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Food Science & Nutrition Sep 2023Coenzyme Q10 is a potent antioxidant and is necessary for energy production in mitochondria. Clinical data have suggested that coenzyme Q10 (CoQ10) has some beneficial... (Review)
Review
Coenzyme Q10 is a potent antioxidant and is necessary for energy production in mitochondria. Clinical data have suggested that coenzyme Q10 (CoQ10) has some beneficial effects on liver function. However, these results are equivocal. This systematic review and meta-analysis aimed to clarify the effect of coenzyme Q10 supplementation on the serum concentration of liver function enzymes. We searched the online databases using relevant keywords up to April 2022. Randomized clinical trials (RCTs) investigating the effect of CoQ10, compared with a control group, on serum concentrations of liver enzymes were included. We found a significant reduction following supplementation with CoQ10 on serum concentrations of alanine aminotransferase (ALT) based on 15 effect sizes from 13 RCTs (weighted mean difference [WMD] = -5.33 IU/L; 95% CI: -10.63, -0.03; = .04), aspartate aminotransferase (AST) based on 15 effect sizes from 13 RCTs (WMD = -4.91 IU/L; 95% CI: -9.35, -0.47; = .03) and gamma-glutamyl transferase (GGT) based on eight effect sizes from six RCTs (WMD = -8.07 IU/L; 95% CI: -12.82, -3.32; = .001; = 91.6%). However, we found no significant effects of CoQ10 supplementation on alkaline phosphatase concentration (WMD = 1.10 IU/L; 95% CI: -5.98, 8.18; = .76). CoQ10 supplementation significantly improves circulating ALT, AST, and GGT levels; therefore, it might positively affect liver function. Further high-quality RCTs with more extended intervention periods and larger sample sizes are recommended to confirm our results.
PubMed: 37701221
DOI: 10.1002/fsn3.3478 -
British Medical Bulletin Jun 2019The present systematic review investigates the biological and chemical mechanisms that affect the health and structure of tendons following the use of fluoroquinolones...
INTRODUCTION
The present systematic review investigates the biological and chemical mechanisms that affect the health and structure of tendons following the use of fluoroquinolones (FQs).
SOURCES OF DATA
A total of 12 articles were included, organized, and reported following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines.
AREAS OF AGREEMENT
Five mechanisms were identified: arrest of proliferation through a decreased activity of cyclin B, CDK-1, CHK-1, and increased PK-1; decrease tenocytes migration through decreased phosphorylation of FAK; decrease type I collagen metabolism through increased MMP-2; chelate effect on ions that influence epigenetics and several enzymes; fluoroquinolones-induced ROS (radical oxygen species) production in mitochondria.
AREAS OF CONTROVERSY
There is no definite structure-damage relationship. The dose-effect relationship is unclear.
GROWING POINTS
Knowing and defining the damage exerted by FQs plays a role in clinical practice, replacing FQs with other antibacterial drugs or using antioxidants to attenuate their pathological effects.
AREAS TIMELY FOR DEVELOPING RESEARCH
Clinical and basic sciences studies for each FQs are necessary.
Topics: Anti-Bacterial Agents; Cyclin B; Dose-Response Relationship, Drug; Fluoroquinolones; Humans; Phosphorylation; Reactive Oxygen Species; Tendinopathy
PubMed: 30811525
DOI: 10.1093/bmb/ldz006 -
Journal of Translational Medicine May 2021Mitochondria are essential organelles that provide energy for cellular functions, participate in cellular signaling and growth, and facilitate cell death. Based on their... (Review)
Review
BACKGROUND
Mitochondria are essential organelles that provide energy for cellular functions, participate in cellular signaling and growth, and facilitate cell death. Based on their multifactorial roles, mitochondria are also critical in the progression of critical illnesses. Transplantation of mitochondria has been reported as a potential promising approach to treat critical illnesses, particularly ischemia reperfusion injury (IRI). However, a systematic review of the relevant literature has not been conducted to date. Here, we systematically reviewed the animal and human studies relevant to IRI to summarize the evidence for mitochondrial transplantation.
