Protective Effect Of Coenzyme Q10 Research Articles

The Effects of Ubiquinone on the Antioxidant System in Male Rats Exposed to Saccharin-Induced the Hepatic Toxicity

Saccharin (Sac) is a widely used artificial sweetener with significant applications in the food industry, pharmaceutical formulations, and tobacco products. Despite its popularity, saccharin has drawn attention due to its potential carcinogenic effects and associations with various health risks, including renal impairment, hepatic dysfunction, obesity, and diabetes. This study aimed to investigate the protective effects of Ubiquinone, or coenzyme Q10 (COQ10), on liver toxicity induced by saccharin, focusing on oxidative stress and antioxidant markers. In this experiment, rats were divided into six groups of ten. The control group received no treatment, while the second group was administered COQ10 at a dosage of 20 mg per kilogram of body weight. The third and fourth groups were given saccharin at 1/10 and 1/20 of the lethal dose 50 (LD50), respectively. The fifth and sixth groups received saccharin at the same dosages as the third and fourth groups, but with additional COQ10 supplementation. All treatments were administered orally for 30 days, after which liver tissues were collected to assess oxidative stress and antioxidant markers. The results revealed that saccharin significantly increased oxidative stress in the liver, as evidenced by elevated levels of malondialdehyde (MDA) and oxidized glutathione (GSSG). Additionally, saccharin-treated groups exhibited a marked decrease in antioxidant markers, including reduced glutathione (GSH) and superoxide dismutase (SOD). However, the groups that received COQ10 alongside saccharin showed significant improvement, with oxidative stress and antioxidant levels nearly returning to those observed in the control group. These findings suggest that saccharin consumption promotes the generation of reactive oxygen species and contributes to liver damage, characterized by necrotic hepatocytes, sinusoidal dilatation, and inflammatory infiltration. The protective effects of COQ10 in mitigating saccharin-induced oxidative stress highlight its potential as a therapeutic agent for preventing liver damage associated with saccharin intake.

Protective Effect of Coenzyme Q10 in Children with Heart Failure

Background: Heart failure is considered a health problem caused by its high mortality, morbidity and high costs of care. The causes of Heart Failure in children differ from that of adults, with the most frequent causes in children being congenital heart disease and cardiomyopathy. Coenzyme Q10 acts as an energy transfer molecule, occurring in organs with high metabolic levels, such as the heart, kidneys and liver. Methodology: A narrative review was carried out through various databases from January 2005 to January 2021; the search and selection of articles was carried out in journals indexed in English. The following keywords were used: Coenzyme Q10, children, Heart Failure, Pediatrics. Results: Supplementation with Coenzyme Q10 has beneficial effects on different etiological variants of heart failure in children, thanks to the prevention of oxidative damage to the defective myocardium, as well as the increase in bioenergetics and its strong antioxidant properties, provided by its important role as an electron carrier in the transport chain. Conclusion: This review offers recommendations to use Coenzyme Q10 as a complementary treatment in Heart Failure in different etiological variants.

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.

Evaluation of the protective effect of coenzyme Q10 against x-ray irradiation-induced ovarian injury.

This study focused on the anti-oxidant and anti-apoptotic effects of CoQ10 in ovaries exposed to pelvic radiation. Thirty-two female rats were randomly assigned into four groups. Group I (control group), Group II: Only 2 Gy pelvic x-ray irradiation (IR) was administered as a single fractioned dose. Group III: 30 mg/kg CoQ10 was administered by oral gavage +2 Gy pelvic IR. Group IV: 150 mg/kg CoQ10 was administered by oral gavage +2 Gy pelvic IR. CoQ10 treatment was started 7 days before pelvic IR and completed 7 days later. The rats in Group III and IV were treated with CoQ10 for a total of 14 days. Histopathological analysis showed severe damage to the ovarian tissue in the radiation group, while both doses of CoQ10 showed normal histological structure. Likewise, while there was a high level of staining in the IR group for necrosis and apoptosis, the CoQ10 treated ones were like the control group. Tissue Malondialdehyde (MDA) levels were like the control group in the low-dose CoQ10 group, while the MDA levels of the high dose CoQ10 group were similar to the radiation group. Usage of low-dose CoQ10 has a radioprotective effect on radiation-induced ovarian damage. Although the use of high doses is morphologically radioprotective, no antioxidative effect was observed in the biochemical evaluation.

The Protective Effects of High-Intensity Interval Training Combined with Q10 Supplementation on Learning and Memory Impairments in Male Rats with Amyloid-β-Induced Alzheimer's Disease.

