Ubiquinone Research Articles

Association of vitamin intake with health-related quality of life in hemodialysis patients.

It is still uncertain whether vitamin intake is associated with better quality of life in hemodialysis patients. This study aims to assess the association between the quantity of supplemented vitamins and health-related quality of life (HRQoL) in this population. This cross-sectional study included all patients on chronic hemodialysis from three units. Vitamins and micronutrients assessed were B1, B6, B12, C, D, folic acid, menaquinone, carnitine, zinc, and coenzyme Q10. Quality of life scores included the 8 domains of SF-36 and the 11 domains of the Kidney Disease Quality of Life (KDQOL). Bivariate analysis compared two groups of patients divided based on the median of vitamin intake. Spearman Rho test assessed the correlation between number of vitamins and different dimensions of HRQoL. A total of 183 patients were included. Median number of vitamins supplemented was 2 (1,3); 112 patients had an intake of ≤ 2 vitamins, and 71 patients were taking > 2 vitamins. There was a significant association between higher vitamin intake and the burden of kidney disease that remained significant in the multivariable analysis (p = 0.03), but no correlation between the number of vitamins (0 - 13) and different HRQoL scores. Sub-analyses of each category of vitamins showed no significant difference in HRQoL scores except for Vitamin B and staff encouragement (p = 0.01) and for multivitamins and quality of social interaction (p = 0.03). A higher number of vitamins in hemodialysis patients is associated with an increased perception of the burden of kidney disease. Interventional studies are needed to assess whether selective vitamin supplementation in case of deficiencies is associated with better quality of life.

Effect of mitochondrial coenzyme-Q10 precursor solanesol in gentamicin-induced experimental nephrotoxicity: Evidence from restoration of ETC-complexes and histopathological alterations.

Nephrotoxicity occurs when the body is exposed to certain drugs or toxins. When kidney damage occurs, the kidney fails to eliminate excess urine and waste. Solanesol (C45H74O) is a tri-sesquiterpenoid alcohol first isolated from tobacco, and it is widely distributed in plants of the Solanaceae family. Solanesol (SNL) is an intermediate in the synthesis of coenzyme Q10 (CoQ10), an antioxidant which protects nerve cells. This study investigated the protective effect of SNL at doses of 30 and 60 mg/kg in gentamicin-induced nephrotoxicity in Wistar albino rats. Animals were distributed into six groups and administered 100 mg/kg gentamicin-intraperitoneal injection for 14 days. Biochemical assessments were performed on kidney homogenate, blood, and serum. Treatment with SNL was shown as lower serum levels of creatinine, blood urea nitrogen (BUN), thiobarbituric acid reactive substances (TBARS), and Tumor necrosis factor alpha)TNF-α ((p < .001). It also restored reduced glutathione (GSH) and mitochondrial complex enzymatic activity as protective measures against gentamicin-induced nephrotoxicity. SNL were shown to reduce inflammation and oxidative stress markers (p < .001). Histological findings furtherly augmented the protective effects of SNL. Long-term SNL therapy also restored mitochondrial electron transport chain complex enzymes, such as complex-I (p < .001). In conclusion, these findings suggest that SNL can represent a protective therapeutic option for drug-induced nephrotoxicity, a long-term adverse effect of aminoglycoside antibiotics such as gentamicin.

Refractory Epilepsy in Adult Patient With COQ8A Variant Improves With CoQ10 Supplementation: A Case for Exome Sequencing in the ICU.

Describe a case of stroke-like episodes and refractory status epilepticus diagnosed with primary CoQ10 deficiency-4 (COQ10D4) using whole-exome sequencing in the intensive care unit (ICU), with treatment implications. A patient presented to the emergency department with 1 month of progressively worsening focal motor status epilepticus and stroke-like imaging abnormalities. Multiple seizure medications, ketogenic diet, and elective intubation for anesthetic drips failed to achieve sustained seizure freedom. Genetic testing was pursued for prognostic information and identified potential treatment. Whole-exome sequencing revealed compound heterozygous variants of COQ8A, including 1 allele not previously described as pathogenic. The patient's history, imaging, and genetic testing supported a diagnosis of COQ10D4. High-dose coenzyme Q10 supplementation was started with gradual clinical improvement. Whole-exome sequencing is a fast and cost-effective means to diagnose rare neurologic disease in critically ill patients and can uncover treatment options. While primarily used in the neonatal ICU, appropriately selected adult patients may also benefit.

