Effects of Coenzyme Q10 Supplementation on Biomarkers of Oxidative Stress in Adults: A GRADE-Assessed Systematic Review and Updated Meta-Analysis of Randomized Controlled Trials

Abstract

Evidence shows that exogenous CoQ10 supplementation may potentially attenuate oxidative stress status. However, its effective dose and evidence certainty require further evaluation in the general population via more updated randomized controlled trials (RCTs). Databases (PubMed, Embase and Cochrane Library) were searched up to 30 March 2022. Evidence certainty was assessed using the Grading of Recommendations, Assessment, Development and Evaluation (GRADE) approach. Thirty-four RCTs containing 2012 participants were included in this review. Pooled effects of significant increase in total antioxidant capacity (TAC) (standardized mean difference: 1.83, 95%CI: [1.07, 2.59], p < 0.001) and significant reduction in malondialdehyde (MDA) concentrations (−0.77, [−1.06, −0.47], p < 0.001) were shown after CoQ10 supplementation compared to placebo. However, we could not determine that there was a significant increase in circulating superoxide dismutase (SOD) levels yet (0.47, [0.00, 0.94], p = 0.05). Subgroup analyses implied that CoQ10 supplementation was more beneficial to people with coronary artery disease or type 2 diabetes. Additionally, taking 100–150 mg/day CoQ10 supplement had better benefits for the levels of TAC, MDA and SOD (all p < 0.01). These results to a statistically significant extent lent support to the efficacy and optimal dose of CoQ10 supplementation on attenuating oxidative stress status in adults.

Calcium voltage-gated channel subunit alpha 1 C and glial fibrillary acidic protein signaling pathways as a selective biomarker in predicting the efficacy of liposomal loaded co-enzyme Q in the autistic rat model

“…From an indirect perspective, Co-Q10 can regenerate tocopherol, the reduced form of vitamin E's active substance, by converting the product of the reaction between vitamin E and lipid peroxidative free radicals. Furthermore, Co-Q10 could eliminate the effects of oxidative stress on the gene aspect by stimulating nuclear factor erythroid 2-related factor 2 (Nrf-2), a transcription factor that regulates cellular responses to oxidative stress by regulating a number of ROS-detoxifying enzymes [31] .…”

Efficacy of Gaseous Ozone Therapy as an adjuvant to Periodontal Treatment on Oxidative Stress Mediators in Patients with Type 2 Diabetes: A Randomized Clinical Trial

“…The effects of long-term exposure to increased levels of pro-oxidant factors exacerbate the outcomes, by triggering a negative chain reaction which affects processes involving the maintenance of homeostasis, as well as a wide variety of cellular functions (mitochondrial dynamics and function, structural modi cation of cellular proteins and the alteration of their functions, nuclear and mitochondrial DNA dysfunction, lipids, and proteins damage) [40]. Mounting evidence has signalled oxidative stress as a core pathophysiology in the development of complications of Diabetes [31]. However, the exact mechanism remains elusive and is not yet entirely clear.…”

“…However, the exact mechanism remains elusive and is not yet entirely clear. The number of experimental studies on the molecular and physiological basis of periodontitis interactions with diabetes has grown considerably in recent years [31][32][33]. Periodontitis also re ects unsuccessful redox homeostasis through indirect mechanisms which impact the intrinsic antioxidant defence system capacity.…”

“…Serum concentrations of glutathione (GSH), and malondialdehyde (MDA) were measured by employing a Sciex API 3000 triple quadrupole mass spectrometer as described previously. Malondialdehyde (MDA) is the most abundant aldehyde produced by the degradation of lipid peroxides [31], and it has been implicated in several oxidative stress-induced in ammatory diseases, including periodontitis. The concentration of MDA was calculated using an extinction coe cient of MDA-TBA complex, which is 1.56 × 105 M − 1 cm − 1 and the results were expressed as nmol MDA/mg protein.…”

“…Oxidative stress plays a pivotal role in the development of diabetes complications by causing excess mitochondrial hydrogen peroxide emission in skeletal muscle, altering redox status, and promoting insulin resistance [23][24][25]28]. Disruption of appropriate physiological function and debilitation of the antioxidant defence system can advance the evolution of diabetes by an elevation in the frequency of oxidative damage to erythrocytes [29][30][31]. Supraphysiological production of reactive oxygen and nitrogen species (ROS/NOS) and the ineffective antioxidant defence modify the structural and mechanical properties of erythrocytes, which result in changes in mechanical properties, elevate susceptibility to the mechanic and osmotic shock, and damaging of N-terminal of band-3 proteins (B3p) by modifying the anion exchange process, and glycophorin, resulting in decline in the cell's surface area [32].…”