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      Effects of coenzyme Q10 supplementation on C-reactive protein and homocysteine as the inflammatory markers in hemodialysis patients; a randomized clinical trial

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          Abstract

          Background: The most leading cause of death in end-stage renal disease (ESRD) patients are cardiovascular disease and inflammatory markers are related to coronary events. CO-Q10 (coenzyme Q10) is a protective supplement from free radical oxidative damage. In addition, hyperhomocysteinemia is an independent coronary artery disease (CAD) risk factor.

          Objectives: Due to increasing oxidative stress in dialysis patients, and the effect of CO-Q10 in decrease oxidative stress, in this work, we assessed the effect of CO-Q10 on C-reactive protein (CRP) level as an inflammatory marker and homocysteine in dialysis patients.

          Patients and Methods: This was a single-blind, randomized cross over clinical trial. Patients with ESRD were randomly allotted to two groups. All patients received placebo and C0- Q10 100mg/d during the three months in each stage, with two week washout period. Plasma level of CRP and homocysteine from the start of the work and at the conclusion of each menses, are evaluated.

          Results: Thirty-four patients randomized, but 26 patients complete study protocol. The treatment effect of CO-Q10 on CRP level is significant ( P < 0.001) (95% CI = -20.1 to -10.5) and it was also significant for the increasing albumin level. ( P = 0.044) (95% CI = 0. 0-0.6), But there was not any substantial effect on serum homocysteine level ( P = 0.630).

          Conclusions: CO-Q10 could significantly decrease CRP level as an inflammatory marker and can protect cardiovascular events.

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          Biochemical, physiological and medical aspects of ubiquinone function.

          G Dallner, L Ernster (1995)
          This presentation is a brief review of current knowledge concerning some biochemical, physiological and medical aspects of the function of ubiquinone (coenzyme Q) in mammalian organisms. In addition to its well-established function as a component of the mitochondrial respiratory chain, ubiquinone has in recent years acquired increasing attention with regard to its function in the reduced form (ubiquinol) as an antioxidant. Ubiquinone, partly in the reduced form, occurs in all cellular membranes as well as in blood serum and in serum lipoproteins. Ubiquinol efficiently protects membrane phospholipids and serum low-density lipoprotein from lipid peroxidation, and, as recent data indicate, also mitochondrial membrane proteins and DNA from free-radical induced oxidative damage. These effects of ubiquinol are independent of those of exogenous antioxidants, such as vitamin E, although ubiquinol can also potentiate the effect of vitamin E by regenerating it from its oxidized form. Tissue ubiquinone levels are regulated through the mevalonate pathway, increasing upon various forms of oxidative stress, and decreasing during aging. Drugs inhibiting cholesterol biosynthesis via the mevalonate pathway may inhibit or stimulate ubiquinone biosynthesis, depending on their site of action. Administration of ubiquinone as a dietary supplement seems to lead primarily to increased serum levels, which may account for most of the reported beneficial effects of ubiquinone intake in various instances of experimental and clinical medicine.
          Article 0 comments Cited 65 times – based on 0 reviews     Review now
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            Effects of coenzyme Q10 supplementation (300 mg/day) on antioxidation and anti-inflammation in coronary artery disease patients during statins therapy: a randomized, placebo-controlled trial

            Bor-Jen Lee, Yu-Fen Tseng, Chi-Hua Yen … (2013)
            Background High oxidative stress and chronic inflammation can contribute to the pathogenesis of coronary artery disease (CAD). Coenzyme Q10 is an endogenous lipid-soluble antioxidant. Statins therapy can reduce the biosynthesis of coenzyme Q10. The purpose of this study was to investigate the effects of a coenzyme Q10 supplement (300 mg/d; 150 mg/b.i.d) on antioxidation and anti-inflammation in patients who have CAD during statins therapy. Methods Patients who were identified by cardiac catheterization as having at least 50% stenosis of one major coronary artery and who were treated with statins for at least one month were enrolled in this study. The subjects (n = 51) were randomly assigned to the placebo (n = 24) and coenzyme Q10 groups (Q10-300 group, n = 27). The intervention was administered for 12 weeks. The concentrations of coenzyme Q10, vitamin E, antioxidant enzymes activities (superoxide dismutase, catalase, and glutathione peroxidase), and inflammatory markers [C-reactive protein (CRP), tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6)] were measured in the 42 subjects (placebo, n = 19; Q10-300, n = 23) who completed the study. Results The levels of the plasma coenzyme Q10 (P < 0.001) and antioxidant enzymes activities (P < 0.05) were significantly higher after coenzyme Q10 supplementation. The levels of inflammatory markers (TNF-α, P = 0.039) were significantly lower after coenzyme Q10 supplementation. The subjects in the Q10-300 group had significantly higher vitamin E (P = 0.043) and the antioxidant enzymes activities (P < 0.05) than the placebo group at week 12. The level of plasma coenzyme Q10 was significantly positively correlated with vitamin E (P = 0.008) and antioxidant enzymes activities (P < 0.05) and was negatively correlated with TNF-α (P = 0.034) and IL-6 (P = 0.027) after coenzyme Q10 supplementation. Conclusion Coenzyme Q10 supplementation at 300 mg/d significantly enhances antioxidant enzymes activities and lowers inflammation in patients who have CAD during statins therapy. Trial registration Clinical Trials.gov Identifier: NCT01424761.
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              Oxidative stress and endothelial function in chronic renal failure.

