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Abstract\nHighlightsParkinson’s disease (PD) is a prevalent neurodegenerative disorder characterized by the loss of dopaminergic neurons in the substantia nigra pars compacta (SNpc) and subsequent depletion of dopamine in the striatum. Solanesol, an alcohol that acts as a precursor to coenzyme Q10, possesses potential applications in managing neurological disorders with antioxidant, anti-inflammatory, and neuromodulatory potential. In this study, a zebrafish model was employed to investigate the effects of solanesol in tramadol induced PD like symptoms. Zebrafish were administered tramadol injections (50 mg/kg) over a 20-day period. Solanesol was administered at doses of 25, 50, and 100 mg/kg, three hours prior to tramadol administration from day 11 to day 20. Behavioral tests assessing motor coordination were conducted on a weekly basis using open field and novel diving tank apparatus. On day 21, the zebrafish were euthanized, and brain tissues were examined for markers of oxidative stress, inflammation, and neurotransmitters level. Chronic tramadol treatment resulted in motor impairment, reduced antioxidant enzyme levels, enhanced release of proinflammatory cytokines in the striatum, and disrupted neurotransmitter balance. However, solanesol administration mitigated these effects and exhibited a neuroprotective effect against neurodegenerative alterations in the zebrafish model of PD. This was evident through improvements in behavior, modulation of biochemical markers, attenuation of neuroinflammation, restoration of neurotransmitters level, and enhancement of mitochondrial activity. The histopathological study also confirmed that solanesol dose dependently restored neuronal cell density which confirmed its neuroprotective potential. Further investigations are required to elucidate the underlying mechanisms of solanesol neuroprotective effects and evaluate its efficacy in human patients.Neuroprotective effects: Solanesol has shown significant neuroprotective effects in a zebrafish model of Parkinson’s disease induced by chronic tramadol usage.Improved behavioral performance: Administration of solanesol resulted in improved motor coordination in the open field test (OFT) and novel diving apparatus in the tramadol-induced zebrafish model of PD.Decreased inflammation: Solanesol treatment significantly reduced pro-inflammatory cytokine levels in the tramadol-induced zebrafish model of PD, indicating its anti-inflammatory properties.Restored oxidative parameters: Solanesol administration restored oxidative stress parameters, as well as catecholamine and neurotransmitter levels in the tramadol-induced zebrafish model of PD.Histopathological improvement: Solanesol administration prevented histopathological alterations induced by tramadol, indicating its ability to protect against neuronal damage in the zebrafish model of PD.Neuroprotective effects: Solanesol has shown significant neuroprotective effects in a zebrafish model of Parkinson’s disease induced by chronic tramadol usage.Improved behavioral performance: Administration of solanesol resulted in improved motor coordination in the open field test (OFT) and novel diving apparatus in the tramadol-induced zebrafish model of PD.Decreased inflammation: Solanesol treatment significantly reduced pro-inflammatory cytokine levels in the tramadol-induced zebrafish model of PD, indicating its anti-inflammatory properties.Restored oxidative parameters: Solanesol administration restored oxidative stress parameters, as well as catecholamine and neurotransmitter levels in the tramadol-induced zebrafish model of PD.Histopathological improvement: Solanesol administration prevented histopathological alterations induced by tramadol, indicating its ability to protect against neuronal damage in the zebrafish model of PD. [ABSTRACT FROM AUTHOR]

AbstractChronic and excessive alcohol consumption leads to liver toxicity. There is a need to investigate effective therapeutic strategies to alleviate alcohol-induced liver injury, which remains the leading cause of liver-related morbidity and mortality worldwide. Therefore here, we looked into and evaluated how ethanol-induced hepatotoxicity was affected by coenzyme Q10 (CoQ10) and its analog, idebenone (IDE), on the NLRP3/caspase-1/IL-1 pathway. Hepatotoxicity induced in rats through the oral administration of gradually increasing dosages of ethanol (from 2 to 6 g/kg/day) over 30 days and the effect of CoQ10 (10 or 20 mg/kg) and IDE (50 or 100 mg/kg) were evaluated. Serum hepatotoxicity markers (ALT, AST, GGT, ALP, and TBIL), tissue oxidative stress markers and the mRNA expressions of IL-1β, IL-18, TGF-β, NF-κB, NLRP3, and caspase-1 were evaluated. Masson’s trichrome staining was also used to visualize fibrosis in the liver tissue. The results indicated that ethanol exposure led to hepatotoxicity as well as considerable NLRP3/caspase-1/IL-1β pathway activation. Moreover, CoQ10 or IDE treatment reduced measured parameters in a dosage-dependent manner. Thus, by inhibiting the NLRP3/caspase-1/IL-1 pathway, CoQ10 and IDE can prevent the hepatotoxicity caused by ethanol, although CoQ10 is more effective than IDE. This study will provide insight into new therapeutic avenues that take advantage of the anti-inflammatory and antioxidant properties of CoQ10 and IDE in ethanol-induced liver diseases. [ABSTRACT FROM AUTHOR]

Coenzyme Q10 (CoQ10) is an essential component of the electron transport chain. It also acts as an antioxidant in cellular membranes. It can be endogenously produced in all cells by a specialized mitochondrial pathway. CoQ10 deficiency, which can result from aging or insufficient enzyme function, has been considered to increase oxidative stress. Some drugs, including statins and bisphosphonates, often used by older individuals, can interfere with enzymes responsible for endogenous CoQ10 synthesis. Oral supplementation with high doses of CoQ10 can increase both its circulating and intracellular levels and several clinical trials observed that its administration provided beneficial effects on different disorders such as cardiovascular disease and inflammation which have been associated with low CoQ10 levels and high oxidative stress. Moreover, CoQ10 has been suggested as a promising therapeutic agent to prevent and slow the progression of other diseases including metabolic syndrome and type 2 diabetes, neurodegenerative and male infertility. However, there is still a need for further studies and well-designed clinical trials involving a large number of participants undergoing longer treatments to assess the benefits of CoQ10 for these disorders. [ABSTRACT FROM AUTHOR]