METHODS
We searched MEDLINE, the Cochrane library, and Embase and performed a systematic review of mitochondrial transplantation for IRI in both preclinical and clinical studies. We developed a search strategy using a combination of keywords and Medical Subject Heading/Emtree terms. Studies including cell-mediated transfer of mitochondria as a transfer method were excluded. Data were extracted to a tailored template, and data synthesis was descriptive because the data were not suitable for meta-analysis.
RESULTS
Overall, we identified 20 animal studies and two human studies. Among animal studies, 14 (70%) studies focused on either brain or heart IRI. Both autograft and allograft mitochondrial transplantation were used in 17 (85%) animal studies. The designs of the animal studies were heterogeneous in terms of the route of administration, timing of transplantation, and dosage used. Twelve (60%) studies were performed in a blinded manner. All animal studies reported that mitochondrial transplantation markedly mitigated IRI in the target tissues, but there was variation in biological biomarkers and pathological changes. The human studies were conducted with a single-arm, unblinded design, in which autologous mitochondrial transplantation was applied to pediatric patients who required extracorporeal membrane oxygenation (ECMO) for IRI-associated myocardial dysfunction after cardiac surgery.
CONCLUSION
The evidence gathered from our systematic review supports the potential beneficial effects of mitochondrial transplantation after IRI, but its clinical translation remains limited. Further investigations are thus required to explore the mechanisms of action and patient outcomes in critical settings after mitochondrial transplantation. Systematic review registration The study was registered at UMIN under the registration number UMIN000043347.
Topics: Animals; Cell Death; Child; Humans; Mitochondria; Reperfusion Injury
PubMed: 34001191
DOI: 10.1186/s12967-021-02878-3 -
BMC Geriatrics Aug 2022Healthy aging relies on mitochondrial functioning because this organelle provides energy and diminishes oxidative stress. Single nucleotide polymorphisms (SNPs) in...
INTRODUCTION
Healthy aging relies on mitochondrial functioning because this organelle provides energy and diminishes oxidative stress. Single nucleotide polymorphisms (SNPs) in TOMM40, a critical gene that produces the outer membrane protein TOM40 of mitochondria, have been associated with mitochondrial dysfunction and neurodegenerative processes. Yet it is not clear whether or how the mitochondria may impact human longevity. We conducted this review to ascertain which SNPs have been associated with markers of healthy aging.
METHODS
Using the PRISMA methodology, we conducted a systematic review on PubMed and Embase databases to identify associations between TOMM40 SNPs and measures of longevity and healthy aging.
RESULTS
Twenty-four articles were selected. The TOMM40 SNPs rs2075650 and rs10524523 were the two most commonly identified and studied SNPs associated with longevity. The outcomes associated with the TOMM40 SNPs were changes in BMI, brain integrity, cognitive functions, altered inflammatory network, vulnerability to vascular risk factors, and longevity.
DISCUSSIONS
Our systematic review identified multiple TOMM40 SNPs potentially associated with healthy aging. Additional research can help to understand mechanisms in aging, including resilience, prevention of disease, and adaptation to the environment.
