Administration Of Coenzyme Q10 Research Articles

Cellular oxygen consumption in patients with diabetic ketoacidosis

BackgroundDiabetic ketoacidosis (DKA) is a potentially life-threatening disorder associated with severe alterations in metabolism and acid–base status. Mitochondrial dysfunction is associated with diabetes and its complications. Thiamine and coenzyme Q10 (CoQ10) are important factors in aerobic metabolism. In this study, we measured cellular oxygen consumption rates (OCRs) and the effects of in vitro administration of thiamine and CoQ10 on OCRs in patients with DKA versus healthy controls.MethodsBlood samples were collected from a prospective cohort of patients with DKA and from controls. Cellular OCRs were measured in peripheral blood mononuclear cells (PBMC) without treatment and after treatment with thiamine, CoQ10, or both. The mitochondrial profile was measured using an XFe96 Extracellular Flux Analyzer and XF Cell Mito Stress Test Kit (Seahorse Bioscience). A linear quantile mixed model was used to compare OCRs and estimate treatment effects.ResultsA total of 62 patients with DKA and 48 controls were included in the study. The median basal and maximal OCRs were lower in the DKA group than in the control group (basal: 4.7 [IQR: 3.3, 7.9] vs. 7.9 [5.0, 9.5], p = 0.036; maximal: 16.4 [9.5, 28.1] vs. 31.5 [20.6, 46.0] pmol/min/µg protein, p < 0.001). In DKA samples, basal and maximal OCRs were significantly increased when treated with thiamine, CoQ10, or both. In controls, basal and maximal OCR were significantly increased only with thiamine treatment.ConclusionMitochondrial metabolic profiles of patients with DKA demonstrated lower cellular oxygen consumption when compared to healthy controls. Oxygen consumption increased significantly in cells of patients with DKA treated with thiamine or CoQ10. These results suggest that thiamine and CoQ10 could potentially have therapeutic benefits in DKA via their metabolic effects on mitochondrial cellular respiration.

Comparative study of the protective effects of coenzyme Q10 and cinnamon extract on possible kidney damage and dysfunction of amiodarone in rats.

An increase in free oxygen radicals and proinflammatory cytokines and decrease in intracellular adenosine triphosphate account for the nephrotoxic effect of amiodarone. This study investigated the protective effects of Coenzyme Q10 (CoQ10), cinnamon extract (CE) and the combination of the two (CoCE) on possible amiodarone-induced renal injury in rats. Thirty male albino Wistar rats were cetegorized into healthy (HG), amiodarone (ADG), CoQ10 + amiodarone (CoQA), CE + amiodarone (CEA), and CoCE + amiodarone (CoCEA) groups. First, CoQ10 (10mg/kg) and CE (100mg/kg) were orally given. After 1h, 50mg/kg amiodarone was orally given to all groups except for HG. Amiodarone, CoQ10, and CE administration was continued orally at the indicated doses once daily for 10days.Then, blood samples were collected from all groups to determine creatinine, blood urea nitrogen (BUN), and kidney injury molecule (KIM-1) levels, followed by euthanasia and removal of kidney tissues. Oxidative stress and inflammatory parameters were analysed in the tissue samples. Histopathological examination was also performed on the tissues. Amiodarone increased malondialdehyde levels and decreased total glutathione, superoxide dismutase, and catalase levels (p < 0.001). Amiodarone increased the expression and tissue levels of tissue nuclear factor kappa B, tumor necrosis factor-alpha, interleukin-1β and interleukin-6, and led to increases in serum creatinine and BUN and KIM-1 levels (p < 0.001). Amiodarone also caused histopathological damage (p < 0.001).CoQ10, CE and especially CoCE inhibited biochemical changes and tissue damage (p < 0.001). Although CoQ10, CE, and CoCE effectively prevent amiodarone-induced oxidative and inflammatory nephrotoxicity, CoCE appears to be superior.

Prenatal and progressive coenzyme Q10 administration to mitigate muscle dysfunction in mitochondrial disease.