The effect of in-vitro sperm incubation with Pentoxifylline (PTX) and Coenzyme Q10 (CoQ10) in Oligoasthenoteratozoospermia (OAT) patients was evaluated. Semen samples were obtained from men with Normozoospermia and men with OAT. Motile sperm from the two groups were subdivided into four subgroups: (i) without incubation with PTX + CoQ10; (ii) incubation with PTX; (iii) Incubation with CoQ10; and (iv) incubation with a combination of PTX + CoQ10. Then, sperm parameters, chromatin, DNA and membrane integrity, protamine deficiency, apoptosis, mitochondrial activity, sperm chromatin dispersion test (SCD), hypo-osmotic swelling test (HOS), chromomycin A3 (CMA3), Terminal deoxynucleotidyl transferase dUTP nick end labelling (TUNEL), and diaminobenzidine (DAB) assays were evaluated, respectively. Sperm incubated with CoQ10 and a combination of CoQ10 and PTX resulted in a significant increase in the sperm parameters. Also, a significant decrease was noted with a combination of PTX and CoQ10 in normal men. There was a significant difference between CoQ10 treated and CoQ10 + PTX treated groups in comparison with the OAT group in the percentage of the DNA fragmentation, sperm apoptosis, AB+, HOS test + and sperm mitochondrial activity. Incubated sperm with CoQ10, PTX, and in combination with each other can improve sperm parameters in OAT patients. [ABSTRACT FROM AUTHOR]

Doxorubicin (Dox) is an anthracycline antibiotic that treats a variety of malignancies. Unfortunately, its cardiotoxicity limits its therapeutic usefulness. Coenzyme Q10 (CoQ10) has effectively treated and prevented various cardiac diseases and toxicities. This study aimed to evaluate the possible antioxidative and anti-apoptotic cardioprotective effects of CoQ10 against doxorubicin-induced histopathological and molecular changes in cardiomyocytes. Twenty-eight adult Wistar rats were divided into positive control, negative control, Dox-treated group, and Dox+CoQ10-treated. On the 16th day after the start of treatment, the hearts of all rats were dissected, and the left ventricles were processed for histological evaluation; immunohistochemical staining with caspase-3 and inducible nitric oxide synthase (iNOS); ultrastructural examination of cardiomyocytes; molecular assessment of proapoptotic gene Bax and anti-apoptotic gene expression Bcl-2; and biochemical study of malondialdehyde (MDA). The Dox-treated group had disorganized cardiomyocytes with increased interstitial space, vacuolated cytoplasm, and multiple small-sized pyknotic nuclei. A significant increase in caspase-3 and iNOS immunoexpression was observed. Ultrastructurally, the mitochondria were large with abnormal shapes, vacuolated cytoplasm, multiple vacuoles and autophagosomes, collagen fibril accumulation, and multiple small hyperchromatic nuclei. The intercalated discs were disorganized with loss of desmosome junction. The cardiomyocytes also showed significantly increased MDA levels and upregulation of Bax/Bcl-2 gene expression ratio. Co-administration of CoQ10 resulted in significant improvement in the histopathological picture, with a significant decrease in caspase-3 and iNOS immunoexpression and downregulation of the Bax/Bcl-2 gene expression ratio. In conclusion, CoQ10 protects against Dox-induced cardiotoxicity through the regulation of proapoptotic and anti-apoptotic gene expression. [ABSTRACT FROM AUTHOR]

Our study aimed to develop a self-microemulsifying drug delivery system for the poorly aqueous-soluble drug Coenzyme Q10, to improve the dissolution and the oral bioavailability. Excipients were selected based on their Coenzyme Q10 solubility, and their concentrations were set for the optimization of the microemulsion by using a D-optimal mixture design to achieve a minimum droplet size and a maximum solubility of Coenzyme Q10 within 15 min. The optimized formulation was composed of an oil (omega-3; 38.55%), a co-surfactant (Lauroglycol® 90; 31.42%), and a surfactant (Gelucire® 44/14; 30%) and exhibited a mean droplet size of 237.6 ± 5.8 nm and a drug solubilization (at 15 min) of 16 ± 2.48%. The drug dissolution of the optimized formulation conducted over 8 h in phosphate buffer medium (pH 6.8) was significantly higher when compared to that of the Coenzyme Q10 suspension. A pharmacokinetic study in rats revealed a 4.5-fold and a 4.1-fold increase in the area under curve and the peak plasma concentration values generated by the optimized formulation respectively, as compared to the Coenzyme Q10 suspension. A Coenzyme Q10 brain distribution study revealed a higher Coenzyme Q10 distribution in the brains of rats treated with the optimized formulation than the Coenzyme Q10 suspension. Coenzyme Q10-loaded self microemulsifying drug delivery system was successfully formulated and optimized by a response surface methodology based on a D-optimal mixture design and could be used as a delivery vehicle for the enhancement of the oral bioavailability and brain distribution of poorly soluble drugs such as Coenzyme Q10. [ABSTRACT FROM AUTHOR]

Our study aimed to develop a self-microemulsifying drug delivery system for the poorly aqueous-soluble drug Coenzyme Q10, to improve the dissolution and the oral bioavailability. Excipients were selected based on their Coenzyme Q10 solubility, and their concentrations were set for the optimization of the microemulsion by using a D-optimal mixture design to achieve a minimum droplet size and a maximum solubility of Coenzyme Q10 within 15 min. The optimized formulation was composed of an oil (omega-3; 38.55%), a co-surfactant (Lauroglycol® 90; 31.42%), and a surfactant (Gelucire® 44/14; 30%) and exhibited a mean droplet size of 237.6 ± 5.8 nm and a drug solubilization (at 15 min) of 16 ± 2.48%. The drug dissolution of the optimized formulation conducted over 8 h in phosphate buffer medium (pH 6.8) was significantly higher when compared to that of the Coenzyme Q10 suspension. A pharmacokinetic study in rats revealed a 4.5-fold and a 4.1-fold increase in the area under curve and the peak plasma concentration values generated by the optimized formulation respectively, as compared to the Coenzyme Q10 suspension. A Coenzyme Q10 brain distribution study revealed a higher Coenzyme Q10 distribution in the brains of rats treated with the optimized formulation than the Coenzyme Q10 suspension. Coenzyme Q10-loaded self microemulsifying drug delivery system was successfully formulated and optimized by a response surface methodology based on a D-optimal mixture design and could be used as a delivery vehicle for the enhancement of the oral bioavailability and brain distribution of poorly soluble drugs such as Coenzyme Q10. [ABSTRACT FROM AUTHOR]

