Cytochrome c oxidase dysfunction in oxidative stress

Srinivasan, Satish; Avadhani, Narayan G.

doi:10.1016/j.freeradbiomed.2012.07.021

Cited by 286 publications

(225 citation statements)

References 166 publications

(229 reference statements)

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“…The results of our study suggest that high levels of UA in hepatocytes significantly reduced CCO activity in the mitochondria. A previous study showed that mitochondrial ATP production can be upregulated via positive regulation of CCO activity, thereby preventing myocardial cell hypoxia (Hayashi et al, 2015), while another study showed that lower CCO vitality can lead to an increase in ROS generation in the mitochondria (Srinivasan and Avadhani, 2012); these studies support our conclusion that UA-induced oxidative stress in liver mitochondria, and alterations to mitochondrial function, result in cell damage.…”

Section: Discussionsupporting

confidence: 82%

Effect of uric acid on mitochondrial function and oxidative stress in hepatocytes

et al. 2016

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ABSTRACT. Here, we investigated the effect of uric acid (UA) on hepatocyte mitochondria. Hepatocytes cultured in vitro were treated with varying concentrations of UA. The change in apoptotic activity was detected by flow cytometry. The DNA damage index 8-hydroxy-deoxyguanosine (8-OHdG) and mitochondrial function indices succinate dehydrogenase (SDH), cytochrome C oxidase (CCO), and adenosine triphosphate (ATP) were detected by enzyme assays. Reactive oxygen species (ROS) accumulation was confirmed by a dichloro-dihydrofluorescein diacetate assay. We observed an increase in apoptotic activity, ROS accumulation, and 8-OHdG activity in hepatocytes treated with UA for extended periods, indicating DNA damage; specifically, we observed a significant increase in these activities 48, 72, and 96 h after UA addition, compared to those observed at 24 h (P < 0.05). Cells treated with 30 mg/dL UA for 96 h showed a peak in apoptotic activity. We also observed a significant decrease in ATP, SDH, and CCO activities with the increase in uric acid concentration over time. Cells treated with 30 mg/dL UA for 96 h showed the highest ATP levels, while SDH and CCO activities at 48, 72, and 96 h post-UA treatment were significantly lower than those at 24 h (P < 0.01). Moreover, cells treated with 30 mg/dL UA showed a 0.02 ± 0.02 and 0.15 ± 0.01 mmol/ mg/min decrease in SDH and CCO levels after 72 h. Therefore, we concluded that high concentrations of UA may induce oxidative stress in hepatocyte mitochondria, increasing ROS production and ultimately resulting in mitochondrial damage.

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Section: Discussionsupporting

confidence: 82%

Effect of uric acid on mitochondrial function and oxidative stress in hepatocytes

et al. 2016

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“…When cytochrome c oxidase is inhibited, electrons were directed toward reacting with oxygen to form superoxide anions and reactive oxygen species. (27,28) To the best of our knowledge, no studies have been carried out to investigate the oxidative stress in Participants of acute zinc phosphide poisoning. However, many studies evaluated oxidative stress markers in acute aluminium phosphide poisoning.…”

Section: Discussionmentioning

confidence: 99%

Evaluation of Potential Oxidative Stress in Egyptian Patients with Acute Zinc Phosphide Poisoning and the Role of Vitamin C

Sagah

Oreby

Elgharabawy³

et al. 2015

IJHS

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Objective: To evaluate potential oxidative stress in patients with acute phosphide poisoning and the effect of vitamin C. Methods:Participants were females and divided into three groups; group I: healthy volunteers group II: healthy volunteers received vitamin C, group III: patients with acute phosphide poisoning received the supportive and symptomatic treatment and group IV: patients with acute phosphide poisoning received the supportive and symptomatic treatment in addition to vitamin C. All the participants were subjected to thorough history, clinical examination, ECG and laboratory investigations were carried on collected blood and gastric lavage samples on admission. Blood samples were divided into two parts, one for measurement of routine investigations and the second part was used for evaluation of malondialdehyde and total thiol levels before and after receiving the treatment regimen.Results: Most of the cases in this study were among the age group of 15-25 years, females, single, secondary school education, from rural areas and suicidal. All vital signs were within normal range and the most common complaint was vomiting and abdominal pain. All cases in this study showed normal routine investigations. The mean MDA levels after receiving treatment decreased significantly in groups II and IV. The mean total thiol levels increased significantly after receiving treatment in groups II and IV. Conclusion:It can be concluded that vitamin C has a potential benefit due to its antioxidant property on zinc phosphide induced-oxidative stress in acute zinc phosphide poisoned patients.

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“…Among the nuclear-encoded subunits of CcO, subunits IVi1 and Vb have been found to be particularly susceptible to damage under various oxidative stress conditions. 7 Our new study examines the nature of signaling initiated by long-term reduction in nuclear CcO subunits and activity and the resulting cellular changes (Fig. 1).…”

Section: Role Of Cco Dysfunction In Cellular Reprogramming and Cancermentioning

confidence: 99%

Mitochondrial respiratory defects promote the Warburg effect and cancer progression

Srinivasan

Guha

Avadhani

2015

Molecular & Cellular Oncology

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Cytochrome c oxidase dysfunction in oxidative stress

Cited by 286 publications

References 166 publications

Effect of uric acid on mitochondrial function and oxidative stress in hepatocytes

Effect of uric acid on mitochondrial function and oxidative stress in hepatocytes

Evaluation of Potential Oxidative Stress in Egyptian Patients with Acute Zinc Phosphide Poisoning and the Role of Vitamin C

Mitochondrial respiratory defects promote the Warburg effect and cancer progression

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