Effects of Coenzyme Q10 Combined With Metformin on Ovarian Function Compared to Metformin Alone in Iraqi PCOS Patients

Background: Data about the response of ovary function in women with polycystic ovary syndrome (PCOS) to metformin treatment are controversial and the use of metformin in women with this syndrome combined with CoQ10 has never been assessed previously using the current study design. Research objective: to figure out the effect of Co Q10 and metformin combination in contrast to monotherapy using metformin on ovary activity in PCOS Patients and methods: The present study included 150 patients with an age range of 20 to less than 35 years. Patients were categorized into five groups: CoQ10 groups who were treated using 10 mg per-oral (bid), metformin group (positive control group) and they received metformin as 500 mg per-oral (bid), combination groups who received both agents with similar doses as above, newly diagnosed group who received no treatment and finally newly diagnosed PCOS. Each group included 30 women. Pediatrics and Maternity Teaching Hospital in Adiwaniyah Province (Iraq) was the location of sample collection. Beginning of study was at September the 21st 2023 and extended to March 31st 2024. Data about age and body mass index were included in the study. Ultrasound assessment of ovarian volume and antral follicle volume was carried out before and after treatment.Results: Comparison of mean ovary volume among research cohorts is shown in table 2. Statistically notable variance was reported in average ovary volume across research cohorts (p &lt; 0.001). Mean ovary volume was highest in newly diagnosed PCOS group and it was lowest in negative control group and combination group. The volume was comparable in CoQ10 group and metformin group; however, combination group had significantly lower mean ovary volume in comparison with either treatment approach alone (p &lt; 0.05). Statistically notable variance was reported in average follicle volume across study cohorts (p &lt; 0.001). Average follicle volume was lowest in newly diagnosed PCOS group and it was highest in negative control group. The volume was comparable in CoQ10 group and metformin group; however, combination group had significantly higher mean follicle volume in comparison with either treatment approach alone (p &lt; 0.05). Conclusion: Both treatment approaches using metformin alone or CoQ10 alone produces significant improvement in ovary volume and antral follicle volume in women with PCOS; however, combination of both agents resulted in more significant improvement.

Quercetin and Coenzyme Q10: A Comparison study of their Hepatoprotective Effects in Paracetamol-Induced Hepatotoxic Rats

Quercetin and Coenzyme Q10: A Comparison study of their Hepatoprotective Effects in Paracetamol-Induced Hepatotoxic Rats

LncRNA DCRT Protects Against Dilated Cardiomyopathy by Preventing NDUFS2 Alternative Splicing by Binding to PTBP1.

Dilated cardiomyopathy is characterized by left ventricular dilation and continuous systolic dysfunction. Mitochondrial impairment is critical in dilated cardiomyopathy; however, the underlying mechanisms remain unclear. Here, we explored the cardioprotective role of a heart-enriched long noncoding RNA, the dilated cardiomyopathy repressive transcript (DCRT), in maintaining mitochondrial function. The DCRT knockout (DCRT-/-) mice and DCRT knockout cells were developed using CRISPR-Cas9 technology. Cardiac-specific DCRT transgenic mice were generated using α-myosin heavy chain promoter. Chromatin coimmunoprecipitation, RNA immunoprecipitation, Western blot, and isoform sequencing were performed to investigate the underlying mechanisms. We found that the long noncoding RNA DCRT was highly enriched in the normal heart tissues and that its expression was significantly downregulated in the myocardium of patients with dilated cardiomyopathy. DCRT-/- mice spontaneously developed cardiac dysfunction and enlargement with mitochondrial impairment. DCRT transgene or overexpression with the recombinant adeno-associated virus system in mice attenuated cardiac dysfunction induced by transverse aortic constriction treatment. Mechanistically, DCRT inhibited the third exon skipping of NDUFS2 (NADH dehydrogenase ubiquinone iron-sulfur protein 2) by directly binding to PTBP1 (polypyrimidine tract binding protein 1) in the nucleus of cardiomyocytes. Skipping of the third exon of NDUFS2 induced mitochondrial dysfunction by competitively inhibiting mitochondrial complex I activity and binding to PRDX5 (peroxiredoxin 5) and suppressing its antioxidant activity. Furthermore, coenzyme Q10 partially alleviated mitochondrial dysfunction in cardiomyocytes caused by DCRT reduction. Our study revealed that the loss of DCRT contributed to PTBP1-mediated exon skipping of NDUFS2, thereby inducing cardiac mitochondrial dysfunction during dilated cardiomyopathy development, which could be partially treated with coenzyme Q10 supplementation.

