Coenzyme Q10, Copper, Zinc, and Lipid Peroxidation Levels in Serum of Patients with Chronic Obstructive Pulmonary Disease

Tanrıkulu, Abdullah Çetin; Abakay, Abdurrahman; Evliyaoğlu, Osman; Palanci, Yılmaz

doi:10.1007/s12011-010-8897-5

Cited by 39 publications

(26 citation statements)

References 23 publications

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“…Our finding is supported by a recent study that a decrease in CoQ10 and increase in zinc levels were observed in chronic obstructive pulmonary disease (COPD) patients [31], which probably result from the defense response of organism against zinc-mediated inflammation. There is no direct evidence in relation to zinc and CoQ10 interactions, but our results suggest that CoQ10 may be neuroprotective against zinc-induced mitochondrial dysfunction.…”

Section: Discussionsupporting

confidence: 90%

Effect of DHA and CoenzymeQ10 Against A�- and Zinc-Induced Mitochondrial Dysfunction in Human Neuronal Cells

Sadli¹,

Barrow²,

McGee

et al. 2013

Cell Physiol Biochem

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Background: Beta-amyloid (Aβ) protein is a key factor in the pathogenesis of Alzheimer's disease (AD) and it has been reported that mitochondria is involved in the biochemical pathway by which Aβ can lead to neuronal dysfunction. Coenzyme Q10 (CoQ10) is an essential cofactor involved in the mitochondrial electron transport chain and has been suggested as a potential therapeutic agent in AD. Zinc toxicity also affects cellular energy production by decreasing oxygen consumption rate (OCR) and ATP turnover in human neuronal cells, which can be restored by the neuroprotective effect of docosahexaenoic acid (DHA). Method: In the present study, using Seahorse XF-24 Metabolic Flux Analysis we investigated the effect of DHA and CoQ10 alone and in combination against Aβ- and zinc-mediated changes in the mitochondrial function of M17 neuroblastoma cell line. Results: Here, we observed that DHA is specifically neuroprotective against zinc-triggered mitochondrial dysfunction, but does not directly affect Aβ neurotoxicity. CoQ10 has shown to be protective against both Aβ- and zinc-induced alterations in mitochondrial function. Conclusion: Our results indicate that DHA and CoQ10 may be useful for the prevention, treatment and management of neurodegenerative diseases such as AD.

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Section: Discussionsupporting

confidence: 90%

Effect of DHA and CoenzymeQ10 Against A�- and Zinc-Induced Mitochondrial Dysfunction in Human Neuronal Cells

Sadli¹,

Barrow²,

McGee

et al. 2013

Cell Physiol Biochem

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“…Consequently, trace element measurement can enable detection of more disorders of the airway and also provide valuable information about pulmonary inflammation in COPD-like conditions. 27 Telomerase is a unique polymerase, and it synthesizes telomeric repeats. 28,29 There are 2 core components of telomerase: the catalytic reverse transcriptase and the RNA component.…”

Section: Discussionmentioning

confidence: 99%

Serum Telomerase Levels and COPD Exacerbations

Bozkuş¹,

Güler

Sımsek

2016

Respir Care

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BACKGROUND: To our knowledge, there is no study on the level of telomerase in subjects with COPD during an exacerbation period. The objective of this work was to compare lipid peroxidation, telomerase, zinc (Zn), copper (Cu), and malondialdehyde levels in asymptomatic smokers and subjects with COPD exacerbation. METHODS: The study included 45 subjects with COPD exacerbation and 42 healthy subjects with tobacco use as a control group. Samples were taken from blood and after the serum levels of telomerase malondialdehyde, Cu, and Zn were measured, the values were compared between the 2 groups. Tests for respiratory function were performed, and sedimentation and C-reactive protein levels were measured. RESULTS: The COPD exacerbation group had a significantly (P < .001) lower Cu/Zn ratio compared with the control group; however, the COPD exacerbation group had significantly (P < .001) higher levels of telomerase malondialdehyde, Cu, and Zn compared with the control group. Malondialdehyde, Cu, Zn, and FEV 1 were found negatively correlated in the COPD exacerbation and control groups (P < .001). The COPD exacerbation group had lower FEV 1 and FVC compared with the control group. The COPD exacerbation group had significantly (P < .001) higher levels of C-reactive protein and a higher blood cell sedimentation rate compared with the control group. CONCLUSIONS: The reason why the subjects had a reduced Cu/Zn ratio and increased levels of telomerase, Cu, and Zn is likely to be oxidative stress, which can be defined as an increased exposure to oxidants and/or decreased antioxidant capacities It is obvious from this study that lung oxidant-antioxidant balance is abnormal in subjects with COPD exacerbation and also that the increased level of telomerase is associated with this imbalance.

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“…In addition, free radicals effects are connected with a formation of atherosclerotic lesions. In body fluids (blood, urine) the increased levels of peroxidation end-products (MDA, 4-HNE, isoprostanes) are present [26,27]. The lipid peroxidation by free radicals occurs in three stages: initiation, propagation and termination [2,26].…”

Section: Introductionmentioning

confidence: 99%