scholarly journals The Paradox of Coenzyme Q10 in Aging

Nutrients ◽  
2019 ◽  
Vol 11 (9) ◽  
pp. 2221 ◽  
Author(s):  
Díaz-Casado ◽  
Quiles ◽  
Barriocanal-Casado ◽  
González-García ◽  
Battino ◽  
...  

Coenzyme Q (CoQ) is an essential endogenously synthesized molecule that links different metabolic pathways to mitochondrial energy production thanks to its location in the mitochondrial inner membrane and its redox capacity, which also provide it with the capability to work as an antioxidant. Although defects in CoQ biosynthesis in human and mouse models cause CoQ deficiency syndrome, some animals models with particular defects in the CoQ biosynthetic pathway have shown an increase in life span, a fact that has been attributed to the concept of mitohormesis. Paradoxically, CoQ levels decline in some tissues in human and rodents during aging and coenzyme Q10 (CoQ10) supplementation has shown benefits as an anti-aging agent, especially under certain conditions associated with increased oxidative stress. Also, CoQ10 has shown therapeutic benefits in aging-related disorders, particularly in cardiovascular and metabolic diseases. Thus, we discuss the paradox of health benefits due to a defect in the CoQ biosynthetic pathway or exogenous supplementation of CoQ10.

2018 ◽  
Vol 24 (23) ◽  
pp. 2729-2742 ◽  
Author(s):  
Nasrin Sharifi ◽  
Reza Tabrizi ◽  
Mahmood Moosazadeh ◽  
Naghmeh Mirhosseini ◽  
Kamran B. Lankarani ◽  
...  

Background and objective: Oxidative stress and inflammation are key parameters in developing metabolic disorders. Hence, antioxidant intake might be an appropriate approach. Several studies have evaluated the effect of coenzyme Q10 (CoQ10) supplementation on lipid profile among patients with metabolic diseases, though findings are controversial. The aim of this systematic review and meta-analysis was to determine the effects of CoQ10 supplementation on lipid profile in patients with metabolic disorders. Methods: We searched PubMed, EMBASE, Web of Science and Cochrane Library databases until July 2017. Prospective clinical trials were selected assessing the effect of CoQ10 supplementation on different biomarkers. Two reviewers independently assessed the eligibility of studies, extracted data, and evaluated the risk of bias of included studies. A fixed- or random-effects model was used to pool the data, which expressed as a standardized mean difference with 95% confidence interval. Heterogeneity was measured using a Q-test and with I2 statistics. Results: A total of twenty-one controlled trials (514 patients and 525 controls) were included. The meta-analysis indicated a significant reduction in serum triglycerides levels (SMD -0.28; 95% CI, -0.56, -0.005). CoQ10 supplementation also decreased total-cholesterol (SMD -0.07; 95% CI, -0.45, 0.31), increased LDL- (SMD 0.04; 95% CI, -0.27, 0.36), and HDL-cholesterol levels (SMD 0.10; 95% CI, -0.32, 0.51), not statistically significant. Conclusion: CoQ10 supplementation may significantly reduce serum triglycerides levels, and help to improve lipid profiles in patients with metabolic disorders. Additional prospective studies are recommended using higher supplementation doses and longer intervention period.


Antioxidants ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 1785
Author(s):  
Juan Diego Hernández-Camacho ◽  
Laura García-Corzo ◽  
Daniel José Moreno Fernández-Ayala ◽  
Plácido Navas ◽  
Guillermo López-Lluch

Coenzyme Q is a unique lipidic molecule highly conserved in evolution and essential to maintaining aerobic metabolism. It is endogenously synthesized in all cells by a very complex pathway involving a group of nuclear genes that share high homology among species. This pathway is tightly regulated at transcription and translation, but also by environment and energy requirements. Here, we review how coenzyme Q reacts within mitochondria to promote ATP synthesis and also integrates a plethora of metabolic pathways and regulates mitochondrial oxidative stress. Coenzyme Q is also located in all cellular membranes and plasma lipoproteins in which it exerts antioxidant function, and its reaction with different extramitochondrial oxidoreductases contributes to regulate the cellular redox homeostasis and cytosolic oxidative stress, providing a key factor in controlling various apoptosis mechanisms. Coenzyme Q levels can be decreased in humans by defects in the biosynthesis pathway or by mitochondrial or cytosolic dysfunctions, leading to a highly heterogeneous group of mitochondrial diseases included in the coenzyme Q deficiency syndrome. We also review the importance of coenzyme Q levels and its reactions involved in aging and age-associated metabolic disorders, and how the strategy of its supplementation has had benefits for combating these diseases and for physical performance in aging.


