

Mildažienė

Crumm

et al. 2000

Biochemical Journal

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Changes in the kinetics and regulation of oxidative phosphorylation were characterized in isolated rat liver mitochondria after 2 months of ethanol consumption. Mitochondrial energy metabolism was conceptually divided into three groups of reactions, either producing protonmotive force (∆p) (the respiratory subsystem) or consuming it (the phosphorylation subsystem and the proton leak). Manifestation of ethanol-induced mitochondrial malfunctioning of the respiratory subsystem was observed with various substrates ; the respiration rate in State 3 was inhibited by 27p4 % with succinate plus amytal, by 20p4 % with glutamate plus malate, and by 17p2 % with N,N,Nh,Nhtetramethyl-p-phenylenediamine\ascorbate. The inhibition of the respiratory activity correlated with the lower activities of cytochrome c oxidase, the bc " complex, and the ATP synthase in mitochondria of ethanol-fed rats. The block of reactions consuming the ∆p to produce ATP (the phosphorylating subsystem)

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Section: Discussionmentioning

confidence: 99%

Kinetics and control of oxidative phosphorylation in rat liver mitochondria after chronic ethanol feeding

Marcinkeviciute

Mildažienė

Crumm

et al. 2000

Biochemical Journal

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“…Mitochondria are important source of ROS under both physiological 12) and pathological conditions such as cerebral I/R injury.…”

Section: Discussionmentioning

confidence: 99%

Schisandrin B Enhances Cerebral Mitochondrial Antioxidant Status and Structural Integrity, and Protects against Cerebral Ischemia/Reperfusion Injury in Rats

Chen

Chiu

2008

Biological & Pharmaceutical Bulletin

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Schisandrin B (Sch B) is the most abundant, active dibenzocyclooctadiene derivative isolated from the fruit of Schisandra chinensis (FS), a traditional Chinese herb clinically used for the treatment of viral and chemical hepatitis. 1)A recent study from our laboratory has demonstrated that long-term treatment with Sch B was able to enhance mitochondrial antioxidant status and the resistance to Ca 2ϩ -induced mitochondrial permeability transition (PT) in an ageindependent manner in various rat organs including the heart and brain.2) The Sch B-induced enhancement of mitochondrial protective parameters in the heart was associated with the protection against myocardial ischemia/reperfusion (I/R) injury in both young and middle-aged rats.2) Given that the maintenance of mitochondrial antioxidant status and structural integrity is crucial for cell survival, 3) Sch B has been proposed to be used as a universal cell protectant against tissue damage caused by endogenous and exogenous oxidants. 2)While the protection of Sch B against I/R injury has been demonstrated in the heart, 2,4) it is still unclear whether Sch B treatment can produce any beneficial effect on cerebral I/R injury.In the present study, we investigated the effect of longterm treatment with Sch B on cerebral I/R injury in rats. To elucidate the biochemical mechanism involved in the cerebroprotection against I/R injury, cerebral mitochondrial antioxidant status as well as mitochondrial structural integrity were assessed in control and Sch B-treated rats, without or with I/R challenge. MATERIALS AND METHODS ChemicalsReduced glutathione (GSH), oxidized glutathione, glutathione reductase, cytochrome c, a-tocopherol (a-TOC), cyclosporin A (Cs A) and 2,3,5-triphenyl tetrazolium chloride (TTC) were purchased from Sigma Chemical Co. (St. Louis, MO, U.S.A.). All other chemicals were of analytical grade. Solvents used for HPLC were of HPLC grade.Herbal Material Dried FS was imported from mainland China. It was authenticated and supplied by a commercial dealer (Lee Hoong Kee Ltd.) in Hong Kong. Sch B was purified from the petroleum ether extract of FS, with the purity being higher than 95% as determined by HPLC analysis. 5)Animal Care Adult female Sprague-Dawley rats (8-10 weeks; 200-250 g) were maintained under a 12-h dark/light cycle at about 22°C, and allowed food and water ad libitum. Experimental protocols were approved by the Research Practice Committee at the Hong Kong University of Science & Technology.Drug Treatment Animals were randomly divided into groups, with five animals in each. In the Sch B treatment groups, rats were intragastrically administered with Sch B (dissolved/suspended in olive oil) at a daily dose of 1, 10 or 30 mg/kg from day 1 to day 15 of the experiment. This dosage regimen was found to be effective in protecting against myocardial ischemia/reperfusion injury in rats.2) Sch B-untreated animals received the vehicle (i.e. olive oil) only. The rat model of cerebral I/R injury was modified from that of Ischikawa and Konishi.6) Phenobarbita...

