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Fatigue
Published in Carolyn Torkelson, Catherine Marienau, Beyond Menopause, 2023
Carolyn Torkelson, Catherine Marienau
CoQ10 levels are lower in people with certain conditions, such as heart disease and chronic fatigue syndrome, and in those who take statins, which are drugs that lower cholesterol. CoQ10 levels also decrease as we age, so taking a supplement as you grow older can help support optimal energy levels. The most commonly available products are ubiquinol and ubiquinone. Both are valid forms of CoQ10, but ubiquinol is better absorbed. A typical dose of 100 mg is considered safe and is available in capsule, chewable tablet, and liquid form.
Implication of Mitochondrial Coenzyme Q10 (Ubiquinone) in Alzheimer’s Disease *
Published in Abhai Kumar, Debasis Bagchi, Antioxidants and Functional Foods for Neurodegenerative Disorders, 2021
Sayantan Maitra, Dibyendu Dutta
In its reduced form (CoQ10·H2), CoQ10 is an effective fat-soluble antioxidant that protects cell membranes and lipoproteins from oxidation. Ubiquinol (CoQ10·H2) exerts its antioxidative property primarily by diminishing the generation of lipid peroxyl radicals (LOO·), whereas vitamin E exerts its effect mainly by quenching these radicals. The preventive activity of ubiquinol is attributable to the reduction of the initiating perferryl radical, subsequently with the formation of ubisemiquinone and H2O2. In addition, ubiquinol also acts by eliminating LOO·, either directly or through the regeneration of vitamin E from the α-tocopheroxyl radical, a process that otherwise must rely on access to water-soluble antioxidants like ascorbate [30].
Antioxidants and AIDS
Published in Ronald R. Watson, NUTRIENTS and FOODS in AIDS, 2017
Zhen Zhang, Paula Inserra, Bailin Liang, Ronald R. Watson
Although ubiquinone (coenzyme Q10 CoQ 10) is known for its activity as a redox component of transmembrane electron transport in mitochondria, its reduced form, ubiquinol, is an active antioxidant. Ubiquinol scavenges products from the peroxidation of membrane lipids even after the peroxidation process has been initiated. Lipid peroxidation will not occur, in fact, until all ubiquinol is consumed, which spares vitamin E in the process.75
The therapeutic effects of coenzyme Q10 on surgically induced endometriosis in Sprague Dawley rats
Published in Journal of Obstetrics and Gynaecology, 2022
Saadet Özen Akarca-Dizakar, Mürşide Ayşe Demirel, Neslihan Coşkun Akçay, Mehmet Sipahi, Lale Karakoç Sökmensüer, Hakan Boyunaga, Ayse Köylü, Suna Ömeroğlu
Coenzyme Q10 (CoQ10, ubiquinol-10, and/or ubiquinone-10) is a powerful anti-inflammatory and antioxidant agent and by inhibiting lipid peroxidation, and protein oxidation, it reduces OS (Rahmani et al. 2018; Testai et al. 2021). CoQ10 is located close to unsaturated lipid chains in membranes and acts as a major scavenger of free radicals (Kunitomo et al. 2008). CoQ10 is an important cofactor in the mitochondrial electron transport system, and plays a role in the production of ATP via oxidative phosphorylation (Kunitomo et al. 2008; Rahmani et al. 2018). Many previous studies proved that CoQ10 is antioxidant (Hargreaves 2014; Liu et al. 2015; Giannubilo et al. 2018), anti-inflammatory (Ben‐Meir et al. 2015; Turk et al. 2017), anti-diabetic (Amin et al. 2014) and anti-carcinogenic (Yuvaraj et al. 2009; Fouad et al. 2013). Especially, many studies have promising evidence of the beneficial effect of CoQ10 therapy on various disorders related to OS and inflammation (Perez-Sanchez et al. 2017; Zhang et al. 2013; Jhun et al. 2015). It is known that the administration of CoQ10 may increase the reproductive capacity by making a positive effect on oocytes, and granulosa/cumulus cells, and improve ovulation rate- and/or the uterine tissue (Ben‐Meir et al. 2015). Considering the constructive effects of CoQ10 on the reproductive system, inflammation, and OS, it may prevent the formation and progression of endometriosis foci. We aimed to evaluate the possible beneficial effects of different doses of CoQ10 in a rat endometriosis model and to compare the effect of the GnRH agonist.
Coenzyme Q10 and the exclusive club of diseases that show a limited response to treatment
Published in Expert Opinion on Orphan Drugs, 2021
Nadia Turton, Nathan Bowers, Sam Khajeh, Iain P Hargreaves, Robert A Heaton
In light of their increased absorption, the use of both gel and oil-based formulations has been recommended over the use of conventional tablet formulations in patients with ETC disorders [90]. In a study by Martinefski, Samassa [91] it was reported that liquid emulsion improved the bioavailability of CoQ10 with respect to solid formulations. Currently, there is considerable debate as to whether formulations of ubiquinol rather than the ubiquinone form of CoQ10 have a better absorption from the gastrointestinal tract (GI). It has been reported that absorption of ubiquinol is three to four times higher than CoQ10 in the GI [91,92]. However, because during absorption in the GI CoQ10 undergoes reduction to ubiquinol, the suggested increased bioavailability of the ubiquinol formulations may be due to the matrix in which the ubiquinol is held in rather than its redox state.
Probiotics maintain the intestinal microbiome homeostasis of the sailors during a long sea voyage
Published in Gut Microbes, 2020
Jiachao Zhang, Jinshan Zhao, Hao Jin, Ruirui Lv, Huiwen Shi, Guozhong De, Bo Yang, Zhihong Sun, Heping Zhang
To investigate the observed differences in the functional profiles of the intestinal microbiota during the long sea voyage, high-quality reads from all samples were assembled and annotated for protein-coding genes. Based on the results, a collective, non-redundant intestinal microbiota gene catalog was created. Next, for each sample, the reads were mapped to the collective gene catalog to reconstruct sample-specific gene profiles, and metabolic pathways were also generated with the Kyoto Encyclopedia of Genes and Genomes Orthology database (Tables S7 and S8). PCoA was performed based on the Bray–Curtis distances of the intestinal microbial functional gene profiles (Figure S3), and the specific changes in the microbial metabolic pathway were represented by a decreased toluene degradation ability and ubiquinol and glycogen synthesis ability (Table 1). Additionally, a significant shift from the intestinal microbial carbohydrate-active enzyme (CAZy) gene profile (Table S9) based on the Bray–Curtis distances (Figure 3(a)) and a sharp decline in the alpha diversity of microbial CAZy genes (Figure 3(b)) were observed at the end of the voyage in the placebo group, which were represented by a decrease in the relative abundance of the gene families glycoside hydrolases (GH), glycosyltransferases (GT) and polysaccharide lyases (PL) (Figure 3(c)). These results indicated that the long sea voyage not only disordered the balance of the intestinal microbiota of sailors but also reduced the diversity of functional features of intestinal microbiota.