ADCK genesencode aarF domain-containing mitochondrial kinases involved in coenzyme Q (CoQ) biosynthesis and regulation. Haploinsufficiency of ADCK2 in humans leads to adult-onset physical incapacity with reduced mitochondrial CoQ levels in skeletal muscle, resulting in mitochondrial myopathy and alterations in fatty acid β-oxidation. The sole current treatment for CoQ deficiencies is oral administration of CoQ10, which causes only partial recovery with postnatal treatment, underscoring the importance of early diagnosis for successful intervention. We used Adck2 heterozygous mice to examine the influence of this gene on muscle structure, function and regeneration throughout development, growth and ageing. This investigation involved techniques including immunohistochemistry, analysis of CoQ levels, mitochondrial respiratory content, muscle transcriptome analysis and functional tests. We demonstrated that Adck2 heterozygous mice exhibit defects from embryonic development, particularly in skeletal muscle (1102 genes deregulated). Adck2 heterozygous embryos were 7% smaller in size and displayed signs of delayed development. Prenatal administration of CoQ10 could mitigate these embryonic defects. Heterozygous Adck2 mice also showed a decrease in myogenic cell differentiation, with more severe consequences in 'aged' mice (41.63% smaller) (P<0.01). Consequently, heterozygous Adck2 mice displayed accelerated muscle wasting associated with ageing in muscle structure (P<0.05), muscle function (less grip strength capacity) (P<0.001) and muscle mitochondrial respiration (P<0.001). Furthermore, progressive CoQ10 administration conferred protective effects on mitochondrial function (P<0.0001) and skeletal muscle (P<0.05). Our work uncovered novel aspects of CoQ deficiencies, revealing defects during embryonic development in mammals for the first time. Additionally, we identified the gradual establishment and progression of the deleterious Adck2 mouse phenotype. Importantly, CoQ10 supplementation demonstrated a protective effect when initiated during development.

The State of Lipid Metabolism in Old Rats in High Altitude Conditions Against the Background of the Use of Coenzyme Q10

The problem of population aging is relevant both in Kyrgyzstan and in the global space. At the same time, the preservation of the functional capabilities of the body of elderly people living in adverse climatic conditions is of particular importance. 20-30% of the inhabitants live in the mountainous area of Kyrgyzstan at an altitude of 2000-4000 meters above sea level. It is known that in high-altitude conditions, the body is influenced by extreme factors of the highlands, which accelerate the aging process and reduce life expectancy. This article presents data from experimental studies of energy metabolism disorders in old rats and its correction of coenzyme Q10 at an altitude of 3200 m above sea level. It was found that in old rats, under conditions of short-term adaptation in the mountains, an increase in the level of total cholesterol, triglycerides and low-density lipoproteins was shown, and the level of high-density lipoproteins decreased, indicating a violation of lipid metabolism. Also, due to oxidative stress in high-altitude conditions, the level of malondialdehyde, superoxide dismutase and catalase in the blood of animals was increased. Oral administration of coenzyme Q10 at a dose of 30 mg/kg of body weight 1 time per day for 30 days to old rats led to a decrease in total cholesterol, low-density lipoproteins, triglycerides and an increase in high-density lipoproteins, due to the fact that coenzyme Q10 protects the plasma membrane of the cell from lipid peroxidation, preventing oxidative modifications lipids, which leads to a reduced risk of coronary heart disease, heart attack and stroke.

Protective Effects of Coenzyme Q10 on Testicular Histology in Rats Exposed via Chronic Mosquito Coil Smoke Inhalation.

To determine the preventive effect of coenzyme Q10 (CoQ10) on the testicular histology of rats exposed chronically to mosquito coil smoke. Experimental study. Place and Duration of the Study: Department of Anatomy, Army Medical College/National University of Medical Sciences, Rawalpindi, Pakistan, from January to December 2020. Thirty male Sprague Dawley rats were divided into three groups of 10 rats each. Group A was the healthy control. Group B rats were exposed to allethrin-based mosquito coil smoke for 12 weeks (4 hours/day). Group C rats received coenzyme Q10 (CoQ10, 10mg/kg/day) through oral gavage, in addition to 12 weeks of mosquito coil smoke exposure (4 hours/day). At the end of the study, testicular histology was compared among three groups including the germinal epithelium height, seminiferous tubule diameter, and testicular capsule thickness, while adjusting for the body weight variations among rats. The rats in Group B, exposed only to mosquito coil smoke showed testicular disruption, characterised by dilated seminiferous tubules (p <0.001), reduced germinal epithelial height (p <0.001), and thickened testicular capsule (p <0.007), as compared to the control group rats. However, the germinal epithelium height (p = 0.73) and testicular capsule thickness (p = 0.31) of rats receiving CoQ10 in addition to mosquito coil smoke inhalation were not significantly different from the control group. Prolonged inhalation of allethrin-based mosquito coil smoke can cause testicular disruption among rats. The oral CoQ10 administration can effectively prevent the histomorphological adverse effects on the testis among rats exposed to mosquito coil smoke. Allethrin, Coenzyme Q10, Germinal epithelium, Mosquito coil, Seminiferous tubules, Testicular capsule.