              M Annuk, Walter Linde-Zwirble, B Fellström … (2001)
              This study aimed to investigate the relationship between oxidative stress and endothelium-dependent vasodilation in patients with chronic renal failure (CRF). Thirty-seven patients with CRF underwent evaluation of endothelium-dependent vasodilation and endothelium-independent vasodilation by means of forearm blood flow measurements with venous occlusion plethysmography during local intra-arterial infusions of methacholine (evaluating endothelium-dependent vasodilation) and sodium nitroprusside (evaluating endothelium-independent vasodilation). Lag phase of lipoprotein fraction to oxidation, total antioxidative activity, diene conjugates, thiobarbituric acid reactive substances, lipid hydroperoxide, reduced glutathione (GSH), oxidized GSH (GSSG), and the GSH redox ratio (GSSG/GSH) were all measured as markers of oxidative stress. Two groups of healthy subjects (61 and 37 subjects, respectively) were used as controls. In one group, oxidative stress markers were measured, whereas endothelium-dependent vasodilation and endothelium-independent vasodilation were assessed in the other group. Compared with controls, the patients with renal insufficiency had an impaired endothelium-dependent vasodilation, a shorter lag phase of lipoprotein fraction, and higher levels of diene conjugates, lipid hydroperoxide, and GSSG levels. The GSSG/GSH ratio was lower in patients with CRF. Endothelium-dependent vasodilation was positively correlated with total antioxidative activity (r = 0.41, P = 0.016), GSH (r = 0.44, P < 0.0098), and lag phase of LDL (r = 0.35, P = 0.036) and negatively correlated with GSSG (r = -0.40, P < 0.018), GSSG/GSH (r = -0.47, P = 0.0057), and diene conjugates (r = -0.53 P < 0.0015) in patients with CRF. These results show that an impaired endothelium vasodilation function and oxidative stress are related to each other in patients with CRF.
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                Author and article information

                Journal
                Journal ID (nlm-ta): J Nephropathol
                Journal ID (iso-abbrev): J Nephropathol
                Journal ID (publisher-id): J Nephropathol
                Journal ID (pmc): J Nephropathol
                Journal ID (publisher-id): JNP
                Title: Journal of Nephropathology
                Publisher: Society of Diabetic Nephropathy Prevention
                ISSN (Print): 2251-8363
                ISSN (Electronic): 2251-8819
                Publication date (Print): January 2016
                Publication date (Electronic): 07 November 2015
                Volume: 5
                Issue: 1
                Pages: 38-43
                Affiliations
                1Departement of Nephrology, Loghman Hakim Hospital, Shahid-Beheshti University of Medical Sciences, Tehran, Iran
                2Department of Internal Medicine, Loghman Hakim Hospital, Shahid-Beheshti University of Medical Sciences , Tehran, Iran
                Author notes
                [* ] Corresponding author: Maryam Ghassami, Department of Internal Medicine, Division of Nephrology, Loghman-Hakim Hospital, Shahid-Beheshti University of Medical sciences, Tehran, Iran. lcrdc.sbum@ 123456gmail.com
                Article
                DOI: 10.15171/jnp.2016.07
                PMC ID: 4790186
                PubMed ID: 27047809
                SO-VID: c39e732d-5885-4950-8f00-64a8c755bfea
                Copyright © © 2016 The Author(s)
                License:

                Published by Society of Diabetic Nephropathy Prevention. This is an open-access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 05 October 2015
                Date accepted : 01 November 2015
                Page count
                Figures: 2, Tables: 4, References: 25, Pages: 6
                Categories
                Subject: Original Article

                Keywords: homocysteine,c-reactive protein,renal insufficiency,coenzyme q10
                Data availability:
                Keywords: homocysteine, c-reactive protein, renal insufficiency, coenzyme q10

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