Topics: Aging; Healthy Aging; Humans; Longevity; Membrane Transport Proteins; Mitochondrial Precursor Protein Import Complex Proteins; Polymorphism, Single Nucleotide
PubMed: 35964003
DOI: 10.1186/s12877-022-03337-4 -
Mitochondrion Jul 2021Cell-free mitochondrial DNA (cf-mtDNA) is a marker of inflammatory disease and a predictor of mortality, but little is known about cf-mtDNA in relation to psychobiology.... (Review)
Review
Cell-free mitochondrial DNA (cf-mtDNA) is a marker of inflammatory disease and a predictor of mortality, but little is known about cf-mtDNA in relation to psychobiology. A systematic review of the literature reveals that blood cf-mtDNA varies in response to common real-world stressors including psychopathology, acute psychological stress, and exercise. Moreover, cf-mtDNA is inducible within minutes and exhibits high intra-individual day-to-day variation, highlighting the dynamic regulation of cf-mtDNA levels. We discuss current knowledge on the mechanisms of cf-mtDNA release, its forms of transport ("cell-free" does not mean "membrane-free"), potential physiological functions, putative cellular and neuroendocrine triggers, and factors that may contribute to cf-mtDNA removal from the circulation. A review of in vitro, pre-clinical, and clinical studies shows conflicting results around the dogma that physiological forms of cf-mtDNA are pro-inflammatory, opening the possibility of other physiological functions, including the cell-to-cell transfer of whole mitochondria. Finally, to enhance the reproducibility and biological interpretation of human cf-mtDNA research, we propose guidelines for blood collection, cf-mtDNA isolation, quantification, and reporting standards, which can promote concerted advances by the community. Defining the mechanistic basis for cf-mtDNA signaling is an opportunity to elucidate the role of mitochondria in brain-body interactions and psychopathology.
Topics: Brain; Cell-Free Nucleic Acids; DNA, Mitochondrial; Humans; Mitochondria; Signal Transduction
PubMed: 33839318
DOI: 10.1016/j.mito.2021.04.002 -
Neurological Sciences : Official... Nov 2021Parkinson's disease (PD) is a chronic and progressive neurodegenerative disorder that affects 1% of the population worldwide. Etiology of PD is likely to be... (Review)
Review
Parkinson's disease (PD) is a chronic and progressive neurodegenerative disorder that affects 1% of the population worldwide. Etiology of PD is likely to be multi-factorial such as protein misfolding, mitochondrial dysfunction, oxidative stress, and neuroinflammation that contributes to the pathology of Parkinson's disease (PD), numerous studies have shown that mitochondrial dysfunction may play a key role in the dopaminergic neuronal loss. In multiple ways, the two most important are the activation of neuroinflammation and mitochondrial dysfunction, while mitochondrial dysfunction could cause neuroinflammation and vice versa. Thus, the mitochondrial proteins are the highly promising target for the development of PD. However, the limited amount of dopaminergic neurons prevented the detailed investigation of Parkinson's disease with regard to mitochondrial dysfunction. Both genetic and environmental factors are also associated with mitochondrial dysfunction and PD pathogenesis. The induction of PD by neurotoxins that inhibit mitochondrial complex I provide direct evidence linking mitochondrial dysfunction to PD. A decrease of mitochondrial complex I activity is observed in PD brain and in neurotoxin- or genetic factor-induced in vitro and in vivo models. Moreover, PINK1, Parkin, DJ-1 and LRRK2 mitochondrial PD gene products have important roles in mitophagy, a cellular process that clear damaged mitochondria. This review paper would discuss the evidence for the mitochondrial dysfunction and neuroinflammation in PD.
Topics: Dopaminergic Neurons; Humans; Mitochondria; Mitochondrial Proteins; Oxidative Stress; Parkinson Disease
PubMed: 34480241
DOI: 10.1007/s10072-021-05551-1 -
Frontiers in Physiology 20238-Hydroxy-2'-deoxyguanosine (8-OHdG) is a byproduct of DNA oxidation resulting from free radical attacks. Paradoxically, treatment with 8-OHdG accelerates tissue...