Comparative Assessment of Beeswax Alcohol and Coenzyme Q10 (CoQ10) to Prevent Liver Aging, Organ Damage, and Oxidative Stress in Hyperlipidemic Zebrafish Exposed to D-Galactose: A 12-Week Dietary Intervention.

The current study was designed to compare in vivo efficacy between beeswax alcohol (BWA) and coenzyme Q10 (CoQ10) to treat fatty liver changes, oxidative stress, and damages in major organs of zebrafish by 12 weeks with high-cholesterol (HC) and galactose (Gal) supplementation. At week 12, the HC control and HC+Gal control groups showed 96% and 92% survivability, respectively, while co-supplementation of the 0.5% BWA and 1.0% BWA groups exhibited 96% and 100% survivability. However, co-supplementation of the 0.5% CoQ10 and 1.0% CoQ10 groups revealed the lowest survivability, around 92% and 89%, respectively. The 0.5% BWA and 1.0% BWA groups showed 21% (p < 0.001) and 41% (p < 0.001), respectively, lower total cholesterol (TC) than the HC+Gal control, while the 1.0% CoQ10 group showed only 15% lower TC than the control. Interestingly, the 0.5% BWA and 1.0% BWA groups showed 22% (p < 0.001) and 38% (p < 0.001), respectively, lower triglyceride (TG) than the HC+Gal control. However, both the 0.5% CoQ10 and 1.0% CoQ10 groups showed similar TG levels as the control, suggesting that CoQ10 supplementation had no effect on lowering serum TG. The 1.0% BWA group showed the highest plasma HDL-C and HDL-C/TC (%) up to 3.2-fold and 5.5-fold, respectively, higher than those of the HC+Gal control, while the 1.0% CoQ10 group showed 2.4-fold and 2.8-fold higher plasma HDL-C and HDL-C/TC (%), respectively, than the control. The plasma aspartate transaminase (AST) and alanine transaminase (ALT) levels were lowest in the 1.0% BWA group, 51% and 72%, respectively, lower than HC+Gal control, suggesting the lowest extent of hepatic damage. In hepatic tissue, neutrophil infiltration and interleukin (IL)-6 production were the lowest in the 1.0% BWA group, around 67% and 85%, respectively, lower than the HC+Gal control. Fatty liver change, cellular apoptosis, and cell senescence in hepatic tissue were remarkably lowered in the 1.0% BWA group, while the CoQ10 group showed much less effect than the BWA group. In kidney, ovary, and testis tissue, the 1.0% BWA group showed the lowest production of reactive oxygen species, the extent of cellular senescence, and cellular apoptosis with the healthiest cell morphology. In conclusion, supplementation of BWA remarkably protected the liver, kidney, ovary, and testis from oxidative damage by cholesterol and galactose consumption, with the least serum AST and ALT levels, inflammatory parameters, and senescence markers.

Mitochondrial Dysfunction in Systemic Lupus Erythematosus: Insights and Therapeutic Potential.

Systemic lupus erythematosus (SLE) is a complex autoimmune disorder characterized by the presence of various serum autoantibodies and multi-system effects, predominantly affecting young female patients. The pathogenesis of SLE involves a combination of genetic factors, environmental triggers, and pathogen invasions that disrupt immune cell activation, leading to the release of autoantibodies and chronic inflammation. Mitochondria, as the primary cellular powerhouses, play a crucial role in SLE development through their control of energy generation, reactive oxygen species (ROS) production, and cellular apoptotic pathways. Dysregulation of mitochondrial structure and function can contribute to the immune dysregulation, oxidative stress, and inflammation seen in SLE. Recent research has highlighted the impact of mitochondrial dysfunction on various immune cells involved in SLE pathogenesis, such as T-lymphocytes, B-lymphocytes, neutrophils, and plasmacytoid dendritic cells. Mitochondrial dysfunction in these immune cells leads to increased ROS production, disrupted mitophagy, and alterations in energy metabolism, contributing to immune dysregulation and inflammation. Moreover, genetic variations in mitochondrial DNA (mtDNA) and abnormalities in mitochondrial dynamics have been linked to the pathogenesis of SLE, exacerbating oxidative stress and immune abnormalities. Targeting mitochondrial function has emerged as a promising therapeutic approach for SLE. Drugs such as sirolimus, N-acetylcysteine, coenzyme Q10, and metformin have shown potential in restoring mitochondrial homeostasis, reducing oxidative stress, and modulating immune responses in SLE. These agents have demonstrated efficacy in preclinical models and clinical studies by improving disease activity, reducing autoantibody titers, and ameliorating organ damage in SLE patients. In conclusion, this review underscores the critical role of mitochondria in the pathogenesis of SLE and the potential of targeting mitochondrial dysfunction as a novel therapeutic strategy for improving outcomes in SLE patients. Further investigation into the mechanisms underlying mitochondrial involvement in SLE and the development of targeted mitochondrial therapies hold promise for advancing SLE treatment and enhancing patient care.

