Co-administration Of Coenzyme Q10 Research Articles

Influence of titanium dioxide nanoparticles and/or cadmium chloride oral exposure on testicular morphology, oxidative stress, and apoptosis in rats: Ameliorative role of co-enzyme Q10

Background and objectivesLittle is known about the implications of titanium dioxide nanoparticles (TiO2NPs) and cadmium chloride (Cd) co-exposure on the male reproductive system in mammals. As a result, this study researched the effects of oral TiO2NPs and/or Cd exposure on male reproduction and testicular functions. Additionally, a mitigation trial with co-enzyme Q10 (CoQ10) has also been conducted. MethodsIn a 60-day experiment, seven experimental groups, each containing 10 male Sprague Dawley rats, were orally given distilled water (control), corn oil (vehicle control), CoQ10 (10 mg/kg b.wt), TiO2NPs (50 mg/kg b.wt), Cd (5 mg/kg b.wt), TiO2NPs + Cd, and TiO2NPs + Cd + CoQ10. Then, sperm quality, male sex hormones, oxidative stress indications, Ti and Cd testicular residues, testes and accessory gland architecture, and apoptotic and inflammatory markers in rat testes were assessed. ResultsTiO2NPs and/or Cd exposure negatively impacted body weight, weight gain, testicular weights, semen quality, serum reproductive hormones, oxidative stress parameters, and Caspase-3 and tumor necrosis factor (TNF-α) immunoreactions. Histopathological changes were recorded in testicular, seminal vesicle, and prostatic tissues. Yet, co-administration of CoQ10 with TiO2NPs and Cd substantially mitigated these adverse consequences. The most notable aspect is that it effectively lowered testicular tissue Ti and Cd levels. It also improved oxidant status, hormonal profile, and sperm picture. CoQ10 minimized the testicular damage implied by histological examination. Furthermore, CoQ10 significantly diminished TiO2NPs and Cd-induced Caspase-3 and TNF-α immunoexpression in testicular tissue. ConclusionAs a result, CoQ10 could be utilized as a safe remedy to protect male reproductive physiology from TiO2NPs and Cd damage.

Co-administration of Coenzyme Q10 and HMG-CoA Reductase Inhibitor Attenuates Oxidative Stress, TGF-β, TNF-α, Nitrite Content and MPO Levels against Experimentally-induced Diabetic Nephropathy in Rats

Co-administration of Coenzyme Q10 and HMG-CoA Reductase Inhibitor Attenuates Oxidative Stress, TGF-β, TNF-α, Nitrite Content and MPO Levels against Experimentally-induced Diabetic Nephropathy in Rats

The Effect of Coenzyme Q10 on Liver Injury Induced by Valproic Acid and Its Antiepileptic Activity in Rats.

Valproic acid (VPA) has toxic metabolites that can elevate oxidative stress markers, and the hepatotoxicity of VPA has been reported. Coenzyme Q10 (CoQ10) is one of the most widely used antioxidants. The effect of CoQ10 on epileptogenesis and VPA hepatotoxicity were examined. Rats were randomly divided into five groups: the control group received 0.5% methylcellulose by oral gavages daily and saline by intraperitoneal injection three times weekly. The PTZ group received 1% methylcellulose by gavages daily and 30 mg/kg PTZ by intraperitoneal injection three times weekly. The valproic acid group received 500 mg/kg valproic acid by gavage and 30 mg/kg PTZ, as above. The CoQ10 group received 200 mg/kg CoQ10 by gavages daily and 30 mg/kg PTZ, as above. The Valproic acid + CoQ10 group received valproic acid and CoQ10, as above. Results: CoQ10 exhibited anticonvulsant activity and potentiated the anticonvulsant effect of VPA. CoQ10 combined with VPA induced a more significant reduction in oxidative stress and improved the histopathological changes in the brain and liver compared to VPA treatment. In addition, CoQ10 reduced the level of toxic VPA metabolites. These findings suggest that the co-administration of CoQ10 with VPA in epilepsy might have therapeutic potential by increasing antiepileptic activity and reducing the hepatotoxicity of VPA.

