Reactive oxygen species are generated by the respiratory complex <scp>II</scp> – evidence for lack of contribution of the reverse electron flow in complex <scp>I</scp>

Moreno‐Sánchez, Rafael; Hernández‐Esquivel, Luz; Rivero-Segura, Nadia Alejandra; Marín‐Hernández, Álvaro; Neužil, Jiřı́; Ralph, Stephen John; Rodrı́guez-Enrı́quez, Sara

doi:10.1111/febs.12086

Cited by 69 publications

(58 citation statements)

References 63 publications

(110 reference statements)

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“…Mitochondrial complex II oxidizes succinate to fumarate as part of the Krebs cycle and reduces ubiquinone in the electron transport system. Succinate-driven oxidation via complex II may contribute significantly to high rates of production of Reactive Oxygen Species (ROS) by mitochondria [36,37].…”

Section: Discussionmentioning

confidence: 99%

Muscle Mitochondrial Dysfunction in Horses Affected by Acute Laminitis

et al. 2014

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Laminitis is a common and debilitating disease affecting horses and ponies. It often leads to the demise of the animal. Energy deficiency is suspected to entrain the disruption of the hemidesmosomes leading to the failure of the dermal-epidermal interface. The aim of this study was to measure the muscle mitochondrial function by high resolution respirometry. Muscle micro-biopsies were obtained from 11 horses affected by acute metabolic laminitis, 6 horses affected by acute laminitis resulting from a systemic inflammation response syndrome and 28 healthy horses distributed in 2 control groups: 17 horses with a body condition score [BSC, ranging from 0 (emaciated) to 5 (obese)] of 2 to 3 and 11 horses with a BSC of 4 to 5. During the acute phase of laminitis, a significant reduction of the muscle mitochondrial respiration was observed. The muscle mitochondrial dysfunction occurred independently of the etiology (metabolic disorder or systemic inflammation) leading to laminitis. The reduction of the oxidative phosphorylation and of the maximal respiratory capacity (after uncoupling) may induce depletion of the cell's ATP content. If the same mitochondrial alteration occurs in the foot lamina, mitochondria targeting should be considered for the future, not only to better understand the physiopathology of the disease but also to maintain and to support the mitochondrial function before reaching the « mitochondrial dysfunction threshold » that may lead to the failure of the dermal-epidermal interface.

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Section: Discussionmentioning

confidence: 99%

Muscle Mitochondrial Dysfunction in Horses Affected by Acute Laminitis

et al. 2014

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“…Many studies reported that critical sites for electron leakage were the ubiquinone binding sites of complex I and complex III, and that of complex II were negligible [13,14]. Some studies also suggest that ROS would be produced from complex II and complex IV [15,16]. However, the mechanism of how excess ROS is produced in hepatic mitochondria exposed to Cr(VI) has not been elaborated clearly.…”

Section: Discussionmentioning

confidence: 99%

Effect of Hexavalent Chromium on Electron Leakage of Respiratory Chain in Mitochondria Isolated from Rat Liver

Xie

Zhong

Zeng

et al. 2013

Cell Physiol Biochem

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Background/Aims: In the present study, we explored reactive axygen species (ROS) production in mitochondria, the mechanism of hexavalent chromium (Cr(VI)) hepatotoxicity, and the role of protection by GSH. Methods: Intact mitochondria were isolated from rat liver tissues and mitochondrial basal respiratory rates of NADH and FADH₂ respiratory chains were determined. Mitochondria were treated with Cr(VI), GSH and several complex inhibitors. Mitochondria energized by glutamate/malate were separately or jointly treated with Rotenone (Rot), diphenyleneiodonium (DPI) and antimycinA (Ant), while mitochondria energized by succinate were separately or jointly treated with Rot, DPI ‚ thenoyltrifluoroacetone (TTFA) and Ant. Results: Cr(VI) concentration-dependently induced ROS production in the NADH and FADH₂ respiratory chain in liver mitochondria. Basal respiratory rate of the mitochondrial FADH₂ respiratory chain was significantly higher than that of NADH respiratory chain. Hepatic mitochondrial electron leakage induced by Cr(VI) from NADH respiratory chain were mainly from ubiquinone binding sites of complex I and complex III. Conclusion: Treatment with 50µM Cr(VI) enhances forward movement of electrons through FADH₂ respiratory chain and leaking through the ubiquinone binding site of complex III. Moreover, the protective effect of GSH on liver mitochondria electron leakage is through removing excess H₂O₂ and reducing total ROS.

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“…However, the detailed mechanism of the effect of complex II on HCC progression remains to be elucidated. Complex II contributes significantly to the production of ROS (14,15), which may explain the strong association between complex II and HCC development. The levels of complex II and ROS demonstrated no association in the present analysis, suggesting that an alternative mechanism may regulate the generation of ROS in patients with HCC.…”

Section: Factorsmentioning

confidence: 99%

“…Complex II is ubiquitous in diverse aerobic species and contributes significantly to the excessive production of ROS by mitochondria (14,15). Recently, several tumors caused by complex II gene mutations have been identified (16).…”

Section: Introductionmentioning

confidence: 99%

“…Although numerous studies have suggested the value of oxidative stress markers, such as ROS and complex II (14)(15)(16), in molecular cancer research, little is known regarding the potential predictive power of oxidative stress markers for the prognosis of HCC patients. The aim of the present study was to evaluate the ability of ROS and complex II mtDNA levels in HCC liver tissues for the survival of patients with HCC.…”

Section: Introductionmentioning

confidence: 99%

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Mitochondrial reactive oxygen species and complex II levels are associated with the outcome of hepatocellular carcinoma

Zhao

et al. 2015

Oncology Letters

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Abstract. In the present study, two oxidative stress parameters, reactive oxygen species (ROS) and mitochondrial respiratory complex II, were evaluated in the mitochondria of hepatocellular carcinoma (HCC) cells to determine the association between these parameters and the carcinogenesis and clinical outcome of HCC. High levels of ROS and low levels of complex II were found to be associated with reduced post-operative survival in HCC patients using the log-rank test. Furthermore, multivariate analysis confirmed that the levels of ROS [relative risk (RR)=2.867; 95% confidence interval (CI), 1.062-7.737; P=0.038] and complex II (RR=5.422; 95% CI, 1.273-23.088; P=0.022) were independent predictors for the survival of patients with HCC. Therefore, the analysis of ROS and complex II levels may provide a useful research and therapeutic tool for the prediction of HCC prognosis and treatment.

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Reactive oxygen species are generated by the respiratory complex II – evidence for lack of contribution of the reverse electron flow in complex I

Cited by 69 publications

References 63 publications

Muscle Mitochondrial Dysfunction in Horses Affected by Acute Laminitis

Muscle Mitochondrial Dysfunction in Horses Affected by Acute Laminitis

Effect of Hexavalent Chromium on Electron Leakage of Respiratory Chain in Mitochondria Isolated from Rat Liver

Mitochondrial reactive oxygen species and complex II levels are associated with the outcome of hepatocellular carcinoma

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