Ethambutol is a widely used drug to treat tuberculosis that may cause visual disturbance including ethambutol toxic optic neuropathy (ETON). The disease disrupts bodily tissues' energy production, including the retinal ganglion cells (RGC). Many have proposed treatment with coenzyme Q10 (coQ10) due to its antioxidant and facilitative effects that can improve mitochondrial electron transport. The present study hence assessed whether coQ10 could protect against ETON through a parallel triple-blinded randomised controlled trial in 18 mice using computer-generated tables for treatment allocation. All of the mice received 25 mg/kg ethambutol daily, while only nine in the treated group also received 100 mg/kg coQ10. After 30 days, blinded pathologists counted RGC numbers in enucleated and dyed orbital tissue. The treated group had significantly denser RGCs at 47.2 (standard deviation [SD] 10.6) cells per 500 µm microscope field vs 33.5 (SD 6.3) in the control group (t = 3.34, p =.004). CoQ10 therefore protected RGCs from ETON. Clinical trials of coQ10 in human subjects treated with ethambutol should be considered. [ABSTRACT FROM AUTHOR]

The aim of this study was to evaluate the effects of coenzyme Q10 in the treatment of endometriosis rat models. Twenty seven Sprague Dawley rats were divided into four groups; Control Group (n = 7; Endometriosis group), Reference Group (n = 6; Endometriosis + Buserelin acetate, 20 mg/kg), CoQ10 Group-I (n = 7; Endometriosis + CoQ10, 50 mg/kg) and CoQ10 Group-II (n = 7; Endometriosis + CoQ10, 100 mg/kg). At the end of the experiment, all the rats were sacrificed, and the volume and histoarchitecture of endometrial implants were evaluated. The mast cells were determined by Toluidine blue and collagen fiber density was analysed by Masson's Trichrome staining. Tumour necrosis factor and vascular endothelial growth factor (VEGF) levels were analysed by enzyme-linked immunosorbent assay in peritoneal fluid and VEGF and matrix metalloproteinase-9 (MMP-9) were evaluated by immunohistochemistry. Terminal deoxynucleotidil transferase-mediated dUTP Nick end labelling (TUNEL) was also used for the detection of apoptotic cells. The CoQ10 treatment significantly decreased the volume of endometriotic implants, VEGF, and MMP-9 immunoreactivity and increased TUNEL-positive cells. The findings of the study suggest that CoQ10 can be used in endometriosis treatment by suppressing the endometriotic implants. What is already known on this subject? Endometriosis is a gynaecological disorder and previous studies have shown that different treatments with antioxidants cause significant regression in the endometriotic implants. What the results of this study add? In this study, CoQ10 reduced intra-abdominal adhesion scores and volume of the endometriotic implants. In addition, CoQ10 treatment affected mast cell, TNF-α, VEGF, and MMP-9. Whatof these findings for clinical practice and/or further research? CoQ10 treatments may be possible to apply, it can contribute to science in terms of a new therapeutic treatment for endometriosis. Further studies are required to evaluate the Coenzyme Q10's effects on pain and subfertility in endometriosis. [ABSTRACT FROM AUTHOR]

Clinical Relevance: Effective treatment of corneal epithelial defects is crucial to prevent secondary infectious keratitis and visual impairment due to loss of corneal transparency. Therefore, it is important to determine the effect of different topical agents on corneal wound healing response.Background: The aim was to compare the effects of three different eye drops on corneal epithelial wound healing in an experimental model.Methods: Twenty-four eyes of 24 female BALB/c mice were included. A 2 mm central corneal epithelial defect was created. Topical Coenzyme Q10 + Vitamin E D-α-TPGS 4 × 1 was applied to Group A (n = 6), topical Sodium hyaluronate + Xanthan Gum + 0.3% Nethylmicine 4 × 1 to Group B (n = 6) and topical Sodium hyaluronate 4 × 1 to Group C (n = 6). Group D (n = 6) was the control group without treatment. Clinical scoring according to corneal fluorescein staining and histopathological evaluations was performed.Results: Clinical scores according to corneal fluorescein staining were similar in all groups on days 1 (p = 0.05), 2 (p = 0.15) and 3 (p = 0.62). Electron microscopy revealed disruption of intercellular junctions between corneal epithelial cells and intracellular vacuole formation in all groups except Group A. Corneal epithelial thickness and superficial epithelial microvillus arrangement were close to normal in Group A.Conclusion: Although there was no difference in clinical scores between groups, electron microscopy revealed a better organised epithelium with normal configuration of microvilli and less vacuolisation in Group A. [ABSTRACT FROM AUTHOR]