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“…Previously, one of the superoxideproducing sites in the respiratory chain was shown to be the co-enzyme Q and cytochrome bc1 complex. 29,30) The production of superoxide at this site results in the leakage of electrons from the respiratory chain, but the superoxide produced from here is also able to reduce cytochrome c, and then transfer an electron to cytochrome c oxidase. However, when modified by peroxynitrite, even if reduced by superoxide, the cytochrome c could be readily oxidized by hydrogen peroxide formed from residual superoxide.…”

Section: Discussionmentioning

confidence: 99%

Functional Modification of Cytochrome c by Peroxynitrite in an Electron Transfer Reaction.

Nakagawa¹,

Ohshima²,

Takusagawa³

et al. 2001

CHEMICAL & PHARMACEUTICAL BULLETIN

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Reactive oxygen species (ROS) such as superoxide and reactive nitrogen species (RNS) such as nitric oxide are considered to be involved in the pathogenesis of various diseases. Although nitric oxide and superoxide are both endogenous compounds and important for physiological reactions including vasodilatation, signal transduction, and protection from infection, they have toxic effects on various biological components when overproduced. Peroxynitrite is produced after the diffusion rate-limiting reaction between nitric oxide and superoxide, and is a strong oxidant for various biological components as well as a nitrating reagent for free tyrosine and protein tyrosine residues. Since peroxynitrite is formed from superoxide and nitric oxide under physiological conditions in vitro, it is also considered to be produced in vivo when sufficient amounts of superoxide and nitric oxide are produced to react directly with one another. Because of its high reactivity, peroxynitrite can cause oxidative damage to important biological components, such as low density lipoprotein (LDL) oxidation, lipid peroxidation, and DNA strand breakage, [1][2][3] as well as the nitration of tyrosine residues to produce nitrotyrosine.4) The presence of nitrotyrosine in tissues and cell cultures is often used as a marker for peroxynitrite production although nitrotyrosine is not the sole product of peroxynitrite.With reports that nitrotyrosine is upregulated in tissue in several kinds of diseases, peroxynitrite is assumed to be produced not only in inflammation, 2,3) but also in neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, and amyotropic lateral sclerosis.1,5-10) Additionally, the tyrosine nitration in the substrate proteins of tyrosine kinases is assumed to prevent the tyrosine phosphorylation by the kinases. Tyrosine phosphorylation is very important to the signal transduction in cells.11,12) Furthermore, the oxidation and nitration activities of peroxynitrite are considered to play important roles in the functional damage to enzymes and receptors. It has been reported that the activity of the respiratory chain in mitochondria is inhibited by peroxynitrite treatment due to the oxidative destruction of iron-sulfur containing proteins, 13) the inhibition of the redox cycling of cytochrome c by the oxidation of ferrocytochrome c, 14) and the inhibition of cytochrome c oxidase.15) It has also been shown that cytochrome c is released from mitochondria and involved in the activation of caspases during the apoptotic process. [16][17][18] Although cytochrome c is an important component of the electron transfer system in mitochondria, few studies have been conducted on the effect of peroxynitrite on the redox activity of cytochrome c. Very recently, Radi and colleagues, reported nitration of cytochrome c by peroxynitrite in vitro, 19,20) and demonstrated that a low concentration of peroxynitrite caused mono-nitration of the tyrosine residue at position 67. Since cytochrome c is a water-soluble protein in the intermembran...

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Cited by 96 publications

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Kinetics and control of oxidative phosphorylation in rat liver mitochondria after chronic ethanol feeding

Kinetics and control of oxidative phosphorylation in rat liver mitochondria after chronic ethanol feeding

Schisandrin B Enhances Cerebral Mitochondrial Antioxidant Status and Structural Integrity, and Protects against Cerebral Ischemia/Reperfusion Injury in Rats

Functional Modification of Cytochrome c by Peroxynitrite in an Electron Transfer Reaction.

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