Oral administration of coenzyme Q10 ameliorates memory impairment induced by nicotine-ethanol abstinence through restoration of biochemical changes in male rat hippocampal tissues

Substance abuse among adolescents has become a growing issue throughout the world. The significance of research on this life period is based on the occurrence of neurobiological changes in adolescent brain which makes the individual more susceptible for risk-taking and impulsive behaviors. Alcohol and nicotine are among the most available drugs of abuse in adolescents. Prolonged consumption of nicotine and alcohol leads to drug dependence and withdrawal which induce various dysfunctions such as memory loss. Coenzyme Q10 (CoQ10) is known to improve learning and memory deficits induced by various pathological conditions such as Diabetes mellitus and Alzheimer's disease. In the present study we investigated whether CoQ10 treatment ameliorates memory loss following a nicotine-ethanol abstinence. Morris water maze and novel object recognition tests were done in male Wistar rats undergone nicotine-ethanol abstinence and the effect of CoQ10 was assessed on at behavioral and biochemical levels. Results indicated that nicotine-ethanol abstinence induces memory dysfunction which is associated with increased oxidative and inflammatory response, reduced cholinergic and neurotrophic function plus elevated Amyloid-B levels in hippocampi. CoQ10 treatment prevented memory deficits and biochemical alterations. Interestingly, this ameliorative effect of CoQ10 was found to be dose-dependent in most experiments and almost equipotential to that of bupropion and naloxone co-administration. CoQ10 treatment could effectively improve memory defects induced by nicotine-ethanol consumption through attenuation of oxidative damage, inflammation, amyloid-B level and enhancement of cholinergic and neurotrophic drive. Further studies are required to assess the unknown side effects and high dose tolerability of the drug in human subjects.

Efficacy of Kirin pill plus vitamin CE and coenzyme Q10 in the treatment of ovarian reserve hypofunction

Purpose: To investigate the efficacy of Kirin pill plus vitamin CE and coenzyme Q10 in the treatment of diminished ovarian reserve (DOR). &#x0D; Methods: 145 patients with ovarian reserve hypofunction hospitalized in Xiangyang Central Hospital, Xiangyang City, China from March 2019 to March 2022 were recruited and assigned randomly to receive either vitamin CE and coenzyme Q10 (control group), or vitamin CE and coenzyme Q10 plus Kirin pills (study group). The parameters/indices determined include menstrual recovery, clinical efficacy, sex hormone and serum anti-mullerian hormone (AMH) levels, changes in the number of ovarian sinus follicles, and levels of CD3+, CD4+ and CD8+ T cell. &#x0D; Results: There were no significant differences (p &gt; 0.05) observed among baseline data, pre-treatment sex hormones, serum AMH, ovarian antral follicle count, CD3+, CD4+, and CD8+ T cell levels. After the intervention, administration of the Kirin pill resulted in significantly lower serum follicle stimulating hormone (FSH) and FSH/luteinizing hormone (LH), elevated AMH levels, and better LH and estradiol (E2) levels in patients compared to the administration of vitamin CE and coenzyme Q10 (control group). The study group also showed superior ovarian reserve function and more ovarian basal sinus follicles than the control group (p &lt; 0.05). &#x0D; Conclusion: Kirin pill plus vitamin CE and coenzyme Q10 treatment regimen optimizes the ovarian reserve function of patients with DOR infertility by improving basal sex hormones, menstrual cycle and menstrual volume, AMH and ovarian basal sinus follicle count. Further clinical trials are required prior to application in clinical practice.

Coenzyme Q10 supplementation in burn patients: a double-blind placebo-controlled randomized clinical trial

