Coenzyme Q10, Ageing and the Nervous System: An Overview

The ageing brain is characterised by changes at the physical, histological, biochemical and physiological levels. This ageing process is associated with an increased risk of developing a number of neurological disorders, notably Alzheimer’s disease and Parkinson’s disease. There is evidence that mitochondrial dysfunction and oxidative stress play a key role in the pathogenesis of such disorders. In this article, we review the potential therapeutic role in these age-related neurological disorders of supplementary coenzyme Q10, a vitamin-like substance of vital importance for normal mitochondrial function and as an antioxidant. This review is concerned primarily with studies in humans rather than in vitro studies or studies in animal models of neurological disease. In particular, the reasons why the outcomes of clinical trials supplementing coenzyme Q10 in these neurological disorders is discussed.

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Impact of Polyphenolic-Food on Longevity: An Elixir of Life. An Overview

Antioxidants ◽

10.3390/antiox10040507 ◽

2021 ◽

Vol 10 (4) ◽

pp. 507

Author(s):

Rosaria Meccariello ◽

Stefania D’Angelo

Keyword(s):

Oxidative Stress ◽

Food Sources ◽

Preventive Action ◽

Nutritional Interventions ◽

Beneficial Effects ◽

Age Related ◽

Macromolecular Damage ◽

And Oxidative Stress

Aging and, particularly, the onset of age-related diseases are associated with tissue dysfunction and macromolecular damage, some of which can be attributed to accumulation of oxidative damage. Recently, growing interest has emerged on the beneficial effects of plant-based diets for the prevention of chronic diseases including obesity, diabetes, and cardiovascular disease. Several studies collectively suggests that the intake of polyphenols and their major food sources may exert beneficial effects on improving insulin resistance and related diabetes risk factors, such as inflammation and oxidative stress. They are the most abundant antioxidants in the diet, and their intake has been associated with a reduced aging in humans. Polyphenolic intake has been shown to be effective at ameliorating several age-related phenotypes, including oxidative stress, inflammation, impaired proteostasis, and cellular senescence, both in vitro and in vivo. In this paper, effects of these phytochemicals (either pure forms or polyphenolic-food) are reviewed and summarized according to affected cellular signaling pathways. Finally, the effectiveness of the anti-aging preventive action of nutritional interventions based on diets rich in polyphenolic food, such as the diets of the Blue zones, are discussed.

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1 INSULIN TREATMENT DURING IN VITRO OOCYTE MATURATION LEADS TO DIFFERENT GENE EXPRESSION AND METHYLATION PATTERNS OF KEY GENES ASSOCIATED WITH METABOLISM AND STEROID SYNTHESIS IN THE BOVINE BLASTOCYST

Reproduction Fertility and Development ◽

10.1071/rdv29n1ab1 ◽

2017 ◽

Vol 29 (1) ◽

pp. 108

Author(s):

D. Laskowski ◽

P. Humblot ◽

M. A. Sirard ◽

Y. Sjunnesson ◽

G. Andersson ◽

...

Keyword(s):

Oxidative Stress ◽

Lipid Metabolism ◽

Oocyte Maturation ◽

Steroid Synthesis ◽

Developmental Potential ◽

Increased Risk ◽

In Vitro Oocyte Maturation ◽

Methylation Patterns ◽

And Oxidative Stress

Obesity and overfeeding are common causes for female infertility, leading to insulin resistance and hyperinsulinemia and associated with an increased risk for type 2 diabetes mellitus (Pasquali et al., http://dx.doi.org/10.1093/humupd/dmg024). We investigated here the effect of insulin during in vitro oocyte maturation on methylation changes in bovine Day 8 blastocysts (BC8) and focused on methylation patterns of candidate genes associated with metabolism and steroidogenesis (Day 0 = day of oocyte collection). Abattoir-derived oocytes (n = 882) were in vitro matured for 22 h with 2 different insulin concentrations, INS10 (10 µg mL−1) and INS0.1 (0.1 µg mL−1) or without insulin (INS0, control). Subsequently, IVF and IVC were performed to equal standardized conditions for all groups. Parallel genomic DNA and total RNA extraction (AllPrepDNA/RNA micro kit, cat no. 80284, Qiagen®, Valencia, CA, USA) from pools of 10 frozen (−80°C) BC8 was followed by transcriptome and epigenome analysis (Laskowski et al., http://dx.doi.org/10.1071/RD15315). An empirical Bayes moderated t-test and the ‘limma’ package in R (www.r-project.org) were used to search for differentially expressed genes between the control and the insulin groups. Analysis of the epigenome by using a specific pipeline, described by Shojaei Saadi et al. (2014 BMC Genomics 15, 451), showed that 7632 and 3914 regions were hypomethylated in the INS0.1 and INS10 v. INS0, whereas 6026 and 8504 regions were hypermethylated in INS0.1 and INS10 v. INS0. Combining epigenetic and transcriptomic data, we found that high methylation and low expression or the reverse (low methylation and high expression) were observed for a set of 14 and 11 genes for INS0.1 and INS10 respectively. Most of these genes are associated with lipid metabolism, steroid synthesis, and oxidative stress. Further investigation of the localization of differentially methylated regions (DMR) in genes showed that the conservation odds (methylation) was in general higher in coding regions and CpG islands than in noncoding regions. We observed a large overlap of DMR in the 2 insulin groups compared with controls (3233 common DMR). These numerous changes illustrate the potential unfavourable effects of elevated insulin during maturation leading to alteration of the methylation patterns of the early embryo. This model may help us better understand the mechanisms by which metabolic disorders observed pre-conception can affect embryonic development and subsequent health of the offspring. Our results based on changes in transcriptome or epigenome did show that insulin challenge during maturation leads to postponed effects associated with steroidogenesis, lipid metabolism and oxidative stress in the BC8. By this early stage, if persistent, specific changes in the expression and methylation patterns of genes associated to hyperinsulinemia may decrease the developmental potential of early embryos or could be responsible for subsequent pathologies. This study was funded by FORMAS.