Impact of ciprofloxacin and coenzyme Q10 on spermatogenesis in mice

Background: Ciprofloxacin is commonly used to treat many bacterial infections. There are controversial reports regarding abnormalities in sperm parameters in laboratory animal and human studies after ciprofloxacin administration. Coenzyme Q10 is a fat-soluble vitamin-like substance that is concentrated in sperm mitochondria, where it acts as an antioxidant and an energy promoter. Various studies found that coenzyme Q10 can improve sperm parameters, whereas other studies showed no significant improvement in sperm parameters. This study aimed at investigating the effect of ciprofloxacin and coenzyme Q10 on spermatogenesis and sperm morphology in male mice. Materials and Methods: Twenty eight-week-old male albino mice were randomly divided into four equal groups: control group, group 1 that received ciprofloxacin (102.78 mg/kg), group 2 that was given coenzyme Q10 (20.56 mg/kg), and group 3 that was given both ciprofloxacin and coenzyme Q10. The drugs were given twice daily for 35 days. On day 36, the mice were sacrificed; sperm were harvested, analyzed for sperm morphology, and stained for detection of sperm abnormalities. Testes were taken to evaluate spermatogenesis histopathologically. Data were statistically analyzed, and a P value of ≤ 0.05 was considered significant. Results: Sperm morphology showed no significant alteration in the groups treated with ciprofloxacin, coenzyme Q10, and a combination of ciprofloxacin and coenzyme Q10 compared with the control. However, histopathological lesions showed a mild decrease in spermatogenesis that was accompanied by mild vein congestion in the testicular tissue sections of mice treated with ciprofloxacin only. Conclusion: Ciprofloxacin had no significant negative impact on sperm morphology; however, it induced mild histopathological alterations in testicular tissue that was ameliorated by the coadministration of coenzyme Q10. This effect should be taken into consideration during ciprofloxacin therapy in males.

Complementary effects of coenzyme Q10 and Lepidium sativum supplementation on the reproductive function of mice: An experimental study.

Background Coenzyme Q10 (CoQ10) and Lepidium sativum (LS) have therapeutic effects on infertility.ObjectiveTo evaluate the combined effects of LS and CoQ10 on reproductive function in adult male NMRI mice.Materials and MethodsEighty three-months-old male mice (35–40 gr) were divided into four groups (n = 10/each): control (treated with water), CoQ10-treated (200, 300, and 400 mg/kg/body weight), LS-treated (200, 400, 600 mg/kg/body weight), and co-treated (LS [600 mg/kg/body weight] + CoQ10 [200 mg/kg/body weight]) groups. Serum testosterone, luteinizing hormone, follicle-stimulating hormone, and gonadotropin realizing hormone (GnRH) levels were measured using ELISA method. The sperm quality was assessed using Sperm Class AnalyzerⓇ (SCA) CASA system and GnRH mRNA expression levels were evaluated by real-time polymerase chain reaction.ResultsThe number of sniffing and following behavior was significantly higher in LS-treated (400 and 600 mg/ml/body weight) groups than the control group (p = 0.0007 and p = 0.0010, respectively). The number of mounting and coupling behaviors was significantly higher in the CoQ10 (300 and 400 mg/ml/body weight)-treated animals than the control group (p = 0.0170 and p = 0.0006, respectively). Co-treatment of CoQ10 (200 mg/ml/body weight) and LS (600 mg/ml/body weight) significantly increased all aspects of sexual behaviors as well as the levels of serum testosterone (p = 0.0011), luteinizing hormone (p = 0.0062), and follicle-stimulating hormone (p = 0.0001); sperm viability (p = 0.0300) and motility (p = 0.0010); and GnRH mRNA levels (p = 0.0016) compared to the control group.ConclusionThe coadministration of CoQ10 and LS significantly improves the activity of the hypothalamic-pituitary-gonadal axis and enhances the reproductive parameters in adult male mice.

Coenzyme Q10 Ameliorates potassium cyanide-induced toxicosis in a mouse model

Potassium cyanide (KCN) is one of the most lethal and feared poison; which devastates cellular respiration resulting in death due to hypoxia. Several antidotes exist, but most face major limitations of safety and efficacy. Moreover, there is a need for new strategies to minimize post-exposure pathological sequel, which includes harmful oxidant and inflammatory changes. Coenzyme Q10 (CoQ10) is a powerful antioxidant, which has shown efficacy against chemical-induced toxicity. In the present study, the potential protective effect of CoQ10 against KCN-induced toxicosis was evaluated. Female Swiss white mice (3–4 weeks old) were divided into three treatment groups. The first group was used as the control, the second group was supplemented with 200 mg/kg of CoQ10 for one month before administration with 8 mg/kg of KCN. For this group, co-administration of CoQ10 and KCN was continued to the end of the experiment. The third group was administered 8 mg/kg of KCN. The experiment was terminated after 42 days post-treatment to enable investigations into the effect of KCN and CoQ10 on various physiological, biochemical, and cellular processes. The results of this study showed that KCN severely impaired the health of mice, more so, the neurological integrity. KCN-driven depletion of cellular glutathione (GSH) was noted in the liver and brain. This constitutes a characteristic impairment of the antioxidant capacity due to the induction of severe oxidative stress. CoQ10 significantly reinforced the neurological integrity and restored cellular glutathione (reduced form) in both the liver and brain, a clear indication of reduced oxidative stress. Remarkably, KCN-induced anemia, leukocytosis, and suppression of platelets were reversed by CoQ10 supplementation. Moreover, histopathological analysis revealed that CoQ10 supplementation blocked KCN-driven liver, kidney, and brain inflammation, and characteristic hypoxia-induced lesions. These findings open possibilities for further scrutiny and development of adjunct therapy utilizing CoQ10 to treat KCN poisoning.