BackgroundBurn injuries are important medical problems that, aside from skin damage, cause a systemic response including inflammation, oxidative stress, endocrine disorders, immune response, and hypermetabolic and catabolic responses which affect all the organs in the body. The aim of this study was to determine the effect of coenzyme Q10 (CoQ10) supplementation on inflammation, oxidative stress, and clinical outcomes in burn patients.MethodsIn a double-blind placebo-controlled randomized clinical trial, 60 burn patients were randomly assigned to receive 100 mg CoQ10 three times a day (total 300 mg/day) or a placebo for 10 days. Inflammatory markers including erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), oxidative stress markers including total antioxidant capacity (TAC), malondialdehyde (MDA) and superoxide dismutase (SOD) activity, fasting blood glucose (FBG), blood urea nitrogen (BUN), creatinine, white blood cells (WBC), and body temperature were assessed as primary outcomes and albumin, prothrombin time (PT), partial thromboplastin time (PTT), international normalized ratio (INR), other hematological parameters, blood pressure, O2 saturation, ICU duration, and 28-mortality rate were assessed as secondary outcomes.ResultsFifty-two participants completed the trial. CRP and ESR levels were not significantly different between CoQ10 and placebo groups at the end of the study (P = 0.550 and P = 0.306, respectively). No significant differences between groups were observed for TAC (P = 0.865), MDA (P = 0.692), and SOD activity (P = 0.633) as well. Administration of CoQ10 resulted in a significant increase in albumin levels compared to placebo (P = 0.031). There was no statistically significant difference between the two groups in other measured outcomes (P > 0.05).ConclusionResults showed that in patients with burn injury, CoQ10 administration had no effect on inflammatory markers and oxidative stress, although serum albumin levels were improved after supplementation. Further studies with albumin as the primary outcome are needed to confirm this finding.

Evaluate The Effect of Coenzyme Q10 on The Prevention of Doxorubicin-Induced Acute Cardiotoxicity in Rats.

Objective: This study will evaluate the potential protective effects of coenzyme Q10 on DOX-induced cardiotoxicity in female rats, manifested by changes in biochemical parameters in tissue and serum samples histopathological differences, and compare their changes. Methods:24 female rats were divided into three groups based on weight. The first group received saline, the second group received a cumulative dose of 15 mg/kg of DOX via IP injection, and the third group was pre-treated with CoQ10 before receiving DOX. The data were analysed using a one-way ANOVA test with a Bonferroni post hoc test to compare the markers and histopathological changes in different groups. The GraphPad Prism version 8.1 was used to do the statistical analysis. Results: As indicated by a statistically significant increase (P&lt;0.0001) in TNFα and ICAM-1 level, doxorubicin-induced cardiotoxicity. Additionally, the level of GSH, SOD, and caspase-3 did not differ significantly between the DOX+CoQ10 group and the control group. Furthermore, lesions and histological alterations were induced by the substance. Significant reductions in cardiotoxicity were observed with the administration of coenzyme Q10, as indicated by notable increases (P&lt;0.0001) in SOD, GSH, and TNFα and significant decreases (P&lt;0.0001) in caspase 3 when compared to the DOX group. Also, the CMYO score and lesions exhibited a substantial improvement. Conclusion: In this investigation, coenzyme Q10 exhibited cardioprotective effects against DOX-induced damage to the mouse heart. This phenomenon potentially pertains to inhibiting and safeguarding against oxidative stress, the pathway of apoptosis, and the inflammatory response.

COENZYME Q10 EFFECT ON NMDA RECEPTOR EXPRESSION AND RETINAL GANGLION CELL DENSITY (Experimental Study in Traumatic Optic Neuropathy Model of Wistar Rat)

Abstract&#x0D; Introduction &amp; Objectives : Traumatic optic neuropathy is a visual disturbance condition after acute injury to optic nerve. This injury results in retinal ganglion cells ischemic leading to excitotoxicity and apoptosis. Coenzyme Q10 (CoQ10) is an antioxidant and cofactor in electron transport within mitochondria that inhibits glutamate excitotoxicity and thereby preventing retinal ganglion cell apoptosis. This research aims to prove the effect of coenzyme Q10 on NMDA receptor expression and retinal ganglion cell density in rat model of traumatic optic neuropathy.&#x0D; Methods : This study use post-test only randomized controlled groups design. Traumatic optic neuropathy wistar rats model was made by optic nerve crushed method, then given oral CoQ10 100mg/kgBW after 1 hour for 14 days in treatment group. Retinal histopathological specimen was made with immunohistochemistry and Haematoxyllin-eosin staining and examined under microscope with 400x magnification. Data was verified and statistically analyzed.&#x0D; Results : The NMDA receptor expression in the treatment group was significantly lower than control (p=0.009). The retinal ganglion cell density in the treatment group was significantly higher than control (p=0.009). There was a significant correlation between NMDA receptor expression and retinal ganglion cell density in the treatment group (p = 0.012) with a strong negative correlation direction (r = - 0.652).&#x0D; Conclusion : Administration of CoQ10 in traumatic optic neuropathy model rats affects NMDA receptor expression and retinal ganglion cell density. NMDA receptor expression was lower with higher retinal ganglion cell density in the treatment group. NMDA receptor expression was inversely proportional to retinal ganglion cell density in the treatment group.