Evaluating the impact of coenzyme Q10 (CoQ10) supplementation on hormonal indices, mental health, and biomarkers of inflammatory responses and oxidative stress among female patients suffering from polycystic ovary syndrome (PCOS). The present double-blinded, placebo-controlled randomized clinical trial consisted of 55 PCOS women (aged 18–40 years old), who were randomized into groups receiving 100 mg/day of CoQ10 (28 cases) or placebo (27 cases) for 12 weeks. The supplementation of CoQ10 decreased significantly the scores of Beck Depression Inventory (BDI) (p =.03) and Beck Anxiety Inventory (BAI) (p =.01) and high-sensitivity C-reactive protein (hs-CRP) level (p =.005) when comparing with the placebo group. Moreover, CoQ10 group exhibited a significant drop in total testosterone (p =.004), dehydroepiandrosterone sulfate (DHEAS) (p <.001), hirsutism (p =.002) and malondialdehyde (MDA) (p =.001) levels in the serum, and a significant rise in sex hormone-binding globulin (SHBG) (p <.001) and total antioxidant capacity (TAC) (p <.001) levels in the serum than the placebo group. 12-week supplementation of CoQ10 to PCOS women showed beneficial impact on BDI, BAI, hs-CRP, total testosterone, DHEAS, hirsutism, SHBG, TAC and MDA levels. [ABSTRACT FROM AUTHOR]

We aimed to create a mechanical optic nerve damage model in rats and to investigate the neuroprotective effects of topical Coenzyme Q10 + Vitamin E TPGS (CoQ10+Vit E) molecule on retinal ganglion cells. In our study, 30 eyes of 20 male Wistar rats were used. Three groups, each consisting of 10 eyes, were formed as control, experimental, and treatment groups. The control group was used to test the formation of optic nerve damage. Topical CoQ10 + Vit E TPGS solution was applied to the rats in the treatment group, one drop twice a day for 3 weeks. On the other hand, physiological drops were applied to the experimental group 2 times a day for 3 weeks. After 3 weeks, the optic nerves of the rats were dissected and examined histopathologically. In electron microscopic examination of the treatment group, it was noted that the myelin sheath in the majority of myelinated nerve fibers and the normal structures of mitochondria, neurotubules, and neurofilaments in the axoplasm were preserved. It was observed that the oligodendrocytes surrounded the myelinated axons. In the experimental group, significant degenerative changes were observed in myelinated nerve fibers in many areas. The number of myelinated axons was significantly increased in the treatment group compared to the experimental group (p =.0028). In the light of the data obtained, the neuroprotective effect of the topically used CoQ10 + Vit E TPGS molecule was found to be histopathologically effective in our experimental study. Abbreviations: NAAION: Nonarteritic anterior ischemic optic neuropathy; CoQ10: Coenzyme q10; CG: Control group; EG: Experimental group; TG: Treatment group. [ABSTRACT FROM AUTHOR]

This research evaluated the efficacy of oral nutritional agents including CoQ10, vitamin E, inositols and vitamin D on androgen-associated hormones, glycolipid metabolism and body weight in women with PCOS. A multi-database search was performed from inception to December 2020. Using multi-variate random effects method, a NMA was conducted by synthesizing data pooled from RCTs. It was registered with PROSPERO (registration number CRD42021230292). Twenty-three RCTs and 1291 participants were included. Based on NMA, CoQ10, vitamin E, CoQ10 combined with vitamin E, and inositols were successful in decreasing TT as compared with PA; vitamin E was superior to other agents. Vitamin E and inositols were successful in increasing SHBG levels; inositols were stronger than vitamin E. CoQ10 alone or combined with vitamin E, and inositols were successful in decreasing HOMA-IR. Inositols had the best results among included nutraceuticals to ameliorate HOMA-IR, FBG, FINS, TG, TC, and LDL-C and correlated to improvements in BMI. There was no significant difference between the CoQ10 or vitamin E group and the PA group in ameliorating lipid metabolism, and vitamin D had no positive effects in ameliorating hyperandrogenism, BMI, glycolipid metabolism profiles compared with PA. For women with PCOS, inositols supplementation have some certain advantages in increasing SHBG and improving glycolipid metabolism when compared with nutraceuticals like CoQ10, vitamin E, vitamin D. Besides, vitamin E may be a better option in reducing TT and increasing SHBG. CoQ10 alone or combined with vitamin E can be helpful in decreasing HOMA-IR as well. [ABSTRACT FROM AUTHOR]

Conventional formulations cannot sufficiently control seizures and influence on cognitive corruption and oxidative stress with chronic usage in patients with epilepsy. To defeat this issue, it was planned to develop polymeric liposome formulations that are using for their bioavailability and enhancer impact in oral epilepsy treatment. In this study, chitosan-coated liposomal formulations that encapsulate carbamazepine (CBZ) and coenzyme Q10 (CoQ10) were prepared and optimized by utilizing response surface methodology (RSM). Encapsulation efficiencies of CBZ and CoQ10, which were chosen as dependent variables for optimized chitosan-coated liposomal formulations were determined as 76.13%±2.34% and 82.36%±3.15%, respectively. Narrow size distribution was provided with an average size of 187.1 ± 2.35 nm, while a spherical and uniform shape was approved with transmission electron microscopy analyses. Cumulative release of 78.23% for CBZ and 27.12% for CoQ10 was obtained after 24 hours of in-vitro release study in sink conditions. Physical stability analyses demonstrated that optimum liposomes were convenient for storage at 5 ± 3 °C for at least 90 days. As a result, optimum chitosan-coated liposome containing CBZ and CoQ10 formulations could be suggested as a hopeful approach concerning their release, particle size, high encapsulation efficiency and stability for the treatment of epilepsy. [ABSTRACT FROM AUTHOR]

Hyaluronic acid (HA) is found in connective tissue and participates in wound healing. We investigated the efficacy of a HA gel (2% hyaluronic acid; 1% antioxidants, coenzyme Q10 and vitamin E; and 5% benzocaine) on healing of palatal wounds in rats. We established two groups of rats: a control group treated with vehicle and an HA group treated with HA gel. The control group was divided into five subgroups and the HA group was divided into four subgroups according to the day on which animals were sacrificed. Wounds were created by elevating 5 mm diameter full thickness flaps. Healed and unhealed wound areas were measured using photographs. Transforming growth factor (TGF)-β, insulin-like growth factor (IGF), and collagen I and III expressions were determined using immunohistochemistry. The number of fibroblasts increased and inflammatory cells decreased from day 0 to 21 in both groups. The HA group exhibited more fibroblasts by day 7 compared to controls; (TGF)-β and IGF levels were similar between HA and control groups. HA groups exhibited fewer inflammatory cells than controls on days 3 and 7. We found significant differences in TGF-β and IGF levels among HA groups between days 3 and 21, and among control groups between days 0 and 21. Collagen I and III levels were greater for the day 3 HA group compared to controls. We observed improved wound healing in HA treated rats within 7 days. [ABSTRACT FROM AUTHOR]