Does coenzyme Q10 supplementation protect spermatogenesis in ciprofloxacin-induced rat testes?

Does coenzyme Q10 supplementation protect spermatogenesis in ciprofloxacin-induced rat testes?

Cancer cell stiffening via CoQ10 and UBIAD1 regulates ECM signaling and ferroptosis in breast cancer

CoQ10 (Coenzyme Q10) is an essential fat-soluble metabolite that plays a key role in cellular metabolism. A less-known function of CoQ10 is whether it may act as a plasma membrane-stabilizing agent and whether this property can affect cancer development and progression. Here, we show that CoQ10 and its biosynthetic enzyme UBIAD1 play a critical role in plasmamembrane mechanical properties that are of interest for breast cancer (BC) progression and treatment. CoQ10 and UBIAD1 increase membrane fluidity leading to increased cell stiffness in BC. Furthermore, CoQ10 and UBIAD1 states impair ECM (extracellular matrix)-mediated oncogenic signaling and reduce ferroptosis resistance in BC settings. Analyses on human patients and mouse models reveal that UBIAD1 loss is associated with BC development and progression and UBIAD1 expression in BC limits CTCs (circulating tumor cells) survival and lung metastasis formation. Overall, this study reveals that CoQ10 and UBIAD1 can be further investigated to develop therapeutic interventions to treat BC patients with poor prognosis.

Coenzyme Q10 and vitamin E alleviate heat stress-induced mood disturbances in male mice: Modulation of inflammatory pathways and the HPA axis

Heat stress, as an environmental stressor, can lead to temperature dysregulation and neuroinflammation, causing depression and anxiety by disrupting brain physiology and functional connectivity. This study looked at how co-enzyme Q10 (Q10) and vitamin E (Vit E), alone and together, affected heat stress-caused anxiety and depression symptoms and inflammation in male mice. Five groups were utilized in the study: control, heat stress (NS), Q10, Vit E, and the combination group (Q10+Vit E). The mice were subjected for 15 min/day to a temperature of 43°C for 14 consecutive days, followed by daily treatments for two weeks with either normal saline, Q10 (500 mg/kg), Vit E (250 mg/kg), or their combination. The forced swimming test (FST) and tail suspension test (TST) were employed to evaluate despair behavior, whereas the elevated plus maze (EPM) and open field test (OFT) were used to assess anxious behaviors. Subsequently, the animals were sacrificed, and serum corticosterone levels, protein expression of inflammasome-related proteins, and hsp70 gene expression were evaluated in the prefrontal cortex (PFC). The study revealed that treatment with Vit E and Q10, alone or together, provided anxiolytic and antidepressant effects in the heat-stress-subjected animals. Also, giving Vit E and Q10 alone or together greatly lowered serum corticosterone levels. In the PFC, they also lowered the levels of hsp70 mRNA and NF-κB, caspase 1, NLRP3, and IL-1β proteins. It is speculated that treatment with Q10 and Vit E can attenuate heat stress-associated anxious and depressive responses by inhibiting the inflammatory pathways and modulating the hypothalamus-pituitary-adrenal axis.