Coenzyme Q10 mitigates macrophage mediated inflammation in heart following myocardial infarction via the NLRP3/IL1β pathway

BackgroundThe protective effect of Coenzyme Q10 (CoQ10) on the cardiovascular system has been reported, however, whether it can promote early recovery of cardiac function and alleviate cardiac remodeling after myocardial infarction (MI) remains to be elucidated. Whether CoQ10 may regulate the macrophage-mediated pro-inflammatory response after MI and its potential mechanism are worth further exploration.MethodsTo determine the baseline plasma levels of CoQ10 by LC-MS/MS, healthy controls and MI patients (n = 11 each) with age- and gender-matched were randomly enrolled. Additional MI patients were consecutively enrolled and randomized into the blank control (n = 59) or CoQ10 group (n = 61). Follow-ups were performed at 1- and 3-month to assess cardiac function after percutaneous coronary intervention (PCI). In the animal study, mice were orally administered CoQ10/vehicle daily and were subjected to left anterior descending coronary artery (LAD) ligation or sham operation. Echocardiography and serum BNP measured by ELISA were analyzed to evaluate cardiac function. Masson staining and WGA staining were performed to analyze the myocardial fibrosis and cardiomyocyte hypertrophy, respectively. Immunofluorescence staining was performed to assess the infiltration of IL1β/ROS-positive macrophages into the ischemic myocardium. Flow cytometry was employed to analyze the recruitment of myeloid immune cells to the ischemic myocardium post-MI. The expression of inflammatory indicators was assessed through RNA-seq, qPCR, and western blotting (WB).ResultsCompared to controls, MI patients showed a plasma deficiency of CoQ10 (0.76 ± 0.31 vs. 0.46 ± 0.10 µg/ml). CoQ10 supplementation significantly promoted the recovery of cardiac function in MI patients at 1 and 3 months after PCI. In mice study, compared to vehicle-treated MI mice, CoQ10-treated MI mice showed a favorable trend in survival rate (42.85% vs. 61.90%), as well as significantly alleviated cardiac dysfunction, myocardial fibrosis, and cardiac hypertrophy. Notably, CoQ10 administration significantly suppressed the recruitment of pro-inflammatory CCR2+ macrophages into infarct myocardium and their mediated inflammatory response, partially by attenuating the activation of the NLR family pyrin domain containing 3 (NLRP3)/Interleukin-1 beta (IL1β) signaling pathway.ConclusionsThese findings suggest that CoQ10 can significantly promote early recovery of cardiac function after MI. CoQ10 may function by inhibiting the recruitment of CCR2+ macrophages and suppressing the activation of the NLRP3/IL1β pathway in macrophages.Trial registrationDate of registration 09/04/2021 (number: ChiCTR2100045256).

Prospects of Intravenous Coenzyme Q10 Administration in Emergency Ischemic Conditions.

Coenzyme CoQ10 (CoQ10) is an endogenous lipid-soluble antioxidant that effectively protects lipids, proteins, and DNA from oxidation due to its ability to undergo redox transitions between oxidized and reduced forms. Various oxidative stress-associated infectious and somatic diseases have been observed to disrupt the balance of CoQ10 concentration in tissues. As a high molecular weight polar lipophilic compound, CoQ10 exhibits very limited oral bioavailability, which restrains its therapeutic potential. Nevertheless, numerous studies have confirmed the clinical efficacy of CoQ10 therapy through oral administration of high doses over extended time periods. Experimental studies have demonstrated that in emergency situations, intravenous administration of both oxidized and reduced-form CoQ10 leads to a rapid increase in its concentration in organ tissues, offering protection for organ tissues in ischemic conditions. This suggests that the cardio- and neuroprotective efficacy of intravenously administered CoQ10 forms could present new opportunities in treating acute ischemic conditions. Based on these findings, the review provides reasoning supporting further research and implementation of CoQ10 dosage forms for intravenous administration in emergency situations into clinical practice.

Evaluation of the protective effect of coenzyme Q10 on hepatotoxicity caused by acute phosphine poisoning.

