Coenzyme Q improves LDL resistance to ex vivo oxidation but does not enhance endothelial function in hypercholesterolemic young adults

Raitakari, Olli T.; McCredie, Robyn J.; Witting, Paul K.; Griffiths, Kalinda; Letters, Jacinta; Sullivan, David; Stocker, Roland; Celermajer, David S.

doi:10.1016/s0891-5849(00)00201-x

Cited by 38 publications

(20 citation statements)

References 46 publications

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“…In addition to this antioxidant activity, supplemental coenzyme Q 10 has been reported to decrease integrin expression by monocytes in humans (962), suggestive of anti-inflammatory activity. There is also some recent evidence that supplemental coenzyme Q 10 may improve blood pressure (403) and endothelium-dependent vasodilation in type 2 diabetics (1022), although similar beneficial effects were not observed in hyperlipidemic patients (751).…”

Section: Nonproteinaceous Antioxidantsmentioning

confidence: 99%

Role of Oxidative Modifications in Atherosclerosis

Stocker¹,

Keaney²

2004

Physiological Reviews

2,240

1,756

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This review focuses on the role of oxidative processes in atherosclerosis and its resultant cardiovascular events. There is now a consensus that atherosclerosis represents a state of heightened oxidative stress characterized by lipid and protein oxidation in the vascular wall. The oxidative modification hypothesis of atherosclerosis predicts that low-density lipoprotein (LDL) oxidation is an early event in atherosclerosis and that oxidized LDL contributes to atherogenesis. In support of this hypothesis, oxidized LDL can support foam cell formation in vitro, the lipid in human lesions is substantially oxidized, there is evidence for the presence of oxidized LDL in vivo, oxidized LDL has a number of potentially proatherogenic activities, and several structurally unrelated antioxidants inhibit atherosclerosis in animals. An emerging consensus also underscores the importance in vascular disease of oxidative events in addition to LDL oxidation. These include the production of reactive oxygen and nitrogen species by vascular cells, as well as oxidative modifications contributing to important clinical manifestations of coronary artery disease such as endothelial dysfunction and plaque disruption. Despite these abundant data however, fundamental problems remain with implicating oxidative modification as a (requisite) pathophysiologically important cause for atherosclerosis. These include the poor performance of antioxidant strategies in limiting either atherosclerosis or cardiovascular events from atherosclerosis, and observations in animals that suggest dissociation between atherosclerosis and lipoprotein oxidation. Indeed, it remains to be established that oxidative events are a cause rather than an injurious response to atherogenesis. In this context, inflammation needs to be considered as a primary process of atherosclerosis, and oxidative stress as a secondary event. To address this issue, we have proposed an “oxidative response to inflammation” model as a means of reconciling the response-to-injury and oxidative modification hypotheses of atherosclerosis.

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Section: Nonproteinaceous Antioxidantsmentioning

confidence: 99%

Role of Oxidative Modifications in Atherosclerosis

Stocker¹,

Keaney²

2004

Physiological Reviews

2,240

1,756

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“…The results of controlled intervention studies that have assessed the effects of CoQ on glycaemic control in diabetic subjects are inconsistent (Singh et al, 1999;Eriksson et al, 1999;Henriksen et al, 1999), and further studies are needed. Supplementation with CoQ can result in the inhibition of LDL oxidisability ex vivo (Raitakari et al, 2000), but there is little evidence for an effect of CoQ to inhibit oxidative damage in vivo.…”

Section: Introductionmentioning

confidence: 99%

Coenzyme Q10 improves blood pressure and glycaemic control: a controlled trial in subjects with type 2 diabetes

et al. 2002

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Objective: Our objective was to assess effects of dietary supplementation with coenzyme Q 10 (CoQ) on blood pressure and glycaemic control in subjects with type 2 diabetes, and to consider oxidative stress as a potential mechanism for any effects. Subjects and design: Seventy-four subjects with uncomplicated type 2 diabetes and dyslipidaemia were involved in a randomised double blind placebo-controlled 2Â2 factorial intervention. Setting: The study was performed at the University of Western Australia, Department of Medicine at Royal Perth Hospital, Australia. Interventions: Subjects were randomly assigned to receive an oral dose of 100 mg CoQ twice daily (200 mg=day), 200 mg fenofibrate each morning, both or neither for 12 weeks. Main outcome measures: We report an analysis and discussion of the effects of CoQ on blood pressure, on long-term glycaemic control measured by glycated haemoglobin (HbA 1c ), and on oxidative stress assessed by measurement of plasma F 2 -isoprostanes. Results: Fenofibrate did not alter blood pressure, HbA 1c , or plasma F 2 -isoprostanes. There was a 3-fold increase in plasma CoQ concentration (3.4 AE 0.3 mmol=l, P < 0.001) as a result of CoQ supplementation. The main effect of CoQ was to significantly decrease systolic ( 7 6.1 AE 2.6 mmHg, P ¼ 0.021) and diastolic ( 7 2.9 AE 1.4 mmHg, P ¼ 0.048) blood pressure and HbA 1c ( 7 0.37 AE 0.17%, P ¼ 0.032). Plasma F 2 -isoprostane concentrations were not altered by CoQ (0.14 AE 0.15 nmol=l, P ¼ 0.345). Conclusions: These results show that CoQ supplementation may improve blood pressure and long-term glycaemic control in subjects with type 2 diabetes, but these improvements were not associated with reduced oxidative stress, as assessed by F 2 -isoprostanes.

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“…Clinically, the antioxidant properties of CoQ10 can decrease the oxidation of low-density lipoprotein (LDL) and/or improve arterial endothelial function (Raitakari et al, 2000). It is well known that the ROS induced by UVA radiation often attack lipids and protein molecules in plasma and mitochondrial membranes, especially of unsaturated fatty acids.…”

Section: Discussionmentioning

confidence: 99%