Efficacy of a mitochondrial drug cocktail in preventing acute encephalopathy with biphasic seizures and late reduced diffusion

Acute encephalopathy with biphasic seizures and late reduced diffusion (AESD) is difficult to differentiate from prolonged febrile seizures during the acute phase. Mitochondrial dysfunction-induced energy depletion is among the key mechanisms underlying acute encephalopathy. Therefore, this study aimed to examine the efficacy of a “mitochondrial cocktail” in preventing AESD. We retrospectively studied children experiencing status epilepticus associated with fever lasting more than 30 min, focusing on those who received the mitochondrial cocktail between February 2016 and December 2020, and those who did not receive it within 24 h between February 2012 and January 2014. The mitochondrial cocktail contained vitamins B1, C, and E; biotin; coenzyme Q10; and l-carnitine. AESD occurred in 1 of 41 (2.4 %) patients in the administration group and 7 of 39 (17.9 %) patients in the non-administration group. The incidence of AESD was lower in the administration group than in the non-administration group, with a significant difference (p = 0.027). The incidence of encephalopathy, including cases classified as AESD and unclassified, was 7/41 (17.1 %) and 7/39 (17.9 %) in the administration and non-administration groups, respectively, with no significant difference. However, the number of cases with worsening pediatric cerebral performance category scores was significantly lower in the administration group compared to the non-administration group (p = 0.015). In conclusion, early administration of the mitochondrial cocktail may help prevent AESD. Some encephalopathy cases do not progress to a biphasic state or develop AESD. Thus, the mitochondrial cocktail should be administered as early as possible to prevent AESD.

Potential Chemotherapeutic Effect of Coenzyme Q10 Against Liver Injury in a Leukemia Rat Model by 7,12-Dimethylbenz[a]anthracene

Potential Chemotherapeutic Effect of Coenzyme Q10 Against Liver Injury in a Leukemia Rat Model by 7,12-Dimethylbenz[a]anthracene

Comparison of The Effectiveness of Thymoquinone, St. John Wort Oil and Silver Sulfadiazine in Experimental Burn Wounds.

We aimed to compare the effectiveness of thymoquinone (TQ), most important bioactive component of black cumin, St. John wort (SJW) oil, a traditional medicinal plant used in burns, and silver sulfadiazine (AgSD), well-known anti-inflammatory agent used in modern medicine, in an experimental burn rat-model. 63 Wistar-Albino rats were randomly divided into 9 groups (n=7). TQ, SJW were administered topically and systemically but AgSD was applied topically. Epithelialization, inflammatory cell response, granulation tissue, vascularization, and fibrosis were evaluated. Malondialdehyde (MDA), total antioxidant status (TAS), total oxidant status (TOS), vitamin E, 8-hydroxy-deoxyguanosine (8-OHdG), coenzyme Q10 (CoQ10) were analyzed in serum. Topical TQ accelerated theepithelialization, enabled granulation, vascularization and fibrosis in wounds (P=0.001). Topical and systemic TQ increased Vitamin-E levels (P=0.003) but reduced TOS and 8-OHdG levels (P=0.001). Topical SJW reduced granulation and vascularization. Topical and systemic SJW decreased TOS, MDA and 8-OHdG levels (P=0.001), but increased TAS (P=0.001), and Vitamin-E levels (P=0.003). Topical AgSD reduced TOS, 8-OHdG, MDA levels (P=0.001). Topical and systemic TQ demonstrated significant advantages in accelerating wound healing process, while also enhancing antioxidant defenses and reducing oxidative damage. SJW oil, particularly in topical application, improved epithelialization and antioxidant status but showed less efficacy in systemic use. AgSD, while effective in reducing oxidative stress, was less successful in promoting wound healing and appeared to delay granulation and fibrosis. TQ offers superior protective and healing benefits, SJW is effective locally but less so systemically, and AgSD should be used cautiously, potentially combined with antioxidants to mitigate its negative impact on wound healing.

Major clinical outcomes of nutrology and lifestyle in the metabolic processes of healthy aging: a systematic review