Oxidative stress plays a major role in the progression of Alzheimer's disease (AD)-related cognitive deficits. This study was done to determine the protective effects of coenzyme Q10 (CoQ10) and high-intensity interval training (HIIT) alone and in combination for eight continuous weeks, on oxidative status, cognitive functions, and histological changes in the hippocampus in amyloid-β (Aβ)-induced AD rats. Ninety male Wistar rats were randomly assigned to the sham, control, Q10 (50 mg/kg of CoQ10; P.O.), HIIT (high intensity: 4 min running at 85-90% VO2max, low intensity: 3 min running at 50-60% VO2max), Q10 + HIIT, AD, AD+Q10, AD+HIIT, and AD+Q10 + HIIT groups. The results showed that Aβ injection reduced cognitive functions in the Morris water maze (MWM) test and recognition memory in the novel object recognition test (NORT), which was accompanied by a decrease in total thiol groups, catalase, and glutathione peroxidase activities, an increase in malondialdehyde levels, and neuronal loss in the hippocampus. Interestingly, pretreatment with CoQ10, HIIT, or both, could markedly improve the oxidative status and cognitive decline in the MWM and NOR tests, and hinder neuronal loss in the hippocampus of Aβ-induced AD rats. Therefore, a combination of CoQ10 and HIIT can improve Aβ-related cognitive deficits, probably through an amelioration in hippocampal oxidative status and prevention of neuronal loss.

Protective effect of co-enzyme Q10 on testicular tissue and sperm parameters in adult male rats treated with Sunset Yellow FCF

Objective: To determine the protective effect of co-enzyme Q10 (CoQ10) on testicular tissue and sperm parameters in male rats treated with Sunset Yellow FCF. Methods: Sixty male Sprague-Dawley rats were randomly divided into 6 groups of the control, CoQ10 (10 mg/kg/day), low dose of Sunset Yellow (2.5 mg/kg), high dose of Sunset Yellow (70 mg/kg), low dose of Sunset Yellow (2.5 mg/kg) plus CoQ10, and high dose of Sunset Yellow (70 mg/kg) plus CoQ10. The drugs were administered via daily oral gavages for 6 weeks. At the end of the experiment, sperm analysis, stereological and histological assessments of the testis were carried out. Results: The normal morphology (by 41.1%) and progressive spermatozoa (by 74.8%), testicle volume (by 33.4%), lumen volume (by 38.3%), interstitial tissue volume (by 44.7%), seminiferous tubule volume (by 40.7%), and number of spermatogonia (by 53.9%) and Leydig cells (by 70.7%) reduced in the rats that received high doses of Sunset Yellow in comparison to the control group. Nonetheless, all these alterations were recovered by CoQ10 treatment in the CoQ10 plus high dose of Sunset Yellow group. Furthermore, low doses of Sunset Yellow did not affect different parameters of the testis and sperm. Conclusions: CoQ10 could, to some extent, prevent structural changes of the testis induced by the high dose of Sunset Yellow.

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 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).

Protective effect of coenzyme Q10 in cyclophosphamide-induced kidney damage in rats.

We aimed to investigate the effect of coenzyme q10 on cyclophosphamide-induced kidney damage in rats. A total of 30 female Wistar-Albino rats were utilized to form three groups. In group 1 (control group) (n=10), no drugs were given. In group 2 (cyclophosphamide group) (n=10), 30 mg/kg intraperitoneal cyclophosphamide was administered for 7 days. In group 3 (cyclophosphamide+coenzyme q10 group) (n=10), 30 mg/kg cyclophosphamide and 10 mg/kg coenzyme q10 were given for 7 days via intraperitoneal route. Right kidneys were removed in all groups. Blood malondialdehyde levels and activities of catalase and superoxide dismutase were measured. Histopathological damage was evaluated by examining the slides prepared from kidney tissue using a light microscope. Tissue damage was significantly higher in the cyclophosphamide group than in the cyclophosphamide+coenzyme q10 group (p<0.05). The malondialdehyde levels were significantly higher and the activities of superoxide dismutase and catalase were lower in the cyclophosphamide group than in the cyclophosphamide+coenzyme q10 group (p<0.05). Coenzyme q10 may be a good option to prevent cyclophosphamide-induced kidney damage.

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.

Coenzyme Q10-Loaded Albumin Nanoparticles Protect against Redox Imbalance and Inflammatory, Apoptotic, and Histopathological Alterations in Mercuric Chloride-Induced Hepatorenal Toxicity in Rats.