Complementary, alternative and integrative medicine includes a myriad of therapies including herbal medicines, vitamins, dietary interventions and more, that are taken alone or in adjunct to standard conventional treatment. Often the main goals are to slow progression of disease, increase effectiveness of a drug, reduce side effects and improve quality of life. The study of these therapies and their influence in heart failure is not new. However, even for an experienced clinician, a gap exists between the literature and the application of knowledge to make a confident recommendation. This review has a focus on specific supplements that are commonly used for individuals with HF. It discusses the mechanism of action, expected benefits, potential adverse effects, suggested doses, forms and drug interactions of these therapies. The literature search methodology included using medical subject headings terms to search in PubMed. Articles used were screened and critically appraised by the authors of this review. There are promising outcomes pertaining to the use of CAM in patients with HF. Advances in large scale, randomized, placebo-controlled trials are necessary to support evidence-based decision making regarding the use of supplements in conjunction, and in comparison, to conventional therapies for heart failure. [ABSTRACT FROM AUTHOR]

Introduction: Migraine is a disabling neurovascular disorder characterized by increasing levels of pro-inflammatory cytokines and oxidative stress biomarkers. Curcumin and coenzyme Q10 (CoQ10) can exert neuroprotective effects through modulation of inflammation and oxidative stress. The aim of the present study was to evaluate the combined effects of nano-curcumin and CoQ10 supplementation on migraine symptoms and quality of life in migraine patients. Methods: One-hundred men and women (mean age 32 years) with episodic migraine based on the International Headache Society (IHS) criteria participated in this study. The subjects were randomly divided into four groups as (1) combination of nano-curcumin (80 mg) plus CoQ10 (300 mg), (2) nano-curcumin (80 mg), (3) CoQ10 (300 mg) and (4) the control (nano-curcumin and CoQ10 placebo included oral paraffin oil) beside usual prophylactic drugs for 8 weeks. Frequency, severity, duration of headache attacks, the headache diary results (HDR) and headache disability based on migraine-specific questionnaires were assessed at the baseline and end of the study. Results: Ninety-one of 100 patients completed the study. The results showed a significant effect of nano-curcumin and CoQ10 supplementation on frequency, severity, duration of migraine attacks and HDR compared to other groups (All P < 0.001). Nano-curcumin and CoQ10 group also had better scores in migraine-specific questionnaires at the end of the study compared to other groups (All P < 0.001). There were no side effects reported by the participants. Conclusions: These findings suggest a possible synergistic effect of nano-curcumin and CoQ10 on clinical features of migraine. Trial registration number: IRCT2017080135444N1. [ABSTRACT FROM AUTHOR]

Conventional formulations can not achieve wound healing efficiently and fail to accelerate wound regeneration. To overcome these problems, it was planned to develop nanoformulations that perform a positive effect on the wound healing duration and are suitable for topical use. In this study, liposomal film formulations that encapsulated d-panthenyl triacetate (PTA) and coenzyme Q10 (CoQ10) were optimized by using response surface methodology (RSM) and were analyzed for their wound healing efficacy and cytotoxicity on fibroblast (CCD1079 Sk) and keratinocyte (HEKa) cells. Swelling index, puncture strength, and puncture deformation values, which were choosen as dependent variables for the liposomal film formulation were found as 556.9% ± 21.3, 3.98 ± 0.98 N/mm2, and 6.57% ± 1.12, respectively. Cumulative release of 65.32% for PTA and 12.23% for CoQ10 was obtained after 24 hours of in vitro release study in sink conditions. The in vitro cytotoxicity and wound healing assay results suggested that optimum formulation could be used safely on fibroblast and keratinocyte cells and provided wound closure entirely after 24 h. Consequently, the optimum liposomal film containing PTA and CoQ10 formulations could be proposed as an innovative approach in wound healing treatment, considering their release, mechanical properties, stability, and effectiveness. [ABSTRACT FROM AUTHOR]

Objective: Coenzyme Q10 is an antioxidant and an essential mitochondrial cofactor which has been suggested to improve the clinical features of migraine. Several randomized clinical trials have examined the effects of Coenzyme Q10 on migraine with inconclusive results. The aim of this systematic review and meta-analysis was to evaluate the impact of Coenzyme Q10 supplementation on the frequency, severity, and duration of migraine attacks. Methods: A systematic review of the literature was conducted using ISI Web of Science, PubMed, Cochrane library and Scopus to identify eligible studies up to April 2018. Studies included were randomized clinical trials of Coenzyme Q10 supplementation that reported the frequency, severity, or duration of migraine attacks as a primary outcome. A meta-analysis of eligible studies was performed using the fixed effects model or the random effects model to estimate pooled effect size. Results: Four randomized clinical trials with 221 participants were included. Coenzyme Q10 supplementation significantly reduced the frequency of migraine attacks (weighted mean difference: −1.87 attacks/month, 95% CI: −2.69 to −1.05, p < 0.001) without significant heterogeneity among the studies (I2 = 36.6%, p = 0.192). Coenzyme Q10 supplementation had no significant effect on severity (weighted mean difference: −2.35 visual analog scale score, 95% CI: −5.19 to 0.49, p = 0.105) and duration of migraine attacks (weighted mean difference: −6.14 h, 95% CI: −13.14 to 0.87, p = 0.086) with high heterogeneity. Conclusion: Pooled analyses of available randomized clinical trials suggest that Coenzyme Q10 supplementation may reduce the frequency of migraine attacks per month without affecting the severity or duration of migraine attacks. [ABSTRACT FROM AUTHOR]