Introduction: Centenarians exemplify the concept of healthy aging and therefore provide an invaluable resource for identifying novel host-intestinal microbiota relationships concerning aging. Approximately 18 micronutrients, composed of minerals and vitamins, facilitate the optimal utilization of macronutrients through their role in catalyzing numerous biochemical processes, increasing their bioavailability and absorption, and balancing the microbiome. In the context of aging, a major challenge to maintaining health in old age is unbalanced nutritional intake, resulting in nutritional deficiency or malnutrition. Objective: The main clinical outcomes of nutrology and lifestyle in the metabolic processes of healthy aging were listed through a systematic review. Methods: The systematic review rules of the PRISMA Platform were followed. The search was carried out from July to August 2024 in the Scopus, PubMed, Science Direct, Scielo, and Google Scholar databases. The quality of the studies was based on the GRADE instrument and the risk of bias was analyzed according to the Cochrane instrument. Results and Conclusion: A total of 118 articles were found. A total of 39 articles were fully evaluated and 29 were included and developed in the present systematic review study. Considering the Cochrane tool for risk of bias, the overall assessment resulted in 21 studies with a high risk of bias and 15 that did not meet the GRADE and AMSTAR-2 criteria. Most studies showed homogeneity in their results, with X2=82.7%&gt;50%. Zinc and copper govern many functions that characterize the so-called “oxy-aging”. Selenium (Se) is a fundamental cofactor in many redox functions, the role of vitamin C in aging has been investigated particularly for skin health and immunity, particularly in inflammatory and degenerative diseases. Retinoids, which represent a synthetic form of vitamin A, appear effective in preventing skin degeneration due to aging. The role of vitamin E in the prevention and reduction of ROS-induced lesions has been well described. Supplementation with selenium and coenzyme Q10 influenced the analyzed biomarkers in a way that indicated an anti-aging effect. It was concluded that an adequate plasma level of trace elements, such as Zn or copper (Cu), promotes an optimal function of the immune response. Selenium (Se) is a key cofactor in many redox functions, which reduces ROS-induced degeneration in the senescent phenotype. The role of vitamin C in aging has been investigated particularly for skin health and immunity, particularly in inflammatory and degenerative diseases. Vitamin A acts in the prevention of skin degeneration due to aging. The role of vitamin E in the prevention and reduction of ROS-induced lesions has been well described, as well as it has been associated with the prevention of cognitive decline during senescence, particularly in Alzheimer's disease. Good fats, vitamins, minerals, or polyphenols can have antioxidant and anti-inflammatory activities, with anti-aging effects. Recent studies have shown that vitamin K is a vital cofactor in the activation of several proteins, which act against age-related syndromes.

Reduced retinol (vitamin A) and α-tocopherol (vitamin E) blood levels and increased myeloperoxidase (MPO) activity in children with high myopia

The study assessed selected parameters of redox status in the plasma of patients suffering from high myopia (HM). Thirty-five children with mean age 13.7 ± 2.7 years with HM and 40 healthy children were included. Plasma redox status parameters were determined using colorimetric kits. The levels of retinol, α-tocopherol and coenzyme Q10 were determined with a high-performance liquid chromatograph. Negative correlations were observed between the concentrations of retinol and the axial length of the eye (r = − 0.514 p < 0.001). Increased myeloperoxidase (MPO) activity (p < 0.018), and decreased concentrations of retinol (p < 0.001) and α-tocopherol (p < 0.023) in patients with HM and the axial length of the eye > 26 mm compared to controls were established. Significantly lower retinol and α-tocopherol concentrations were found in patients with the axial length of the eye > 26 mm compared to those with the axial length of the eye ≤ 26 mm (p < 0.001, p < 0.021, respectively). Increased MPO activity in advanced stages of HM may confirm an inflammatory process in HM patients. Reduced retinol and α-tocopherol concentrations and their link to disease progression indicate a need for monitoring their levels and supplementation in children with HM.

Metallothionein ameliorates airway epithelial apoptosis upon particulate matter exposure: role of oxidative stress and ion homeostasis

PurposeTo investigate the mechanism underlying particulate matter (PM) exposure-induced oxidative stress and potential rescue strategies against pulmonary damage in this context.MethodsA combination of omics technology and bioinformatic analysis were used to uncover mechanisms underlying cellular responses to PM exposure in human bronchial epithelia (HBE) cells and imply the potential rescue.ResultsOur results implicated that oxidative stress, metal ion homeostasis, and apoptosis were the major cellular responses to PM exposure in HBE cells. PM exposure disrupted oxidative phosphorylation (OXPHOS)-related gene expressions in HBE cells. Rescuing the expression of these genes with supplemental coenzyme Q10 (Co Q10) inhibited reactive oxygen species (ROS) generation; however, it only partially protected HBEs against PM exposure-induced apoptosis. Further, metallothionein (MT)-encoding genes associated with metal ion homeostasis were significantly induced in HBE cells, which was transcriptionally regulated by specificity protein 1 (SP1). SP1 knock-down (KD) aggravated PM-induced apoptosis in HBE cells, suggesting it plays a role in MT induction. Subsequent studies corroborated the protective role of MT by showing that exogenous MT supplement demonstrated effective protection against PM-induced oxidative stress and apoptosis in HBE cells. Importantly, exogenous MT supplement was shown to reduce ROS generation and apoptosis in airway epithelia in both HBE cells and a PM-inhaled murine model.ConclusionThis study demonstrates that the impact of MT on airway epithelia by suppressing oxidative stress and maintaining metal ion homeostasis is beneficial in attenuating damage to pulmonary cells undergoing PM exposure.