Exposure to mercuric chloride (HgCl2), either accidental or occupational, induces substantial liver and kidney damage. Coenzyme Q10 (CoQ10) is a natural antioxidant that also has anti-inflammatory and anti-apoptotic activities. Herein, our study aimed to investigate the possible protective effects of CoQ10 alone or loaded with albumin nanoparticles (CoQ10NPs) against HgCl2-induced hepatorenal toxicity in rats. Experimental animals received CoQ10 (10 mg/kg/oral) or CoQ10NPs (10 mg/kg/oral) and were injected intraperitoneally with HgCl2 (5 mg/kg; three times/week) for two weeks. The results indicated that CoQ10NP pretreatment caused a significant decrease in serum liver and kidney function markers. Moreover, lowered MDA and NO levels were associated with an increase in antioxidant enzyme activities (SOD, GPx, GR, and CAT), along with higher GSH contents, in both the liver and kidneys of intoxicated rats treated with CoQ10NPs. Moreover, HgCl2-intoxicated rats that received CoQ10NPs revealed a significant reduction in the hepatorenal levels of TNF-α, IL-1β, NF-κB, and TGF-β, as well as an increase in the hepatic level of the fibrotic marker (α-SMA). Notably, CoQ10NPs counteracted hepatorenal apoptosis by diminishing the levels of Bax and caspase-3 and boosting the level of Bcl-2. The hepatic and renal histopathological findings supported the abovementioned changes. In conclusion, these data suggest that CoQ10, alone or loaded with albumin nanoparticles, has great power in reversing the hepatic and renal tissue impairment induced by HgCl2 via the modulation of hepatorenal oxidative damage, inflammation, and apoptosis. Therefore, this study provides a valuable therapeutic agent (CoQ10NPs) for preventing and treating several HgCl2-induced hepatorenal disorders.

P26-09: Protective effects of coenzyme Q10 and idebenone on ethanol induced liver fibrosis through inhibiting NLRP3/Caspase-1/IL-1β inflammasome pathway

P26-09: Protective effects of coenzyme Q10 and idebenone on ethanol induced liver fibrosis through inhibiting NLRP3/Caspase-1/IL-1β inflammasome pathway

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.

Post-Weaning Exposure to Sunset Yellow FCF Induces Changes in Testicular Tight and Gap Junctions in Rats: Protective Effects of Coenzyme Q10.

Studies on adverse health consequences of azo dyes are limited and conflicting. Coenzyme Q10 (CoQ10) supplementation has been shown to have benefits associated with antioxidant and anti-inflammatory characteristics on several body systems. This work investigates the possible toxic effects of the widely used food additive sunset yellow and the probable protective effects of CoQ10 on testicular tight and gap junctions in rats by assessing molecular, immunohistochemical, and histopathological changes. Sixty Sprague-Dawley male weanling rats were randomly divided into six groups (n = 10). The rats received their treatments via daily oral gavages for 6weeks. The treatments included as follows: low dose of sunset yellow (SY-LD) (2.5mg/kg/day), high dose of sunset yellow (SY-HD) (70mg/kg/day), CoQ10 (10mg/kg/day), CoQ10 with low dose of sunset yellow (CoQ10 + LD), CoQ10 with high dose of sunset yellow (CoQ10 + HD), and distilled water as the control treatment. At the end of the experiment, the rats were anesthetized, and the testes were removed for molecular (real-time quantitative PCR), immunohistochemical, and histopathological (H & E staining) assessments. Claudin 11 and occludin gene expression significantly decreased in HD and CoQ10 + HD groups compared with the controls. Connexin 43 (Cx43) expression in the control and CoQ10 groups was significantly higher than in the HD group. The immunohistochemical and histopathological data were largely in line with these findings. The results showed that exposure to a high dose of sunset yellow led to disturbances in cell-to-cell interactions and testicular function. Simultaneous treatment with CoQ10 had some beneficial effects but did not completely improve these undesirable effects.