Evaluation of the neuroprotective effects of electromagnetic fields and coenzyme Q10 on hippocampal injury in mouse.

Electromagnetic fields (EMFs) are reported to interfere with chemical reactions involving free radical production. Coenzyme Q10 (CoQ10) is a strong antioxidant with some neuroprotective activities. The purpose of this study was to examine and compare the neuroprotective effects of EMF and CoQ10 in a mouse model of hippocampal injury. Hippocampal injury was induced in mature female mice (25-30 g), using an intraperitoneal injection of trimethyltin hydroxide (TMT; 2.5 mg/kg). The experimental groups were exposed to EMF at a frequency of 50 Hz and intensity of 5.9 mT for 7 hr daily over 1 week or treated with CoQ10 (10 mg/kg) for 2 weeks following TMT injection. A Morris water maze apparatus was used to assess learning and spatial memory. Nissl staining and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) tests were also performed for the histopathological analysis of the hippocampus. Antiapoptotic genes were studied, using the Western blot technique. The water maze test showed memory improvement following treatment with CoQ10 and coadministration of CoQ10 + EMF. The Nissl staining and TUNEL tests indicated a decline in necrotic and apoptotic cell count following treatment with CoQ10 and coadministration of CoQ10 + EMF. The Western blot study indicated the upregulation of antiapoptotic genes in treatment with CoQ10, as well as coadministration. Also, treatment with EMF had no significant effects on reducing damage induced by TMT in the hippocampus. According to the results, EMF had no significant neuroprotective effects in comparison with CoQ10 on hippocampal injury in mice. Nevertheless, coadministration of EMF and CoQ10 could improve the neuroprotective effects of CoQ10.

Histological study on the effect of rosuvastatin (Crestor) on the skeletal muscle of adult male albino rats and the possible protective effect of coenzyme Q10

Objective The aim of this study was to evaluate the effect of rosuvastatin drug on the histological structure of the skeletal muscle fiber of adult male albino rats and the possible protective role of coenzyme Q10. Background Rosuvastatin has been proven to be effective in improving serum lipid profiles. It decreases the risk for mortality in patients with coronary heart disease. It was reported that some patients treated with various statins have developed symptoms of myopathy. Coenzyme Q10 has a powerful antioxidant activity and affects membrane stability in many tissues, including skeletal muscle. Materials and methods A total of 54 adult male albino rats were used in this study and divided into four groups: group I rats served as negative controls, group II rats served as positive controls, group III rats were treated with rosuvastatin orally for 4 and 12 weeks, and group IV rats were treated with rosuvastatin and Coenzyme Q10 orally for 4 and 12 weeks. The gastrocnemius muscle was dissected and prepared for light and electron microscopic study. Results The light microscopic study of the gastrocnemius muscle of rats treated with a high therapeutic dose of rosuvastatin for 4 and 12 weeks (group III) showed variation in size, mononuclear cellular infiltration, splitting, and focal degeneration of myofibers with increased collagen fiber deposition between muscle fibers. Electron microscopic study showed mitochondrial accumulation between myofibrils and in the subsarcolemmal space, mitochondrial degeneration, and dilatation of sarcoplasmic reticulum cisterna. Coadministration of coenzyme Q10 with rosuvastatin for 4 and 12 weeks ameliorated most of the above-mentioned histological alterations in the rat skeletal muscles. Conclusion Rosuvastatin drug caused skeletal muscle fiber damage. Coenzyme Q10 leads to the protection of the skeletal muscle fibers when given concomitantly with rosuvastatin.

Protective effects of coenzyme Q10 and L-carnitine against statin-induced pancreatic mitochondrial toxicity in rats.

