PMID: 

Environ Health Perspect. 2009 Mar ;117(3):316-24. Epub 2008 Sep 26. PMID: 19337502

Abstract Title: 

The controversy about a possible relationship between mobile phone use and cancer.

Abstract: 

OBJECTIVE: During the last decade, mobile phone use increased to almost 100% prevalence in many countries of the world. Evidence for potential health hazards accumulated in parallel by epidemiologic investigations has raised controversies about the appropriate interpretation and the degree of bias and confounding responsible for reduced or increased risk estimates.DATA SOURCES: Overall, I identified 33 epidemiologic studies in the peer-reviewed literature, most of which (25) were about brain tumors. Two groups have collected data for>or=10 years of mobile phone use: Hardell and colleagues from Sweden and the Interphone group, an international consortium from 13 countries coordinated by the International Agency for Research on Cancer.DATA SYNTHESIS: Combined odds ratios (95% confidence intervals) from these studies for glioma, acoustic neuroma, and meningioma were 1.5 (1.2-1.8); 1.3 (0.95-1.9); and 1.1 (0.8-1.4), respectively.CONCLUSIONS: Methodologic considerations revealed that three important conditions for epidemiologic studies to detect an increased risk are not met: a ) no evidence-based exposure metric is available; b) the observed duration of mobile phone use is generally still too low; c) no evidence-based selection of end points among the grossly different types of neoplasias is possible because of lack of etiologic hypotheses. Concerning risk estimates, selection bias, misclassification bias, and effects of the disease on mobile phone use could have reduced estimates, and recall bias may have led to spuriously increased risks. The overall evidence speaks in favor of an increased risk, but its magnitude cannot be assessed at present because of insufficient information on long-term use.

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PMID: 

Cardiovasc Toxicol. 2019 Apr 24. Epub 2019 Apr 24. PMID: 31020509

Abstract Title: 

Coenzyme Q10 Alleviates Chronic Nucleoside Reverse Transcriptase Inhibitor-Induced Premature Endothelial Senescence.

Abstract: 

Human immunodeficiency virus (HIV)-infected patients undergoing antiretroviral therapy are afforded an increased lifespan but also exhibit an elevated incidence of cardiovascular disease. HIV therapy uses a combination drug approach, and nucleoside reverse transcriptase inhibitors (NRTI) are a backbone of this therapy. Endothelial dysfunction is an initiating event in cardiovascular disease etiology, and in our prior studies, NRTIs induced an endothelial dysfunction that was dependent upon mitochondrial oxidative stress. Moreover, short-term NRTI administration induced a mitophagy-associated endothelial toxicity and increased reactive oxygen species (ROS) production that was rescued by coenzyme Q10 (Q10) or overexpression of a mitochondrial antioxidant enzyme. Thus, our objective was to examine mitochondrial toxicity in endothelial cells after chronic NRTI treatment and evaluate Q10 as a potential adjunct therapy for preventing NRTI-induced mitochondrial toxicity. Human aortic endothelial cells (HAEC) were exposed to chronic NRTI treatment, with or without Q10. ROS production, cell proliferation rate, levels of senescence, and mitochondrial bioenergetic function were determined. Chronic NRTI increased ROS production but decreased population doubling. In addition, NRTI increased the accumulation ofβ-galactosidase, indicative of an accelerated rate of senescence. Moreover, ATP-linked respiration was diminished. Co-treatment with Q10 delayed the onset of NRTI-induced senescence, decreased ROS production and rescued the cells' mitochondrial respiration rate. Thus, our findings may suggest antioxidant enrichment approaches for reducing the cardiovascular side effects of NRTI therapy.

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PMID: 

Molecules. 2019 May 2 ;24(9). Epub 2019 May 2. PMID: 31052590

Abstract Title: 

Aspalathin-Rich Green Rooibos Extract Lowers LDL-Cholesterol and Oxidative Status in High-Fat Diet-Induced Diabetic Vervet Monkeys.