Coenzyme Q10 and N-acetyl cysteine modulates the haematological parameters, markers of oxidative stress and membrane bound phosphatase in spleen toxicity induced by aniline hydrochloride

Aniline is widely used chemical for industrial purpose. Exposure to aniline can lead to various health issues in human being. The most common toxic effect of aniline is splenotoxicity which is produced via the generation of oxidative stress. The present study examines the protective effect of coenzyme Q10 and N-acetyl cysteine on spleen weight, body weight, endogenous antioxidants and membrane bound ATPases in aniline hydrochloride (AH) induced spleen toxicity in rats. Adult male albino rats were divided into five groups, each group consists of six rats. Toxicity was induced by administration of AH (100 ppm, p. o) in drinking water for 30 days. Body weight, markers of oxidative stress and haematological parameters were assessed at the end of treatment period. Treatment rats received Coenzyme Q10 (CoQ10, 10 mg/kg/day/p.o) and N- acetyl cysteine (NAC, 300mg/kg/ day p.o) alone and in combination for 30. AH toxic rats showed a significant elevation of spleen weight, WBC count, iron content, LPO level, NO level and Ca ATPase whereas a significant decrease in body weight, haemoglobin, RBCs level, Protein content, GSH and Na/ K and Mg ATPase were observed. Administration of Coenzyme Q10 (CoQ10, 10 mg/kg/day/p.o) and N- acetyl cysteine (NAC, 300mg/kg/ day p.o) together for 30 consecutive days shows a significant decrease in spleen weight, WBC level, iron content, LPO level, NO level whereas significant increase in body weight, hemoglobin level, RBCs level Protein content, GSH level, Na/ K ATPase, Ca and Mg ATPase when compared with aniline treated group and CoQ10 or NAC alone treated groups. These findings indicate the synergistic &amp; protective effect of CoQ10 and NAC in aniline induced spleen toxicity in rats compared to alone antioxidants.

Role of Gender in the Protection Against Doxorubicin-Induced Oxidative Stress

Background: There are gender differences in the oxidation-reduction reactions. Doxorubicin (Dox) is a chemotherapeutic drug that can produce oxidative stress which may require prevention by antioxidants. Aim: The study aimed to investigate the gender-dependent changes in Dox-induced oxidative stress, and the protective effects of coenzyme Q10 (CoQ10). Materials and Methods: Rats were administered CoQ10 orally for 17 days. On day 13, some rats receiving CoQ10 received a single intraperitoneal dosage of Dox, whereas other rats received normal saline. Glutathione (GSH), malondialdehyde (MDA), and total anti-oxidant capacity (T-AOC) were measured in both genders of albino rats. Results: Dox significantly reduced both GSH and T-AOC levels and caused a significant increase in MDA. The administration of CoQ10 significantly prevented these changes. Dox caused a larger reduction in GSH in males than in females, while CoQ10 caused more protection in females. Dox caused a higher increase in MDA levels in males. Conclusion: Pre-treatments with CoQ10 may protect against Dox-induced oxidative stress, with gender-dependent variations in the extent of these Dox/CoQ10 effects.

Coenzyme Q10 Attenuates Human Platelet Aggregation Induced by SARS-CoV-2 Spike Protein via Reducing Oxidative Stress In Vitro.

Platelet hyperreactivity and oxidative stress are the important causes of thrombotic disorders in patients with COVID-19. Oxidative stress, induced by the excessive generation of reactive oxygen species (ROS), could increase platelet function and the risk of thrombus formation. Coenzyme Q10 (CoQ10), exhibits strong antioxidative activity and anti-platelet effect. However, the effects and mechanisms of CoQ10 on attenuating platelet aggregation induced by spike protein have never been studied. This study aims to investigate whether the SARS-CoV-2 spike protein potentiates human platelet function via ROS signaling and the protective effect of CoQ10 in vitro. Using a series of platelet function assays, we found that spike protein potentiated platelet aggregation and oxidative stress, such as ROS level, mitochondrial membrane potential depolarization, and lipid damage level (MDA and 8-iso-PGF2α) in vitro. Furthermore, CoQ10 attenuated platelet aggregation induced by spike protein. As an anti-platelet mechanism, we showed that CoQ10 significantly decreased the excess production of ROS induced by spike protein. Our findings show that the protective effect of CoQ10 on spike protein-potentiated platelet aggregation is probably associated with its strong antioxidative ability.

Coenzyme Q10 Supplementation Increases Removal of the ATXN3 Polyglutamine Repeat, Reducing Cerebellar Degeneration and Improving Motor Dysfunction in Murine Spinocerebellar Ataxia Type 3.