Antioxidants ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 759
Author(s):  
David Mantle ◽  
Robert A. Heaton ◽  
Iain P. Hargreaves

Coenzyme Q10 (CoQ10) has a number of important roles in the cell that are required for optimal functioning of the immune system. These include its essential role as an electron carrier in the mitochondrial respiratory chain, enabling the process of oxidative phosphorylation to occur with the concomitant production of ATP, together with its role as a potential lipid-soluble antioxidant, protecting the cell against free radical-induced oxidation. Furthermore, CoQ10 has also been reported to have an anti-inflammatory role via its ability to repress inflammatory gene expression. Recently, CoQ10 has also been reported to play an important function within the lysosome, an organelle central to the immune response. In view of the differing roles CoQ10 plays in the immune system, together with the reported ability of CoQ10 supplementation to improve the functioning of this system, the aim of this article is to review the current literature available on both the role of CoQ10 in human immune function and the effect of CoQ10 supplementation on this system.


BMJ Open ◽  
2021 ◽  
Vol 11 (1) ◽  
pp. e039358
Author(s):  
Suhairul Sazali ◽  
Salziyan Badrin ◽  
Mohd Noor Norhayati ◽  
Nur Suhaila Idris

ObjectiveTo determine the effects of coenzyme Q10 (CoQ10) for reduction in the severity, frequency of migraine attacks and duration of headache in adult patients with migraine.DesignSystematic review and meta-analysis.Data sourcesCochrane Central Register of Controlled Trials, CENTRAL, MEDLINE, EMBASE, Cumulative Index to Nursing and Allied Health Literature (CINAHL) and Psychological Information Database (PsycINFO) from inception till December 2019.Study selectionAll randomised control trials comparing CoQ10 with placebo or used as an adjunct treatment included in this meta-analysis. Cross-over designs and controlled clinical trials were excluded.Data synthesisHeterogeneity at face value by comparing populations, settings, interventions and outcomes were measured and statistical heterogeneity was assessed by means of the I2 statistic. The treatment effect for dichotomous outcomes were using risk ratios and risk difference, and for continuous outcomes, mean differences (MDs) or standardised mean difference; both with 95% CIs were used. Subgroup analyses were carried out for dosage of CoQ10 and if CoQ10 combined with another supplementation. Sensitivity analysis was used to investigate the impact risk of bias for sequence generation and allocation concealment of included studies.ResultsSix studies with a total of 371 participants were included in the meta-analysis. There is no statistically significant reduction in severity of migraine headache with CoQ10 supplementation. CoQ10 supplementation reduced the duration of headache attacks compared with the control group (MD: −0.19; 95% CI: −0.27 to −0.11; random effects; I2 statistic=0%; p<0.00001). CoQ10 usage reduced the frequency of migraine headache compared with the control group (MD: −1.52; 95% CI: −2.40 to −0.65; random effects; I2 statistic=0%; p<0.001).ConclusionCoQ10 appears to have beneficial effects in reducing duration and frequency of migraine attack.PROSPERO registration numberCRD42019126127.


Cells ◽  
2022 ◽  
Vol 11 (1) ◽  
pp. 141
Author(s):  
Anne-Sophie Archambault ◽  
Julyanne Brassard ◽  
Émilie Bernatchez ◽  
Cyril Martin ◽  
Vincenzo Di Marzo ◽  
...  

High eosinophil (EOS) counts are a key feature of eosinophilic asthma. EOS notably affect asthmatic response by generating several lipid mediators. Mice have been utilized in hopes of defining new pharmacological targets to treat asthma. However, many pinpointed targets in mice did not translate into clinics, underscoring that key differences exist between the two species. In this study, we compared the ability of human (h) and mouse (m) EOS to biosynthesize key bioactive lipids derived from arachidonic acid (AA), eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). hEOS were isolated from the blood of healthy subjects and mild asthmatics, while mEOSs were differentiated from the bone marrow. EOSs were treated with fatty acids and lipid mediator biosynthesis assessed by LC-MS/MS. We found that hEOS biosynthesized leukotriene (LT) C4 and LTB4 in a 5:1 ratio while mEOS almost exclusively biosynthesized LTB4. The biosynthesis of the 15-lipoxygenase (LO) metabolites 15-HETE and 12-HETE also differed, with a 15-HETE:12-HETE ratio of 6.3 for hEOS and 0.727 for mEOS. EOS biosynthesized some specialized pro-resolving mediators, and the levels from mEOS were 9-times higher than those of hEOS. In contrast, hEOS produced important amounts of the endocannabinoid 2-arachidonoyl-glycerol (2-AG) and its congeners from EPA and DHA, a biosynthetic pathway that was up to ~100-fold less prominent in mEOS. Our data show that hEOS and mEOS biosynthesize the same lipid mediators but in different amounts. Compared to asthmatics, mouse models likely have an amplified involvement of LTB4 and specialized pro-resolving mediators and a diminished impact of the endocannabinoid 2-arachidonoyl-glycerol and its congeners.