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Ceratonia siliqua leaves exert a strong ROS-scavenging effect in human neutrophils, inhibit myeloperoxydase in vitro and protect against intestinal fluid and electrolytes secretion in rats

RSC Advances ◽

10.1039/c6ra11297h ◽

2016 ◽

Vol 6 (70) ◽

pp. 65483-65493 ◽

Cited By ~ 3

Author(s):

Kaïs Rtibi ◽

Mohammed-Amine Jabri ◽

Slimen Selmi ◽

Hichem Sebai ◽

Mohamed Amri ◽

...

Keyword(s):

Oxidative Stress ◽

Human Neutrophils ◽

Physical Factors ◽

Ceratonia Siliqua ◽

Intestinal Fluid ◽

Ros Scavenging ◽

Scavenging Effect ◽

Increased Risk ◽

And Oxidative Stress

Chronic inflammation and oxidative stress are induced by biological, chemical and physical factors which are, in turn, associated with an increased risk of several human diseases.

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Hypoxia and oxidative stress induce sterile placental inflammation in vitro

Scientific Reports ◽

10.1038/s41598-021-86268-1 ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Bernadette C. Baker ◽

Alexander E. P. Heazell ◽

Colin Sibley ◽

Rachael Wright ◽

Helen Bischof ◽

...

Keyword(s):

Oxidative Stress ◽

Placental Tissue ◽

Nitrative Stress ◽

Increased Risk ◽

Cell Free Fetal Dna ◽

Placental Inflammation ◽

Inflammatory Profile ◽

Conditioned Culture Medium ◽

And Oxidative Stress

AbstractFetal growth restriction (FGR) and stillbirth are associated with placental dysfunction and inflammation and hypoxia, oxidative and nitrative stress are implicated in placental damage. Damage-associated molecular patterns (DAMPs) are elevated in pregnancies at increased risk of FGR and stillbirth and are associated with increase in pro-inflammatory placental cytokines. We hypothesised that placental insults lead to release of DAMPs, promoting placental inflammation. Placental tissue from uncomplicated pregnancies was exposed in vitro to hypoxia, oxidative or nitrative stress. Tissue production and release of DAMPs and cytokines was determined. Oxidative stress and hypoxia caused differential release of DAMPs including uric acid, HMGB1, S100A8, cell-free fetal DNA, S100A12 and HSP70. After oxidative stress pro-inflammatory cytokines (IL-1α, IL-1β, IL-6, IL-8, TNFα, CCL2) were increased both within explants and in conditioned culture medium. Hypoxia increased tissue IL-1α/β, IL-6, IL-8 and TNFα levels, and release of IL-1α, IL-6 and IL-8, whereas CCL2 and IL-10 were reduced. IL1 receptor antagonist (IL1Ra) treatment prevented hypoxia- and oxidative stress-induced IL-6 and IL-8 release. These findings provide evidence that relevant stressors induce a sterile inflammatory profile in placental tissue which can be partially blocked by IL1Ra suggesting this agent has translational potential to prevent placental inflammation evident in FGR and stillbirth.

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Oocyte mitochondrial bioenergy potential and oxidative stress: within-/between-subject, in vivo versus in vitro maturation, and age-related variations in a sheep model

Fertility and Sterility ◽

10.1016/j.fertnstert.2011.12.014 ◽

2012 ◽

Vol 97 (3) ◽

pp. 720-728.e1 ◽

Cited By ~ 25

Author(s):

Nicola Antonio Martino ◽

Giovanni Michele Lacalandra ◽

Manuel Filioli Uranio ◽

Barbara Ambruosi ◽

Michele Caira ◽

...