Background: Aluminum phosphide (AlP) poisoning is prevalent in numerous countries, resulting in high mortality rates. Phosphine gas, the primary agent responsible for AlP poisoning, exerts detrimental effects on various organs, notably the heart, liver and kidneys. Numerous studies have documented the advantageous impact of Coenzyme Q10 (CoQ10) in mitigating hepatic injuries. The objective of this investigation is to explore the potential protective efficacy of CoQ10 against hepatic toxicity arising from AlP poisoning. Method: The study encompassed distinct groups receiving almond oil, normal saline, exclusive CoQ10 (at a dosage of 100mg/kg), AlP at 12mg/kg; LD50 (lethal dose for 50%), and four groups subjected to AlP along with CoQ10 administration (post-AlP gavage). CoQ10 was administered at 10, 50, and 100mg/kg doses via Intraparietal (ip) injections. After 24h, liver tissue specimens were scrutinized for mitochondrial complex activities, oxidative stress parameters, and apoptosis as well as biomarkers such as aspartate transaminase (AST) and alanine transaminase (ALT). Results: AlP induced a significant decrease in the activity of mitochondrial complexes I and IV, as well as a reduction in catalase activity, Ferric Reducing Antioxidant Power (FRAP), and Thiol levels. Additionally, AlP significantly elevated oxidative stress levels, indicated by elevated reactive oxygen species (ROS) production, and resulted in the increment of hepatic biomarkers such as AST and ALT. Administration of CoQ10 led to a substantial improvement in the aforementioned biochemical markers. Furthermore, phosphine exposure resulted in a significant reduction in viable hepatocytes and an increase in apoptosis. Co-treatment with CoQ10 exhibited a dose-dependent reversal of these observed alterations. Conclusion: CoQ10 preserved mitochondrial function, consequently mitigating oxidative damage. This preventive action impeded the progression of heart cells toward apoptosis.

Effects of antioxidant treatment on cell differentiation in rabbit embryos

The antioxidant coenzyme Q10 can influence the expression of genes involved in apoptosis and energy metabolism of oocytes and quercetin can improve oocyte maturation and early embryonic development. In this study, the gene expression of GATA6 and NANOG in rabbit embryos was assessed using the qRT-PCR reaction. The groups were: group A- control group (no treatment added), group B (hormonal treatment of superovulation, which included the administration of PMSG and hCG), group C (administration of quercitin) and group D (administration of Coenzyme Q10). Our results show that the expression of the two genes was different depending on both the stage of embryonic development and the treatment administered. The highest values of gene expression for GATA6 and NANOG were obtained in groups 2, 4, 7, 8 and 9, corresponding to morula and blastocyst stages. In addition to the fact that NANOG and GATA6 are factors that are involved in early embryonic development, we believe that the administration of extrapituitary gonadotropins and antioxidants contributed to the increase in gene expression.

RETRACTED: Coenzyme Q10 attenuates neurodegeneration in the cerebellum induced by chronic exposure to tramadol

BackgroundChronic use of tramadol can cause neurotoxic effects and subsequently cause neurodegeneration in the cerebellum. The main damage mechanisms identified are oxidative stress and inflammation. Currently, we investigated the effects of coenzyme Q10 (CoQ10) in attenuates of neurodegeneration in the cerebellum induced by chronic exposure to tramadol. Material and methodsSeventy-two male mature albino rats were allocated into four equal groups, including; non-treated group, CoQ10 group (which received CoQ10 at 200 mg/kg/day orally for three weeks), tramadol group (which received tramadol hydrochloride at 50 mg/kg/day orally for three weeks), and tramadol+CoQ10 group (which received tramadol and CoQ10 at the same doses as the previous groups). Tissue samples were obtained for stereological, immunohistochemical, biochemical, and molecular evaluations. Also, functional tests were performed to evaluate behavioral properties. ResultsWe found a significant increase in stereological parameters, antioxidant factors (catalase, glutathione, and superoxide dismutase), and behavioral function scores in the tramadol+CoQ10 group compared to the tramadol group (p < 0.05). In addition, malondialdehyde levels, the density of apoptotic cells, as well as the expression of pro-inflammatory (tumor necrosis factor-alpha, interleukin 1 beta, and interleukin 6) and autophagy (lysosome-associated membrane protein 2, autophagy-related 5, beclin 1, and autophagy-related 12) genes were considerably reduced in the tramadol+CoQ10 group compared to the tramadol group (p < 0.05). ConclusionWe conclude that the administration of CoQ10 has neuroprotective effects in the cerebellum of rats that have chronic exposure to tramadol.