Objective: Mitochondrial dysfunction has been implicated in the pathophysiology of schizophrenia and other neuropsychiatric disorders. Though the exact mechanisms and clinical implications for this dysfunction are not fully determined, there is a hypothesis that deficiency in coenzyme Q10 (CoQ10) may contribute to mitochondrial impairments and be reflected in cognitive, affective, and energy disturbances in the disorders. CoQ10 is a critical component of the mitochondrial respiratory chain and an essential free radical scavenger, necessary for mitochondrial function. Here, we review the results of CoQ10 supplementation interventions for adults with various neurological and neuropsychiatric disorders and consider the therapeutic potential of CoQ10 supplementation for schizophrenia in light of these studies. Methods: A literature review of randomised controlled trials and open-label studies investigating the effect of CoQ10 as a single intervention in adults with neurological and neuropsychiatric disorders was conducted. Results: CoQ10 supplementation has some positive effects on fatigue, cognitive impairment and affective difficulties in several neurological and neuropsychiatric conditions with associated mitochondrial dysfunction. Discussion: CoQ10 may be of therapeutic value to schizophrenia given evidence of mitochondrial dysfunction in the disorder. [ABSTRACT FROM AUTHOR]

1. This study was performed to evaluate the effects of dietary supplementation of coenzyme Q10 (CoQ10) on laying rate, body weight, plasma metabolites and some liver gene expression in broiler breeder hens. 2. A total of 128 broiler breeder hens (Arbor Acres Plus, 47 weeks of age) were randomly distributed to four dietary groups supplemented with different levels of CoQ10 (0, 300, 600 or 900 mg/kg diet) with four replicates of eight hens each. During 47–54 weeks of age, laying rate, egg mass and body weight were recorded weekly. To assay plasma biochemical indicators, blood samples were collected at 54 weeks of age. At the end of the experiment, for evaluating the abdominal fat weight, liver weight and expression of the adiponectin and proliferator-activated receptor-α (PPAR-α) genes in the liver, eight hens per treatment were selected, weighed and humanely killed by decapitation. 3. Dietary supplementation of CoQ10 linearly decreased abdominal fat weight, alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities by increased levels of CoQ10. The plasma levels of glucose, cholesterol and alkaline phosphatase (ALP) activity were quadratically decreased by increased levels of CoQ10. The best plasma levels of glucose, cholesterol and ALP activity were estimated at 562.5, 633.3 and 517.8 mg CoQ10/kg diet, respectively. Adiponectin and PPARα gene expression exhibited a linear increased by increased levels of CoQ10. 4. In conclusion, addition of CoQ10 to the diet influenced lipid metabolism and expression of the adiponectin and PPAR-α genes, which might be partially due to the improvement in mitochondrial metabolism and energy production. However, further studies are necessary to determine the effects of CoQ10 on these indicators in broiler breeder hens during ageing. [ABSTRACT FROM AUTHOR]

Interactions between drugs and micronutrients have received only little or no attention in the medical and pharmaceutical world in the past. Since more and more pharmaceutics are used for the treatment of patients, this topic is increasingly relevant. As such interactions - depending on the duration of treatment and the status of micronutrients - impact the health of the patient and the action of the drugs, physicians and pharmacists should pay more attention to such interactions in the future. This review aims to sensitize physicians and pharmacists on drug micronutrient interactions with selected examples of widely pescribed drugs that can precipitate micronutrient deficiencies. In this context, the pharmacist, as a drug expert, assumes a particular role. Like no other professional in the health care sector, he is particularly predestined and called up to respond to this task. The following article intends to point out the relevance of mutual interactions between micronutrients and various examples of widely used drugs, without claiming to be exhaustive. [ABSTRACT FROM AUTHOR]

Background: Glycemia is related to energy production during exercise. Coenzyme Q10 is an antioxidant that participates in adenosine triphosphate synthesis in mitochondria. The aim of this study was to investigate the level of coenzyme Q10, glucose parameters, and antioxidant capacity in athletes. Methods: This study was designed as a cross-sectional study. Well-trained college athletes (n = 43) and age-gender matched healthy subjects (n = 25) were recruited from a college. The levels of glucose parameters, oxidative stress, antioxidant enzymes activity, Trolox equivalent antioxidant capacity (TAC), and coenzyme Q10 status were measured in the present study. Results: The athletes had a significantly lower level of white blood cells (WBC) coenzyme Q10 than the healthy subjects (0.34 ± 0.24 vs. 0.65 ± 0.43 nmol/g, p < 0.01); however, no significant difference was detected in plasma coenzyme Q10 between the two groups. Regarding the glucose parameters, the athletes had significantly higher values for HbA1c (5.5 ± 0.3 vs. 5.3 ± 0.3%, p < 0.05) and quantitative insulin sensitivity check index (QUICKI, 0.37 ± 0.03 vs. 0.34 ± 0.03, p < 0.05), and lower homeostatic model assessment-insulin resistance (HOMA-IR, 1.5 ± 0.8 vs. 2.9 ± 3.8, p < 0.05) than the healthy subjects. A higher level of TAC was found in the athletes (serum, 5.7 ± 0.3 vs. 5.4 ± 0.2 mM Trolox; erythrocyte, 10.5 ± 0.6 vs. 10.0 ± 0.5 mM Trolox, p < 0.05). In addition, WBC coenzyme Q10 status was significantly correlated with catalase activity (r = 0.56, p < 0.01), GPx activity (r = 0.56, p < 0.01), serum TAC (r = 0.54, p < 0.01), fasting glucose (β = − 1.10, p < 0.01), HbA1c (β = − 0.82, p < 0.01), HOMA-IR (β = − 1.81, p < 0.01), and QUICK (β = 0.08, p < 0.01). Conclusions: Athletes may suffer from a marginal coenzyme Q10 deficiency, and the level was related to glycemic control and antioxidant capacity. Further interventional studies are needed to clarify an adequate dose of coenzyme Q10 supplementation in athletes to optimize their coenzyme Q10 status and athletic performance or recovery during exercise. [ABSTRACT FROM AUTHOR]