Novel Therapeutic Approaches in Alzheimer's Disease

Alzheimer's disease (AD) is a neurological condition associated with a decrease in levels of acetylcholine and diminished cholinergic functions. This may be caused by the degeneration of cholinergic neurons in the brain, leading to cognitive deficits. Due to the difficulty and invasiveness of collecting cerebrospinal fluid (CSF) required for assessing conventional biomarkers, researchers are currently exploring less intrusive, less expensive, and more straightforward methods for diagnosing AD. Additionally, conventional interventions such as cholinesterase inhibitors like rivastigmine, donepezil, and galantamine are US FDA-approved drugs that are still effective for managing AD. The goal of this therapy is to increase acetylcholine levels in the brain by inhibiting the enzymes that degrade acetylcholine. Therefore, this therapeutic approach is useful for treating mild-to-moderate AD. However, only symptomatic treatment is currently available, and it can lead to serious adverse effects from conventional therapy. Thus, novel therapies for AD are needed in a growing global population. This manuscript provides information on various biomarkers with possible pathogenesis mechanisms, novel treatment strategies such as microalgae, HupA, cannabinoids, and the beneficial effects of coenzyme Q10, bacterial probiotics, omega-3 fatty acids, vitamin B12, and D3 in memory impairment for managing AD. Non-pharmacological treatments such as music therapy, Electroacupuncture (EA), or manual acupuncture (MA) also play an important role in enhancing the effectiveness of conventional pharmacological treatments for AD.

Recovery Supplementation Strategies Applied to Elite Soccer Players

Purpose of review: During soccer seasons, athletes have canned a 48 number of matches. Therefore, recovery supplementation strategies that optimize recovery and/or reduce the damage caused by the number of matches during a season are important to help elite football players in their state of recovery. This way, the purpose of this review is to provide a holistic view of the mainly recovery supplements and their effects on elite soccer players recovery, based on what the literature recommends decreasing the oxidative stress, muscle damage and help them in the status recovery. Recent findings: Vitamin C e vitamin E in co-administration (500 mg vitamin C with 1200 IU vitamin E per day), 6 g per day of glutamine supplementation, and 60 mL drinks per day of Turmeric Original Shot (1400 mg curcumin combined with 10 mg of piperine), were able to decrease oxidative stress and lower rates of injury. 1000 mg magnesium citrate twice a day and 5000 IU (international units) cholecalciferol supplement daily were improving the recovery status. Coenzyme Q10 100 mg twice daily and omega 3 (550 mg DHA and 550 mg EPA) proven a reduction in the levels of the muscle-damage marker. Summary: Recovery supplements should include the vitamin's C, E, and D, besides that glutamine, magnesium, and turmeric with piperine to be able supplements to help the elite soccer players recovery, decreasing oxidative stress and rates of injury.

Therapeutic Effects of Coenzyme Q10 in the Treatment of Ischemic Stroke.

Ischemic stroke is the second deadly disease worldwide, but current treatment is very limited. The brain, rich in lipids and high in oxygen consumption, is susceptible to damage from oxidative stress after ischemic stroke. Thus, antioxidants are promising neuroprotective agents for treatment and prevention of ischemic stroke. Coenzyme Q10 is the only lipophilic antioxidant that can be synthesized de novo by cells and plays a key role as an electron carrier in the oxidative phosphorylation of the mitochondrial electron transport chain. However, the reduced form of coenzyme Q10 (Ubiquinol) levels are significantly deficient in the brain. The aim of this article is to review the therapeutic effects and mechanisms of coenzyme Q10 in ischemic stroke. Current studies have found that coenzyme Q10 protects and treats ischemic stroke through multiple mechanisms based on the evidence from in vitro experiments, in vivo experiments, and clinical observations. For the first time, we reviewed the neuroprotective effects of coenzyme Q10 in ischemic stroke. Coenzyme Q10 exerts neuroprotective effects after ischemic stroke through anti-oxidative stress, anti-nitrosative stress, anti-inflammation, and anti-cell death. Here, we provided the evidence on the therapeutic and preventive effects of coenzyme Q10 in ischemic stroke and suggested the potential value of coenzyme Q10 as a medication candidate.