Abstract: 

Type 2 diabetic patients possess a two to four fold-increased risk for Cardiovascular Diseases (CVD). Hyperglycemia, oxidative stress associated with endothelial dysfunction and dyslipidemia are regarded as pro-atherogenic mechanisms of CVD. In this study, high-fat diet-induced diabetic and non-diabetic vervet monkeys were treated with 90 mg/kg of aspalathin-rich green rooibos extract (Afriplex GRT) for 28 days, followed by a 1-month wash-out period. Supplementation showed improvements in both the intravenous glucose tolerance test (IVGTT) glycemic area under curve (AUC) and total cholesterol (due to a decrease of the low-density lipoprotein [LDL]) values in diabetics, while non-diabetic monkeys benefited from an increase in high-density lipoprotein (HDL) levels. No variation of plasma coenzyme Q10 (CoQ) were found, suggesting that the LDL-lowering effect of Afriplex GRT could be related to its ability to modulate the mevalonate pathway differently from statins. Concerning the plasma oxidative status, a decrease in percentage of oxidized CoQand circulating oxidized LDL (ox-LDL) levels after supplementation was observed in diabetics. Finally, the direct correlation between the amount of oxidized LDL and total LDL concentration, and the inverse correlation between ox-LDL and plasma CoQlevels, detected in the diabetic monkeys highlighted the potential cardiovascular protective role of green rooibos extract. Taken together, these findings suggest that Afriplex GRT could counteract hyperglycemia, oxidative stress and dyslipidemia, thereby lowering fundamental cardiovascular risk factors associated with diabetes.

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PMID: 

Expert Rev Clin Pharmacol. 2019 Apr 27:1-10. Epub 2019 Apr 27. PMID: 31030614

Abstract Title: 

Evidence and mechanisms for statin-induced cognitive decline.

Abstract: 

Statin drugs have become the most highly prescribed drugs for cardiovascular disease. However, there is disagreement as to the existence of adverse effects of statin administration on cognitive function. Therefore, it is important to better understand the effects of statins on cognition and possible mechanisms of these effects. Areas covered: We analyzed relevant studies of the relationship between cognitive performance and statin and usage. We included articles published between 2018 and 1992. We identified three randomized trials, one observational study and 66 case reports that provided credible evidence of statin-induced cognitive impairment. We also identified seven randomized trials and two observational studies reporting no significant evidence of statin-induced cognitive impairment. Expert opinion: We found methodological differences that may have contributed to the divergence of these results. Evaluation of all these studies indicated that statin-associated cognitive decline is a real entity. Likely mechanisms to explain the adverse effects include 1. Reduction of synthesis of coenzyme Qwith consequent increasing oxidative stress and reduction of cerebral energy production; 2. Depletion of central nervous system myelin by inhibition of cholesterol synthesis. We conclude that statin-induced cognitive decline does exist, needs to be better recognized and requires more studies of prevention and treatment.

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PMID: 

Vopr Pitan. 2019;88(2):40-49. Epub 2019 Mar 13. PMID: 31233687

Abstract Title: 

[Immunomodulating effects of using L-carnitine and coenzyme Qin the nutrition of junior athletes].

Abstract: 

Nowdays, much attention is paid to the study of disorders of immune regulation and methods of effective immune correction in athletes. In this regard, the use of specialized sport foods (SSF), containing nutrients with immunomodulatory properties, is of particular relevance in youth sports.of the work is to study the immunomodulating activity of L-carnitine and coenzyme Qin junior athletes during the training period.. The object of the study were 30 junior athletes (masters of sports and candidates for masters of sports in swimming) aged 14-18 years, including 9 girls and 21 boys. Athletes were divided into 3 groups of 10 people each. Athletes of the 1st and 2nd main groups received L-carnitine (600 mg per day) and coenzyme Q(60 mg/day), respectively, for 4 weeks in addition to the basic diet. The dosage of SSF used in the study was 200% of the adequate level of consumption and did not exceed the upper permissible level of consumption. Athletes of the 3rd group (control) received only basic diet without sports' nutrition. Examination of athletes of all groups was performed at the beginning and after 4 weeks of the observation period.. As a result of a comprehensive survey of junior athletes, the positive effect of L-carnitine intake on erythrocyte hemoglobin content (30.2±0.4 vs 28.3±0.3 pg at the beginning) was observed. The relative content of basophilic leukocytes in athletes of the main groups statistically significantly decreased by the end of the observation period: in the L-carnitine group, from 0.64±0.05 to 0.45±0.04%, in the coenzyme Qgroup, from 0.66±0.07 to 0.50±0.04%, which indicated an increase in the body's resistance to allergic reactions.. The biomarkers of the immunotropic effect of L-carnitine and coenzyme Qare a decrease in the expression of the apoptotic marker CD95/Fas on peripheral blood lymphocytes and suppression of the production of pro-inflammatory cytokines synthesized by Th1-lymphocytes with switching the response to humoral immunity. An evidence base for the effectiveness of the use of L-carnitine and coenzyme Qin sports nutrition for restoring immune dysfunction and adaptive potential of junior athletes has been provided.