Background: Work-related fatigue is common among nurses and may negatively affect patient safety and nurses' well-being. Pharmacological interventions with stimulants have had mixed results. The aim of this study was to determine whether coenzyme Q10 (CoQ10) supplementation improved work-related fatigue in nurses. Methods: In phase one, all nurses working at our institution filled out questionnaires to assess fatigue and sleep quality. In phase two, a randomized, double-blind, placebo-controlled trial, nurses with significant work-related fatigue were randomly assigned to either 200 mg daily CoQ10 (n = 54) or placebo (n = 51). The primary endpoint was changed in fatigue from baseline to week 4 using a validated questionnaire, the nurses' fatigue scale. The secondary outcome, sleep quality, was measured with the Pittsburgh Sleep Quality Index. Results: At baseline, 53.6% of 539 nurses had significant fatigue on the nurses' fatigue scale. A total of 68.8% of all nurses worked over 25 shifts a month and 40.7% of them had significant fatigue. A significant correlation was found between fatigue and number of work shifts in those nurses (p =.004). A significant improvement in fatigue and sleep quality was found in the CoQ10 group as compared to the baseline and the placebo group (p =.06 and p =.001, respectively). Conclusion: Preferred multifactorial approaches, e.g. reduced work hours, to fatigue reduction are not currently feasible at our center. Given this practical limitation, CoQ10 supplementation was effective in improving fatigue in nurses and maybe a safe approach, ideally in conjunction with other work condition changes. [ABSTRACT FROM AUTHOR]

Objectives: Coenzyme Q10, incorporated in DOPC lyposomes or naturally present in liver bovine mitochondria or in human blood plasma, was reacted with nitrogen dioxide •NO2 or with a •NO/•NO2 mixture. Methods and Results: The reaction course was monitored by Electron Paramagnetic Resonance (EPR) spectroscopy and in all cases the formation of a di-tert-alkyl nitroxide was observed, deriving from the addition of •NO2 to one of the double bonds, most likely the terminal one, of the isoprenic chain. The rate constant for nitroxide formation was also determined by EPR spectroscopy and an initial rate of ca. 7 × 10−8 M s−1 was obtained. [ABSTRACT FROM AUTHOR]

Objective: To assess whether supplementation with Coenzyme Q10 (CoQ10) during pregnancy alleviate preeclampsia symptoms and the underlying mechanism in the rats with preeclampsia. Methods: Forty-five pregnant Wistar rats were equally divided into three groups randomly and received subcutaneous saline injection (control group, n = 15) or 200 mg/kg L-NAME injection to induce preeclampsia symptoms (PE group, n = 30). The PE rats were treated by distilled water (PE+DW group, n = 15) and CoQ10 (PE+CoQ10 group, n = 15) on day 15 to 21 of gestation randomly. Physiological characteristics such as urine volume, total urine protein, blood pressure, number and weight of pups were recorded. Fluorescent dye was used to detect mitochondrial membrane potential in placenta. Real-time fluorescent quantitative PCR was used to detect the expression of mitochondrial DNA(mtDNA) in placenta. Results: There was no statistic difference among all the three groups on day 10 of gestation in SBP and 24-h proteinuria (P > 0.05). Whereas, SBP and 24-h proteinuria were significantly higher in PE group than control group on day 15 and 21 of gestation (P < 0.05). SBP and 24-h proteinuria were significantly lower in PE+CoQ10 group than PE+DW group on day 21 of gestation (P < 0.05). The number and weight of normal pups were significantly lower in PE group than the control group (P < 0.05), which were most notably in distilled water group, and the number and weight of normal pups were markedly bigger in PE+CoQ10 group rats compared to PE+DW (P < 0.05). The PE+CoQ10 group showed a significantly higher in level of mitochondrial membrane potential than PE+DW group. The expression of mtDNA was significantly higher in the PE+CoQ10 group compared with PE+DW group (P < 0.05). Conclusions: CoQ10 can alleviate preeclampsia symptoms and enhance the function of mitochondria in the placenta. [ABSTRACT FROM AUTHOR]

Backgrounds and aims: Migraine and inflammation are correlated. Coenzyme Q10 (CoQ10) as an anti-inflammatory agent has shown useful effects in other diseases. The present study aimed to assess the effect of CoQ10 supplementation on inflammation and clinical features of migraine. Methods: This randomized double-blind placebo-controlled clinical trial was conducted among 45 non-menopausal women aged 18–50 years, diagnosed for episodic migraine according to the International Headache Society. After one month run-in period, subjects received CoQ10 (400 mg/day CoQ10, n = 23) or placebo (wheat starch, n = 22) for three months. All the patients got prophylactic medication too. Serum CoQ10 concentration, Calcitonin gene-related peptide (CGRP), interleukin (IL)-6, IL-10 and tumor necrosis factor-α (TNF-α) were measured at the beginning and end of the study. Results: CoQ10 supplementation reduced CGRP and TNF-α significantly (p = 0.011 and p = 0.044, respectively), but there were no significant differences in serum IL-6 and IL-10 between the two groups. Significant increase in serum CoQ10 levels was evident with CoQ10 therapy (P < 0.001). A significant improvement was found in frequency (p = 0.018), severity (p = 0.001) and duration (p = 0.012) of migraine attacks in CoQ10 group compared to placebo. Conclusion: CoQ10 supplementation may decrease CGRP and TNF-α with no favorable effects on IL-6 and IL-10 in patients with migraine. [ABSTRACT FROM AUTHOR]