Coenzyme Q10 (CoQ10), a well-known antioxidant, has been explored as a treatment in several neurodegenerative diseases, but its utility in spinocerebellar ataxia type 3 (SCA3) has not been explored. Herein, the protective effect of CoQ10 was examined using a transgenic mouse model of SCA3 onset. These results demonstrated that a diet supplemented with CoQ10 significantly improved murine locomotion, revealed by rotarod and open-field tests, compared with untreated controls. Additionally, a histological analysis showed the stratification of cerebellar layers indistinguishable from that of wild-type littermates. The increased survival of Purkinje cells was reflected by the reduced abundance of TUNEL-positive nuclei and apoptosis markers of activated p53, as well as lower levels of cleaved caspase 3 and cleaved poly-ADP-ribose polymerase. CoQ10 effects were related to the facilitation of the autophagy-mediated clearance of mutant ataxin-3 protein, as evidenced by the increased expression of heat shock protein 27 and autophagic markers p62, Beclin-1 and LC3II. The expression of antioxidant enzymes heme oxygenase 1 (HO-1), glutathione peroxidase 1 (GPx1) and superoxide dismutase 1 (SOD1) and 2 (SOD2), but not of glutathione peroxidase 2 (GPx2), were restored in 84Q SCA3 mice treated with CoQ10 to levels even higher than those measured in wild-type control mice. Furthermore, CoQ10 treatment also prevented skeletal muscle weight loss and muscle atrophy in diseased mice, revealed by significantly increased muscle fiber area and upregulated muscle protein synthesis pathways. In summary, our results demonstrated biochemical and pharmacological bases for the possible use of CoQ10 in SCA3 therapy.

Coenzyme Q10 alleviates testicular endocrine and spermatogenic dysfunction induced by high-fat diet in male Wistar rats: Role of adipokines, oxidative stress and MAPK/ERK/JNK pathway.

The current study investigated the possible protective effects of Coenzyme Q10 (Co Q10 ) on rat model of high-fat diet (HFD) induced testicular dysfunction. Thirty male Wistar rats were allocated randomly into three groups: control, HFD, HFD + Co Q10 (75 mg/kg/day) groups. Animals were sacrificed after 3 months and epididymal sperm suspension, blood, and testes were collected for further analysis. In comparison to the untreated HFD group, the Co Q10 treated group revealed significantly increased serum testosterone, adiponectin levels, and decreased LH, FSH, and leptin levels. In addition, HFD resulted in significant increase in testicular oxidative stress (increased MDA, iNOS, NO, XO & decreased catalase, SOD, GSH) and inflammation (increased pJNK/JNK, pERK/ERK, and p-p38MAPK/MAPK), while Co Q10 was effective to ameliorate these changes. In addition, Co Q10 significantly increased sperm count, motility and viability that were markedly deteriorated by HFD. Regarding testicular ultrastructure, seminiferous tubular diameter and epithelium height were reduced in HFD group and Co Q10 significantly improved these testicular changes. Finally, a significant reduction in spermatogenic cell proliferation was detected by PCNA fluorescent expression and Co Q10 significantly reversed this change. In summary, our results indicated that Co Q10 could suppress testicular dysfunction produced by HFD. This protective effect could be attributed to its antioxidant, anti-inflammatory properties and to its effect on adipokines and spermatogenic cell proliferation. So, Co Q10 may be a promising food supplement to protect against testicular dysfunction induced by HFD.

Protective Effects of Coenzyme Q10 Along with Fe2O3 Nanoparticles On Sperm Parameters in Rats with Scrotal Hyperthermia: Effects of CoQ 10 and Fe2O3 Nanoparticles On Sperm Parameters.

Background: One of the most important factors in reducing the birth rate is male infertility, and one of the main reasons for male infertility is scrotal hyperthermia (SH). Therefore, this study aimed to investigate the protective effect of coenzyme Q10 (CoQ10) along with Fe2O3 nanoparticles on semen parameters in rats with SH. Materials and Methods: Forty-eight adult male Wistar rats were divided into eight groups: healthy control, control group receiving Fe2O3 nanoparticles, control group receiving CoQ10, control group receiving Fe2O3 nanoparticles plus CoQ10, SH group, SH group receiving CoQ10, SH group receiving Fe2O3 nanoparticle, and SH group receiving Fe2O3 nanoparticles plus CoQ10. After killing rats, semen was collected from epididymal tissue, and parameters such as sperm viability, motility, concentration, and morphology were studied. Results: SH significantly reduced sperm concentration, motility, and viability, as well as altering sperm morphology in rats. Nevertheless, CoQ10 strongly improved sperm parameters in SH rats. Fe2O3 nanoparticles led to a sharp decrease in sperm parameters; however, during the simultaneous administration of Fe2O3 nanoparticles with CoQ10, improvement in sperm parameters was seen in the SH rats. Conclusion: Our findings suggest that CoQ10, along with Fe2O3 nanoparticles, has a protective effect against spermatogenic cell death induced by SH. Thus, green synthesis of nanoparticles with the administration of antioxidants, including CoQ10 is recommended for the treatment of SH.