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PMID: 

Nutr Neurosci. 2019 Jun 26:1-10. Epub 2019 Jun 26. PMID: 31241007

Abstract Title: 

The synergistic effects of nano-curcumin and coenzyme Q10 supplementation in migraine prophylaxis: a randomized, placebo-controlled, double-blind trial.

Abstract: 

Migraine is a disabling neurovascular disorder characterized by increasing levels of pro-inflammatory cytokines and oxidative stress biomarkers. Curcumin and coenzyme Q10 (CoQ10) can exert neuroprotective effects through modulation of inflammation and oxidative stress. The aim of the present study was to evaluate the combined effects of nano-curcumin and CoQ10 supplementation on migraine symptoms and quality of life in migraine patients.One-hundred men and women (mean age 32 years) with episodic migraine based on the International Headache Society (IHS) criteria participated in this study. The subjects were randomly divided into four groups as (1) combination of nano-curcumin (80 mg) plus CoQ10 (300 mg), (2) nano-curcumin (80 mg), (3) CoQ10 (300 mg) and (4) the control (nano-curcumin and CoQ10 placebo included oral paraffin oil) beside usual prophylactic drugs for 8 weeks. Frequency, severity, duration of headache attacks, the headache diary results (HDR) and headache disability based on migraine-specific questionnaires were assessed at the baseline and end of the study.Ninety-one of 100 patients completed the study. The results showed a significant effect of nano-curcumin and CoQ10 supplementation on frequency, severity, duration of migraine attacks and HDR compared to other groups (All 

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PMID: 

Arch Med Res. 2019 Feb ;50(2):1-10. Epub 2019 May 21. PMID: 31349945

Abstract Title: 

Independent and Additive Effects of Coenzyme Q10 and Vitamin E on Cardiometabolic Outcomes and Visceral Adiposity in Women With Polycystic Ovary Syndrome.

Abstract: 

BACKGROUND: Polycystic ovary syndrome (PCOS) is the most common endocrine disorder in reproductive age women.OBJECTIVE: This study was conducted to investigate the effects of CoQ10 and/or vitamin E on cardiometabolic outcomes in patients with PCOS.METHODS: This randomized clinical trial was carried out among 86 women with PCOS. Patients were assigned to take CoQ10, vitamin E, CoQ10 plus vitamin E or placebo for 8 weeks. Fasting blood samples were obtained at the beginning and end of the study.RESULTS: A significant decrease in serum triglycerides (TG) (p 

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PMID: 

Int J Environ Res Public Health. 2019 Aug 13 ;16(16). Epub 2019 Aug 13. PMID: 31412628

Abstract Title: 

The Neuroprotective Role of Coenzyme Q10 Against Lead Acetate-Induced Neurotoxicity Is Mediated by Antioxidant, Anti-Inflammatory and Anti-Apoptotic Activities.

Abstract: 

Heavy metal exposure, in lead (Pb) particularly, is associated with severe neuronal impairment though oxidative stress mediated by reactive oxygen species, and antioxidants may be used to abolish these adverse effects. This study investigated the potential neuroprotective role of coenzyme Q10 (CoQ) against lead acetate (PbAc)-induced neurotoxicity. Twenty-eight male Wistar albino rats were divided into four equal groups (= 7) and treated as follows: the control group was injected with physiological saline (0.9% NaCl); the CoQgroup was injected with CoQ(10 mg/kg); PbAc group was injected with PbAc (20 mg/kg); PbAc + CoQgroup was injected first with PbAc, and after 1 h with CoQ. All groups were injected intraperitoneally for seven days. PbAc significantly increased cortical lipid peroxidation, nitrate/nitrite levels, and inducible nitric oxide synthase expression, and decreased glutathione content, superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase activity and mRNA expression, as well as nuclear factor erythroid 2-related factor 2 (Nrf2) and homoxygenase-1 (HO-1) expression. PbAc also promoted the secretion of interleukin-1ß and tumor necrosis factor-α, inhibited interleukin-10 production, triggered the activation of pro-apoptotic proteins, and suppressed anti-apoptotic proteins. Additionally, PbAc increased the cortical levels of serotonin, dopamine, norepinephrine, GABA, and glutamate, and decreased the level of ATP. However, treatment with CoQrescued cortical neurons from PbAc-induced neurotoxicity by restoring the balance between oxidants and antioxidants, activating the Nrf2/HO-1 pathway, suppressing inflammation, inhibiting the apoptotic cascade, and modulating cortical neurotransmission and energy metabolism. Altogether, our findings indicate that CoQhas beneficial effects against PbAc-induced neuronal damage through its antioxidant, anti-inflammatory, anti-apoptotic, and neuromodulatory activities.