Keyword(s):

Oxidative Stress ◽

In Vitro Maturation ◽

Sheep Model ◽

Age Related ◽

And Oxidative Stress

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Age-related changes in brain mitochondrial DNA deletion and oxidative stress are differentially modulated by dietary fat type and coenzyme Q10

Free Radical Biology and Medicine ◽

10.1016/j.freeradbiomed.2011.02.004 ◽

2011 ◽

Vol 50 (9) ◽

pp. 1053-1064 ◽

Cited By ~ 63

Author(s):

Julio J. Ochoa ◽

Reinald Pamplona ◽

M. Carmen Ramirez-Tortosa ◽

Sergio Granados-Principal ◽

Patricia Perez-Lopez ◽

...

Keyword(s):

Oxidative Stress ◽

Mitochondrial Dna ◽

Coenzyme Q10 ◽

Dietary Fat ◽

Mitochondrial Dna Deletion ◽

Dna Deletion ◽

Age Related ◽

And Oxidative Stress ◽

Age Related Changes

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Coenzyme Q10 Regulation of Apoptosis and Oxidative Stress in H2O2 Induced BMSC Death by Modulating the Nrf-2/NQO-1 Signaling Pathway and Its Application in a Model of Spinal Cord Injury

Oxidative Medicine and Cellular Longevity ◽

10.1155/2019/6493081 ◽

2019 ◽

Vol 2019 ◽

pp. 1-15 ◽

Cited By ~ 3

Author(s):

Xing Li ◽

Jiheng Zhan ◽

Yu Hou ◽

Yonghui Hou ◽

Shudong Chen ◽

...

Keyword(s):

Oxidative Stress ◽

Spinal Cord ◽

Spinal Cord Injury ◽

Signaling Pathway ◽

Coenzyme Q10 ◽

Therapeutic Efficiency ◽

Cord Injury ◽

And Oxidative Stress

Spinal cord injury (SCI) has always been considered to be a devastating problem that results in catastrophic dysfunction, high disability rate, low mortality rate, and huge cost for the patient. Stem cell-based therapy, especially using bone marrow mesenchymal stem cells (BMSCs), is a promising strategy for the treatment of SCI. However, SCI results in low rates of cell survival and a poor microenvironment, which limits the therapeutic efficiency of BMSC transplantation. Coenzyme Q10 (CoQ10) is known as a powerful antioxidant, which inhibits lipid peroxidation and scavenges free radicals, and its combined effect with BMSC transplantation has been shown to have a powerful impact on protecting the vitality of cells, as well as antioxidant and antiapoptotic compounds in SCI. Therefore, we aimed to evaluate whether CoQ10 could decrease oxidative stress against the apoptosis of BMSCs in vitro and explored its molecular mechanisms. Furthermore, we investigated the protective effect of CoQ10 combined with BMSCs transplanted into a SCI model to verify its ability. Our results demonstrate that CoQ10 treatment significantly decreases the expression of the proapoptotic proteins Bax and Caspase-3, as shown through TUNEL-positive staining and the products of oxidative stress (ROS), while increasing the expression of the antiapoptotic protein Bcl-2 and the products of antioxidation, such as glutathione (GSH), against apoptosis and oxidative stress, in a H2O2-induced model. We also identified consistent results from the CoQ10 treatment of BMSCs transplanted into SCI rats in vivo. Moreover, the Nrf-2 signaling pathway was also investigated in order to detail its molecular mechanism, and the results show that it plays an important role, both in vitro and in vivo. Thus, CoQ10 exerts an antiapoptotic and antioxidant effect, as well as improves the microenvironment in vitro and in vivo. It may also protect BMSCs from oxidative stress and enhance their therapeutic efficiency when transplanted for SCI treatment.

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Uremic Toxins and Their Relation with Oxidative Stress Induced in Patients with CKD

International Journal of Molecular Sciences ◽

10.3390/ijms22126196 ◽

2021 ◽

Vol 22 (12) ◽

pp. 6196

Author(s):

Anna Pieniazek ◽

Joanna Bernasinska-Slomczewska ◽

Lukasz Gwozdzinski

Keyword(s):

Oxidative Stress ◽

Uremic Toxins ◽

Water Medium ◽

Induce Insulin Resistance ◽

Risk Of Mortality ◽

Increased Risk ◽

Stage Renal Disease ◽

End Stage

The presence of toxins is believed to be a major factor in the development of uremia in patients with chronic kidney disease (CKD) and end-stage renal disease (ESRD). Uremic toxins have been divided into 3 groups: small substances dissolved in water, medium molecules: peptides and low molecular weight proteins, and protein-bound toxins. One of the earliest known toxins is urea, the concentration of which was considered negligible in CKD patients. However, subsequent studies have shown that it can lead to increased production of reactive oxygen species (ROS), and induce insulin resistance in vitro and in vivo, as well as cause carbamylation of proteins, peptides, and amino acids. Other uremic toxins and their participation in the damage caused by oxidative stress to biological material are also presented. Macromolecules and molecules modified as a result of carbamylation, oxidative stress, and their adducts with uremic toxins, may lead to cardiovascular diseases, and increased risk of mortality in patients with CKD.

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