Investigación del efecto de la coenzima Q10 sobre el daño testicular inducido por ciclofosfamida en ratas macho

Cyclophosphamide (CP) is one of the frequently preferred chemotherapeutic agents Worldwide. CP has negative effects on the testes, spermatogenesis, and reproductive hormones. The aim of this study was to determine the protective effect of Coenzyme Q10 (CoQ10) on the damage caused by CP. CoQ10 is use in the treatment of infertility problems and is naturally found in the testes and seminal fluid. Thirty–six Albino Wistar male rats were divided into six groups (Control, Sham, Cyclophosphamide (CP), Coenzyme Q10 (CoQ10), CP + CoQ10 I, CP + CoQ10 II), with six animals in each group. Semen analysis included investigations of sperm DNA damage, motility, abnormal sperm ratio, and density. Histopathological examination and assessment of oxidative stress parameters in the testes were conducted. Additionally, serum levels of FSH, LH, and Testosterone were measured. CoQ10 administration increased the motility rate, density, and Testosterone levels in testicular damage caused by CP (P&lt;0.05). Furthermore, it was observed that the abnormal sperm ratio, sperm DNA damage, and oxidative stress were reduced (P&lt;0.05). Based on the results of this study, the use of CoQ10 in conjunction with CP has the potential to alleviate male infertility problems that may arise from CP administration.

The Effect Of Coenzim Q10 On The Number Of Lymfocite Cells In Male Wistar Rats With Periodontitis

Periodontal disease is a dental and oral health problem in adult society. One of the periodontal diseases is periodontitis which is an inflammation of the periodontal tissue caused by accumulation of dental plaque which can lead to impaired masticatory function, tooth loss, alveolar bone damage, periodontal ligament damage, pocket formation, and gingival recession. Coenzyme Q10 acts as an antioxidant, the reduced form is ready to give electrons to deactivate ROS or block free radicals which can prevent oxidative stress thereby protecting lymphocyte cells and reducing the immune response which can lead to a reduction in inflammation in the periodontal tissues. The purpose of this study was to determine the effect of coenzyme Q10 on the number of lymphocyte cells in the gingiva of male wistar rats with periodontitis. The research method used is true experimental laboratory quantitative research with a research design that is a posttest only control group design with observation or observing the control group and the treatment group. The number of samples used was 24 rats. Observation of lymphocyte cells was carried out using a light microscope with a magnification of 200x and a magnification of 400x and then counted manually by the observer. The results showed that the significance value obtained in the One-Way ANOVA test was 0.000 (&lt;0.05). Then, based on the results of the Post Hoc Least Significant Difference (LSD) test, it was found that the biggest difference in effect was in the K(-)5 group and the P5 group, where the difference was 59.00 with a significance value of 0.000 (&lt;0.05). It can be concluded that there is an effect of coenzyme Q10 administration on the number of lymphocyte cells in the gingiva of male Wistar rats with periodontitis.

Effects of coenzyme Q10 in a propofol infusion syndrome model of rabbits.

Coenzyme Q (CoQ) might be the main site of interaction with propofol on the mitochondrial respiratory chain in the propofol infusion syndrome (PRIS) because of the structural similarity between coenzyme Q10 (CoQ10) and propofol. To investigate the effects of CoQ10 on survival and organ injury in a PRIS model in rabbits. Sixteen male New Zealand white rabbits were divided into 4 groups: (1) propofol infusion group, (2) propofol infusion and CoQ10, 100 mg/kg was administered intravenously, (3) sevoflurane inhalation was administered, and (4) sevoflurane inhalation and CoQ10, 100 mg/kg intravenously, was administered. Arterial blood gas and biochemical analyses were repeated every 2 h and every 12 h, respectively. Animals that were alive on the 24th hour after anesthesia induction were euthanized. The organ damages were investigated under light and transmission electron microscopy (TEM). The propofol infusion group had the highest troponin T levels when compared with the other three groups at the 12th hour. The propofol + CoQ10 group had lower troponin T levels when compared with the propofol and sevoflurane groups (P < 0.05). Administration of CoQ10 decreased total liver injury scores and total organ injury scores both in the propofol and sevoflurane groups. The propofol and sevoflurane organ toxicities were attenuated with CoQ10 in liver, gallbladder, urinary bladder, and spleen. The addition of CoQ10 to propofol and sevoflurane anesthesia prevented the propofol-associated increase in troponin T levels at the 12th hour of infusion and decreased anesthetic-induced total liver and organ injury scores.