Statins are widely used in patients with hyperlipidemia and whom with high risk of cardiovascular diseases. Unfortunately, statins also exert some adverse effects on the liver and pancreas and enhance the risk of type 2 diabetes mellitus. The objective of the present research was to investigate the protective effects of coenzyme Q10 (Co-Q10) and L-carnitine (LC) on statins induced toxicity on pancreatic mitochondria in vivo. Seven groups of male Wistar rats received atorvastatin (20 mg/kg, p.o.), atorvastatin + Co-Q10 (10 mg/kg, i.p.), atorvastatin + LC (500 mg/kg, i.p.), lovastatin (80 mg/kg, p.o), lovastatin + Co-Q10 (10 mg/kg, i.p.), and lovastatin + LC (500 mg/kg, i.p.). Serum glucose and insulin levels were measured before and after two weeks of treatment, while the pancreas was removed and toxic effects of statins, as well as the protective effects of Co-Q10 and LC were assessed. The results showed that atorvastatin and lovastatin significantly increased glucose level and decreased insulin secretion. The glucose level in Co-Q10 and LC groups was significantly lower than statins alone groups. The findings also showed that statin groups had higher rate of pancreatic toxicity including higher level of reactive oxygen species production, decreased cytochrome c oxidase activity, collapse of mitochondrial membrane potential and swelling in comparison to controls. These factors were significantly diminished by co-administration of Co-Q10 or LC compared to statin groups alone. Additionally, supplements caused a significant increase in serum insulin and succinate dehydrogenase activity. Our study provided new evidence supporting beneficial effects of Co-Q10 and LC on statin-induced pancreatic toxicity.

Effect of Coenzyme Q10 Supplementation in Statin-Treated Obese Rats.

Statins, HMG-CoA reductase inhibitors, are known to cause serious muscle injuries (e.g. myopathy, myositis and rhabdomyolysis), and these adverse effects can be rescued by co-administration of coenzyme Q10 (CoQ10) with statins. The goal of the current research is to assess the efficacy of combined treatment of CoQ10 with Atorvastatin for hyperlipidemia induced by high-fat diet in SD rats. 4-week-old Sprague-Dawley male rats were fed normal diet or high-fat diet for 6 weeks. Then, rats were treated with either Statin or Statin with various dosages of CoQ10 (30, 90 or 270 mg/kg/day, p.o.) for another 6 weeks. Compared to Statin only-treatment, CoQ10 supplementation significantly reduced creatine kinase and aspartate aminotransferase levels in serum which are markers for myopathy. Moreover, CoQ10 supplementation with Statin further reduced total fat, triglycerides, total cholesterol, and low-density lipoprotein-cholesterol. In contrast, the levels of high-density lipoprotein-cholesterol and CoQ10 were increased in the CoQ10 co-treated group. These results indicate that CoQ10 treatment not only reduces the side effects of Statin, but also has an anti-obesity effect. Therefore an intake of supplementary CoQ10 is helpful for solving problem of obese metabolism, so the multiple prescription of CoQ10 makes us think a possibility that can be solved in being contiguous to the obesity problem, a sort of disease of the obese metabolism.

Atorvastatin Reduces the Myocardial Content of Coenzyme Q10 in Isoproterenol-induced Heart Failure in Rats

The present study was aimed to study the effects of different doses of atorvastatin on Co Q10 content in the myocardium tissue in rats. A subcutaneous injection of isoproterenol (5 mg/kg/day) for 10 days was used for the induction of heart failure. Rats were randomly assigned to control, treatment with atorvastatin (5, 10, 20 mg/kg/day) and treatment with atorvastatin plus coenzyme Q10 (10 mg/kg/day). Coenzyme Q10 content of myocardium was measured using HPLC method with UV detector after hemodynamic parameters measurements. The malondialdehyde (MDA) content of the myocardium was evaluated in order to determine coenzyme Q10 antioxidative effect. A high dose of atorvastatin (20 mg/kg/day) was significantly reduced the myocardium content of coenzyme Q10 as compared with isoproterenol treated group (p<0.001). Compared with atorvastatin alone treated animals, co-administration of coenzyme Q10 with atorvastatin was improved the level of coenzyme Q10 in the myocardium (p<0.05, p<0.001). Increasing the dose of atorvastatin also led to increase in MDA content of the myocardium (p<0.01). Serum lipid profile showed no changes in atorvastatin treated groups. The results of this study demonstrate that high doses of atorvastatin reduce coenzyme Q10 content of the myocardium and increase lipid peroxidation in myocardium which is reversed by coenzyme Q10 co-administration.