8-Hydroxy-2'-deoxyguanosine (8-OHdG) is a byproduct of DNA oxidation resulting from free radical attacks. Paradoxically, treatment with 8-OHdG accelerates tissue healing. The aim of this study is to quantify the 8-OHdG response after a single session of exercise in both trained and untrained adults. A systematic review and meta-analysis of exercise intervention studies measuring changes in blood 8-OHdG following resistance exercise and aerobic exercise were conducted. The literature search included Web of Science, PubMed, BASE, and Scopus, with publications up to February 2023 included. Subgroup analysis of training status was also conducted. Sixteen studies involving 431 participants met the eligibility criteria. Resistance exercise showed a medium effect on increasing circulating 8-OHdG levels (SMD = 0.66, < 0.001), which was similar for both trained and untrained participants. However, studies on aerobic exercise presented mixed results. For trained participants, a small effect of aerobic exercise on increasing circulating 8-OHdG levels was observed (SMD = 0.42; < 0.001). In contrast, for untrained participants, a large effect of decreasing circulating 8-OHdG levels was observed, mostly after long-duration aerobic exercise (SMD = -1.16; < 0.05). Similar to resistance exercise, high-intensity aerobic exercise (5-45 min, ≥75% VO) significantly increased circulating 8-OHdG levels, primarily in trained participants. Pooled results from the studies confirm an increase in circulating 8-OHdG levels after resistance exercise. However, further studies are needed to fully confirm the circulating 8-OHdG response to aerobic exercise. Increases in 8-OHdG after high-intensity aerobic exercise are observed only in trained individuals, implicating its role in training adaptation. : [https://Systematicreview.gov/], identifier [CRD42022324180].
PubMed: 38028771
DOI: 10.3389/fphys.2023.1275867 -
BJOG : An International Journal of... Aug 2022Normal mature sperm have a considerably reduced number of mitochondria, which provide the energy required for progressive sperm motility. Literature suggests that... (Meta-Analysis)
Meta-Analysis Review
BACKGROUND
Normal mature sperm have a considerably reduced number of mitochondria, which provide the energy required for progressive sperm motility. Literature suggests that disorders of sperm motility may be linked to abnormal sperm mitochondrial number and function.
OBJECTIVES
To summarise the evidence from literature regarding the association of mitochondrial DNA copy numbers and semen quality with a particular emphasis on the sperm motility.
SEARCH STRATEGY
Standard methodology recommended by Cochrane.
SELECTION CRITERIA
All published primary research reporting on the association between mitochondrial DNA copy numbers and semen quality.
DATA COLLECTION AND ANALYSIS
Using standard methodology recommended by Cochrane we pooled results using a random effects model and the findings were reported as a standardised mean difference.
MAIN RESULTS
We included ten studies. The primary outcome was sperm mitochondrial DNA copy numbers. A meta-analysis including five studies showed significantly higher mitochondrial DNA copy numbers in abnormal semen analysis compared with normal semen analysis (standardised mean difference 1.08, 95% CI 0.74-1.43). Seven studies included in the meta-analysis showed a significant negative correlation between mitochondrial DNA copy numbers and semen parameters. The quality of evidence was assessed as good to very good in 60% of studies.
CONCLUSIONS
Our review demonstrates significantly higher mitochondrial DNA in human sperm cells of men with abnormal semen analysis in comparison to men with normal semen analysis.
TWEETABLE ABSTRACT
There is significantly higher mitochondrial DNA in sperm cells of men with abnormal semen analysis in comparison to men with normal semen analysis.
Topics: DNA Copy Number Variations; DNA, Mitochondrial; Humans; Male; Mitochondria; Semen; Semen Analysis; Sperm Motility; Spermatozoa
PubMed: 34954901
DOI: 10.1111/1471-0528.17078 -
Journal of Clinical Pharmacy and... Aug 2015CoenzymeQ10 (CoQ10 ), or ubiquinone, is an endogenous enzyme cofactor produced by most human cells. It is a potent antioxidant and is necessary for energy production in... (Meta-Analysis)
Meta-Analysis Review
WHAT IS KNOWN AND OBJECTIVE
CoenzymeQ10 (CoQ10 ), or ubiquinone, is an endogenous enzyme cofactor produced by most human cells. It is a potent antioxidant and is necessary for energy production in mitochondria. Diabetes mellitus is a chronic disease with multiple metabolic abnormalities, principally resulting from the inflammation and oxidative stress associated with mitochondrial dysfunctions. Clinical trials of the effects of supplementary CoQ10 on metabolic control in diabetes have reported inconsistent results. We undertook a systematic review and meta-analysis of randomized controlled trials to assess the effects of CoQ10 supplementation on glycaemic control, lipid profile and blood pressure in patients with diabetes.