Coenzyme Q 10 in Infertile Men with Idiopathic Asthenozoospermia: A Single Blind Placebo-Controlled, Randomized Trial

Background: Many studies have focused on male infertility. There is limited evidence about the influence of nutrition on quality of semen. Accumulating evidence suggests that oxidative stress plays an important role in the development of male infertility and recently antioxidants have been tried to treat men with idiopathic infertility. Objective: To evaluate the effectiveness of coenzyme Q-10 treatment in improving sperm motility in men with idiopathic asthenozoospermia. Methods: This randomized controlled study conducted in the Department of Reproductive Endocrinology and Infertility, Bangabandhu Sheikh Mujib Medical University (BSMMU), Dhaka, from January 2021 to December 2021. Total 74 diagnosed cases of idiopathic asthenozoospermia were selected for medication was included in this study. Eligible man who gave their informed consent was allocated into either Group A (Coenzyme Q-10) or Group B (Placebo) on the basis of computer generated table. Group A received coenzyme Q-10 100 mg two times daily and Group B received placebo for same doses for 12 weeks. Then pretreatment and post treatment semen parameters, including sperm concentration, total motility, progressive motility and morphology was assessed. Results: Post treatment motility (37.8±11.1 vs 26.3±8.8%), progressive motility (30.0±7.9 vs 22.4±7.7) and total motile sperm count (33.5±24.4 vs 21.4±14.3 million) were significantly higher in coenzyme Q-10 group than placebo group (p&lt;0.05). In coenzyme Q-10 group, motility (37.8±11.1 vs 25.2±8.1%), progressive motility (30.0±7.9 vs 22.5±7.0) and total motile sperm count (33.5±24.4 vs 20.0±13.6 million) were significantly increased in post treatment than pretreatment patients (p&lt;0.05), but not found in placebo group. Improvement of sperm motility was significantly higher in coenzyme Q-10 group than placebo group (60.0% vs 5.6%). Conclusion: In conclusion, coenzyme Q10 administration, total motility, progressive motility and total motile sperm count were .....

Coenzyme Q10 exhibits anti-inflammatory and immune-modulatory thereby decelerating the occurrence of experimental cerebral malaria

Cerebral Malaria (CM) is associated with the complex neurological syndrome, whose pathology is mediated by severe inflammatory processes following infection with Plasmodium falciparum. Coenzyme-Q10 (Co-Q10) is a potent anti-inflammatory, anti-oxidant, and anti-apoptotic agent with numerous clinical applications. The aim of this study was to elucidate the role of oral administration of Co-Q10 on the initiation or regulation of inflammatory immune response during experimental cerebral malaria (ECM). For this purpose, the pre-clinical effect of Co-Q10 was evaluated in C57BL/6 J mice infected with Plasmodium berghei ANKA (PbA). Treatment with Co-Q10 resulted in the reduction of infiltrating parasite load, greatly improved the survival rate of PbA-infected mice that occurred independent of parasitaemia and prevented PbA-induced disruption of the blood-brain barrier (BBB) integrity. Exposure to Co-Q10 resulted in the reduction of infiltration of effector CD8 + T cells in the brain and secretion of cytolytic Granzyme B molecules. Notably, Co-Q10-treated mice had reduced levels of CD8 +T cell chemokines CXCR3, CCR2, and CCR5 in the brain following PbA-infection. Brain tissue analysis showed a reduction in the levels of inflammatory mediators TNF- α, CCL3, and RANTES in Co-Q10 administered mice. In addition, Co-Q10 modulated the differentiation and maturation of both splenic and brain dendritic cells and cross-presentation (CD8α+DCs) during ECM. Remarkably, Co-Q10 was very effective in decreasing levels of CD86, MHC-II, and CD40 in macrophages associated with ECM pathology. Exposure to Co-Q10 resulted in increased expression levels of Arginase-1 and Ym1/chitinase 3–like 3, which is linked to ECM protection. Furthermore, Co-Q10 supplementation prevented PbA-induced depletion of Arginase and CD206 mannose receptor levels. Co-Q10 abrogated PbA-driven elevation in pro-inflammatory cytokines IL-1β, IL-18, and IL-6 levels. In conclusion, the oral supplementation with Co-Q10 decelerates the occurrence of ECM by preventing lethal inflammatory immune responses and dampening genes associated with inflammation and immune-pathology during ECM, and offers an inimitable opening for developing an anti-inflammatory agent against cerebral malaria.