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PMID: 

Hypertens Pregnancy. 2019 Jul 31:1-6. Epub 2019 Jul 31. PMID: 31366258

Abstract Title: 

CoQ10 alleviate preeclampsia symptoms by enhancing the function of mitochondria in the placenta of pregnant rats with preeclampsia.

Abstract: 

: To assess whether supplementation with Coenzyme Q10 (CoQ10) during pregnancy alleviate preeclampsia symptoms and the underlying mechanism in the rats with preeclampsia.: Forty-five pregnant Wistar rats were equally divided into three groups randomly and received subcutaneous saline injection (control group,= 15) or 200 mg/kg L-NAME injection to induce preeclampsia symptoms (PE group,= 30). The PE rats were treated by distilled water (PE+DW group,= 15) and CoQ10 (PE+CoQ10 group,= 15) on day 15 to 21 of gestation randomly. Physiological characteristics such as urine volume, total urine protein, blood pressure, number and weight of pups were recorded. Fluorescent dye was used to detect mitochondrial membrane potential in placenta. Real-time fluorescent quantitative PCR was used to detect the expression of mitochondrial DNA(mtDNA) in placenta.: There was no statistic difference among all the three groups on day 10 of gestation in SBP and 24-h proteinuria (>0.05). Whereas, SBP and 24-h proteinuria were significantly higher in PE group than control group on day 15 and 21 of gestation (

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PMID: 

Free Radic Res. 2019 Aug 7:1-9. Epub 2019 Aug 7. PMID: 31387429

Abstract Title: 

Coenzyme Q10 supplementation alleviates pain in pregabalin-treated fibromyalgia patientsreducing brain activity and mitochondrial dysfunction.

Abstract: 

Although coenzyme Q10 (CoQ10) supplementation has shown to reduce pain levels in chronic pain, the effects of CoQ10 supplementation on pain, anxiety, brain activity, mitochondrial oxidative stress, antioxidants, and inflammation in pregabalin-treated fibromyalgia (FM) patients have not clearly elucidated. We hypothesised that CoQ10 supplementation reduced pain better than pregabalin alonereducing brain activity, mitochondrial oxidative stress, inflammation, and increasing antioxidant levels in pregabalin-treated FM patients. A double-blind randomised placebo-controlled trial was conducted. Eleven FM patients were enrolled with 2 weeks wash-out then randomly allocated to 2 treatment groups; pregabalin with CoQ10 or pregabalin with placebo for 40 d. Then, patients in CoQ10 group were switched to placebo, and patients in placebo group were switched to CoQ10 for another 40 d. Pain pressure threshold (PPT), FM questionnaire,anxiety, and pain score were examined. Peripheral blood mononuclear cells (PBMCs) were isolated to investigate mitochondrial oxidative stress and inflammation at day 0, 40, and 80. The level of antioxidants and brain positron emission tomography (PET) scan were also determined at these time points.Pregabalin alone reduced pain and anxietydecreasing brain activity compared with their baseline. However, it did not affect mitochondrial oxidative stress and inflammation. Supplementation with CoQ10 effectively reduced greater pain, anxiety and brain activity, mitochondrial oxidative stress, and inflammation. CoQ10 also increased a reduced glutathione levels and superoxide dismutase (SOD) levels in FM patients. These findings provide new evidence that CoQ10 supplementation provides further benefit for relieving pain sensation in pregabalin-treated FM patients, possiblyimproving mitochondrial function, reducing inflammation, and decreasing brain activity.

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