Mitophagy Is Required for Acute Cardioprotection by Simvastatin

We have shown that autophagy and mitophagy are required for preconditioning. While statin's cardioprotective effects are well known, the role of autophagy/mitophagy in statin-mediated cardioprotection is not. In this study, we used HL-1 cardiomyocytes and mice subjected to ischemia/reperfusion to elucidate the mechanism of statin-mediated cardioprotection. HL-1 cardiomyocytes exposed to simvastatin for 24 h exhibited diminished protein kinase B (Akt)/mammalian target of rapamycin (mTOR) signaling, increased activation of unc-51-like kinase 1, and upregulation of autophagy and mitophagy. Similar findings were obtained in hearts of mice given simvastatin. Mevalonate abolished simvastatin's effects on Akt/mTOR signaling and autophagy induction in HL-1 cells, indicating that the effects are mediated through inhibition of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase. Simvastatin-treated HL-1 cells exhibited mitochondrial translocation of Parkin and p62/SQSTM1, fission, and mitophagy. Because Parkin is required for mitophagy and is expressed in heart, we investigated the effect of simvastatin on infarct size in Parkin knockout mice. Simvastatin reduced infarct size in wild-type mice but showed no benefit in Parkin knockout mice. Inhibition of HMG-CoA reductase limits mevalonate availability for both cholesterol and coenzyme Q10 (CoQ) biosynthesis. CoQ supplementation had no effect on statin-induced Akt/mTOR dephosphorylation or macroautophagy in HL-1 cells, but it potently blocked mitophagy. Importantly, CoQ supplementation abolished statin-mediated cardioprotection in vivo. Acute simvastatin treatment suppresses mTOR signaling and triggers Parkin-dependent mitophagy, the latter which is required for cardioprotection. Coadministration of CoQ with simvastatin impairs mitophagy and cardioprotection. These results raise the concern that CoQ may interfere with anti-ischemic benefits of statins mediated through stimulation of mitophagy.

Combined atorvastatin and coenzyme Q10 improve the left ventricular function in isoproterenol-induced heart failure in rat

The effect of atorvastatin on cardiac remodeling, function, and homodynamic parameters in isoproterenol-induced heart failure was evaluated in the present study. A subcutaneous injection of isoproterenol (5 mg/kg/day) for 10 days was used for the induction of heart failure. Isoproterenol administration produced intensive myocardial necrosis and fibrosis with a significant decrease in the arterial pressure indices, heart rate, contractility (LVdP/dt max) and relaxation (LVdP/dt min), but an increase in the left ventricular end-diastolic pressure. Rats were randomly assigned to control, treatment with only atorvastatin, and treatment with atorvastatin plus coenzyme Q10. Histopathological analysis showed a marked attenuation of myocyte necrosis and interstitial fibrosis in all atorvastatin treated groups (P < 0.001). A low dose of atorvastatin (5 mg/kg/day) significantly improved the left ventricular systolic pressure, contractility and relaxation (P < 0.01). On the contrary, a high dose of atorvastatin (20 mg/kg/day) worsened the isoproterenol-induced left ventricular dysfunction by a further reduction of LV dP/ dt max from + 2780 ± 94 to + 1588 ± 248 (mm Hg/s; P < 0.01) and LV dP/ dt min from − 2007 ± 190 to − 2939 ± 291 (mm Hg/s; P < 0.05). Co-administration of coenzyme Q10 with atorvastatin reversed the hemodynamic depression and the left ventricular dysfunction to a high level (P < 0.001). There was a lower level of LVEDPs in the atorvastatin + coenzyme Q10 treated groups (3 ± 1 and 4 ± 1.4 versus 8 ± 3.5 and 14 ± 3.6 mm Hg, respectively), thereby suggesting improvement in the myocardial stiffness by the combined coenzyme Q10 and atorvastatin treatment. The atorvastatin therapy attenuated myocardial necrosis and fibrosis in isoproterenol-induced heart failure. However, a high dose of the drug considerably worsened the left ventricular dysfunction and hemodynamic depression, which was reversed by coenzyme Q10 co-administration.

Antiangiogenic and hypolipidemic activity of coenzyme Q10 supplementation to breast cancer patients undergoing Tamoxifen therapy

Tamoxifen, a non-steroidal anti-estrogen is now widely used and has led to an increase in both disease-free and overall survival of women after primary surgery. Tamoxifen therapy is found to cause hypertriglyceridemia by reducing activity of lipolytic enzymes on triglycerides, and thereby increasing the risk of cardiovascular disease. Angiogenesis promotes local tumour progression and invasion and enables tumour cell dissemination and metastasis formation. Our study has found that co-administration of Coenzyme Q10 (100 mg) along with tamoxifen (10 mg, twice a day) to breast cancer patients reduced the level of angiogenesis markers and lipid levels.