METHODS
A systematic search was conducted on MEDLINE, The Cochrane Library, CINAHL, NCCAM, Web of Science, Scopus, ClinicalTrials.gov and historical search of reference lists of relevant articles. The bibliographic databases were searched from inception to February 2015. We included randomized, placebo-controlled trials of CoQ10 in diabetes lasting at least 12 weeks. HbA1c or fasting plasma glucose had to be reported. Primary outcome was glycemic control, and secondary outcomes were lipid profile and blood pressure. Treatment effect was estimated with mean difference.
RESULTS AND DISCUSSION
Seven trials were included in the meta-analysis, involving 356 patients. Neither CoQ10 alone nor CoQ10 plus fenofibrate improved glycemic control. In addition, CoQ10, alone or in combination with fenofibrate, did not alter LDL-C, HDL-C and blood pressure. Triglycerides levels were significantly reduced with CoQ10 (mean difference -0·26 mmol/L, 95% CI -0·05 mmol/L to -0·47 mmol/L, P = 0·02) and CoQ10 plus fenofibrate (mean difference -0·72 mmol/L, 95% CI -0·32 mmol/L to -1·12 mmol/L, P = 0·0004). CoQ10 plus fenofibrate also effectively reduced total cholesterol (mean difference: -0·45 mmol/L, 95% CI -0·06 mmol/L to -0·84 mmol/L, P = 0·02).
WHAT IS NEW AND CONCLUSIONS
CoQ10 supplementation has no beneficial effects on glycemic control, lipid profile or blood pressure in patients with diabetes. However, it may reduce triglycerides levels. Due to limited data availability, well-powered and well-designed randomized controlled trials are needed to clearly determine the effect of CoQ10 on metabolic profile in diabetes. Dosage effects should also be explored.
Topics: Antioxidants; Blood Glucose; Blood Pressure; Diabetes Mellitus; Dietary Supplements; Humans; Lipids; Randomized Controlled Trials as Topic; Ubiquinone; Vitamins
PubMed: 25913756
DOI: 10.1111/jcpt.12280 -
Environmental Pollution (Barking, Essex... Nov 2022This systematic review aims to discover the plausible mechanism of Ozone in A.D., to boost translational research. The main focus of our review lies in understanding the... (Review)
Review
This systematic review aims to discover the plausible mechanism of Ozone in A.D., to boost translational research. The main focus of our review lies in understanding the effects of ozone pollution on the human brain and causing degenerative disease. Owing to the number of works carried out as preclinical evidence in association with oxidative stress and Alzheimer's disease and the lack of systematic review or meta-analysis prompted us to initiate a study on Alzheimer's risk due to ground-level ozone. We found relevant studies from PubMed, ScienceDirect, Proquest, DOAJ, and Scopus, narrowing to animal studies and the English language without any time limit. The searches will be re-run before the final analysis. This work was registered in Prospero with Reg ID CRD42022319360, followed the PRISMA-P framework, and followed the PICO approach involving Population, Intervention/Exposure, Comparison, and Outcomes data. Bibliographic details of 16 included studies were studied for Exposure dose of ozone, duration, exposure, and frequency with control and exposure groups. Primary and secondary outcomes were assessed based on pathology significance, and results were significant in inducing Alzheimer-like pathology by ozone. In conclusion, ozone altered oxidative stress, metabolic pathway, and amyloid plaque accumulation besides endothelial stress response involving mitochondria as the critical factor in ATP degeneration, caspase pathway, and neuronal damage. Thus, ozone is a criteria pollutant to be focused on in mitigating Alzheimer's Disease pathology.
Topics: Animals; Humans; Adenosine Triphosphate; Alzheimer Disease; Amyloid beta-Peptides; Caspases; Environmental Pollutants; Memory Disorders; Meta-Analysis as Topic; Ozone
PubMed: 36089140
DOI: 10.1016/j.envpol.2022.120136