2018 ◽  
Vol 14 (3) ◽  
pp. 164-174 ◽  
Author(s):  
Vladlena I. Zozina ◽  
Serghei Covantev ◽  
Olga A. Goroshko ◽  
Liudmila M. Krasnykh ◽  
Vladimir G. Kukes

2020 ◽  
Vol 2020 ◽  
pp. 1-12 ◽  
Author(s):  
Manal El-khadragy ◽  
Wafa A. Al-Megrin ◽  
Norah A. AlSadhan ◽  
Dina M. Metwally ◽  
Rehab E. El-Hennamy ◽  
...  

Exposure to lead (Pb) causes multiorgan dysfunction including reproductive impairments. Here, we examined the protective effects of coenzyme Q10 (CoQ10) administration on testicular injury induced by lead acetate (PbAc) exposure in rats. This study employed four experimental groups (n=7) that underwent seven days of treatment as follows: control group intraperitoneally (i.p.) treated with 0.1 ml of 0.9% NaCl containing 1% Tween 80 (v:v), CoQ10 group that was i.p. injected with 10 mg/kg CoQ10, PbAc group that was i.p. treated with PbAc (20 mg/kg), and PbAc+CoQ10 group that was i.p. injected with CoQ10 2 h after PbAc. PbAc injection resulted in increasing residual Pb levels in the testis and reducing testosterone, luteinizing hormone, and follicle-stimulating hormone levels. Additionally, PbAc exposure resulted in significant oxidative damage to the tissues on the testes. PbAc raised the levels of prooxidants (malondialdehyde and nitric oxide) and reduced the amount of endogenous antioxidative proteins (glutathione and its derivative enzymes, catalase, and superoxide dismutase) available in the cell. Moreover, PbAc induced the inflammatory response as evidenced by the upregulation of inflammatory mediators (tumor necrosis factor-alpha and interleukin-1 beta). Further, PbAc treatment induced apoptosis in the testicular cells, as indicated by an increase in Bax and caspase 3 expression, and reduced Bcl2 expression. CoQ10 supplementation improved testicular function by inhibiting Pb accumulation, oxidative stress, inflammation, cell death, and histopathological changes following PbAc exposure. Our findings suggest that CoQ10 can act as a natural therapeutic agent to protect against the reproductive impairments associated with PbAc exposure.


2019 ◽  
Vol 5 (1) ◽  
Author(s):  
Minoru Ando ◽  
Yoko Ando

AbstractKidneys are affected by human immunodeficiency virus (HIV) infection and its associated therapies. Antiretroviral therapy (ART) has markedly reduced acquired immune deficiency syndrome–related deaths and opportunistic infectious diseases among HIV-infected patients. This contributed to their prolonged survival; however, the improvement in survival has been accompanied by an increase in the incidence of non-infectious chronic complications, including hypertension, metabolic diseases, and chronic kidney disease (CKD). Recent studies showed that estimated prevalence of any CKD and end-stage renal disease (ESRD) among HIV-infected patients is approximately 20% and 0.5%, respectively, in Japan. Both a rapid decrease in renal function and a high positive rate of albuminuria and proteinuria are clinical characteristics of HIV-infected patients. Moreover, considering higher complication rates of hypertension and diabetes compared with non-HIV-infected individuals of the similar aging, HIV-infected patients who develop CKD and ESRD are very likely to increase. Furthermore, as the survival rate is favorable after the initiation of dialysis, the cumulative number of ESRD patients is supposed to increase. The corporation for treatment of HIV-positive hemodialysis patients by general dialysis clinics will be urgently required; however, there still remain some preoccupations and prejudices about HIV per se in Japan, which may provoke hesitation from accepting those patients.


2014 ◽  
Vol 5 (3-4) ◽  
pp. 180-186 ◽  
Author(s):  
Floriana Licitra ◽  
Hélène Puccio

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