Although coenzyme Q10 (CoQ10) supplementation has shown to reduce pain levels in chronic pain, the effects of CoQ10 supplementation on pain, anxiety, brain activity, mitochondrial oxidative stress, antioxidants, and inflammation in pregabalin-treated fibromyalgia (FM) patients have not clearly elucidated. We hypothesised that CoQ10 supplementation reduced pain better than pregabalin alone via reducing brain activity, mitochondrial oxidative stress, inflammation, and increasing antioxidant levels in pregabalin-treated FM patients. A double-blind randomised placebo-controlled trial was conducted. Eleven FM patients were enrolled with 2 weeks wash-out then randomly allocated to 2 treatment groups; pregabalin with CoQ10 or pregabalin with placebo for 40 d. Then, patients in CoQ10 group were switched to placebo, and patients in placebo group were switched to CoQ10 for another 40 d. Pain pressure threshold (PPT), FM questionnaire, anxiety, and pain score were examined. Peripheral blood mononuclear cells (PBMCs) were isolated to investigate mitochondrial oxidative stress and inflammation at day 0, 40, and 80. The level of antioxidants and brain positron emission tomography (PET) scan were also determined at these time points. Pregabalin alone reduced pain and anxiety via decreasing brain activity compared with their baseline. However, it did not affect mitochondrial oxidative stress and inflammation. Supplementation with CoQ10 effectively reduced greater pain, anxiety and brain activity, mitochondrial oxidative stress, and inflammation. CoQ10 also increased a reduced glutathione levels and superoxide dismutase (SOD) levels in FM patients. These findings provide new evidence that CoQ10 supplementation provides further benefit for relieving pain sensation in pregabalin-treated FM patients, possibly via improving mitochondrial function, reducing inflammation, and decreasing brain activity. [ABSTRACT FROM AUTHOR]

Background: Multiple micronutrient supplementation has been suggested to have a role on health outcomes in patients with heart failure (HF), but the evidence is inconclusive.Objective: To elucidate the role of multiple micronutrient supplementation in heart failure we performed a comprehensive review of the literature.Methods and Results: The search in databases included PUBMED (until June 2018) to detect randomized controlled trials (RCTs) and meta-analyzes that investigated the impact of micronutrient supplementation in HF.Results: With more than 2357 titles and abstracts reviewed, we included only the studies suitable for the final review. Whether alone or in combination, micronutrients have been found to improve the health outcomes of patients with HF by improving symptoms, work capacity and left ventricular ejection fraction (LVEF), thus increasing the quality of life in these patients.Conclusion: Future studies are needed to document the effects of multiple micronutrient associations in order to include them in nutritional guidelines to increase survival and to improve quality of life in patients with heart failure. [ABSTRACT FROM AUTHOR]

Introduction: Statin drugs have become the most highly prescribed drugs for cardiovascular disease. However, there is disagreement as to the existence of adverse effects of statin administration on cognitive function. Therefore, it is important to better understand the effects of statins on cognition and possible mechanisms of these effects. Areas covered: We analyzed relevant studies of the relationship between cognitive performance and statin and usage. We included articles published between 2018 and 1992. We identified three randomized trials, one observational study and 66 case reports that provided credible evidence of statin-induced cognitive impairment. We also identified seven randomized trials and two observational studies reporting no significant evidence of statin-induced cognitive impairment. Expert opinion: We found methodological differences that may have contributed to the divergence of these results. Evaluation of all these studies indicated that statin-associated cognitive decline is a real entity. Likely mechanisms to explain the adverse effects include 1. Reduction of synthesis of coenzyme Q10 with consequent increasing oxidative stress and reduction of cerebral energy production; 2. Depletion of central nervous system myelin by inhibition of cholesterol synthesis. We conclude that statin-induced cognitive decline does exist, needs to be better recognized and requires more studies of prevention and treatment. [ABSTRACT FROM AUTHOR]

Objectives: Coenzyme Q10 (CoQ10, ubiquinone) stands among the safest supplements in the elderly to protect against cardiovascular disorders. Noteworthy, CoQ10 deficiency is common in many surviving stroke patients as they are mostly prescribed statins for the secondary prevention of stroke incidence lifelong. Accordingly, the current study aims to experimentally examine whether CoQ10 supplementation in animals receiving atorvastatin may affect acute stroke-induced injury. Methods: Adult rats underwent transient middle cerebral artery occlusion after atorvastatin pretreatment (5 or 10 mg/ kg/day; po; 30 days) with or without CoQ10 (200 mg/kg/day). After 24 hours ischemic/reperfusion injury, animals were subjected to functional assessments followed by cerebral molecular and histological to detect inflammation, apoptosis and oxidative stress. Results: Animals dosed with 10 mg/kg presented the worst neurological function and brain damage in the acute phase of stroke injury. CoQ10 supplementation efficiently improved functional deficit and cerebral infarction in all stroke animals, particularly those exhibiting statin toxicity. Such benefits were associated with remarkable anti-inflammatory and anti-apoptotic effects, based on the analyzed tumor necrosis factor-α, interleukin-6, Bax/Bcl2 and cleaved caspase 3/9 immunoblots. Importantly, our fluoro-jade staining data indicated CoQ10 may revert the stroke-induced neurodegeneration. No parallel alteration was detected in stroke-induced oxidative stress as determined by malondialdehyde and 8-oxo-2′-deoxyguanosine levels. Discussion: These data suggest that all stroke animals may benefit from CoQ10 administration through modulating inflammatory and degenerative pathways. This study provides empirical evidence for potential advantages of CoQ10 supplementation in atorvastatin-receiving patients which may not shadow its antioxidant properties. [ABSTRACT FROM AUTHOR]

Objective: The aim of this study was to develop, characterize and evaluate stability of a gel containing coenzyme Q10 (Q10)-loaded liposomes, and enhance the stability of Q10 in the nanocarrier-containing gel compared to the conventional gel. Methods: Q10-loaded liposome dispersions prepared from unsaturated or saturated lecithin, were characterized for particle size, polydispersity index (PDI), zeta-potential, pH value, oxidation index, Q10-content and morphology, and incorporated into carbomer gel. Liposome gels and liposome-free gel were analyzed for flow properties, pH values, Q10-content, and liposomes size and PDI (liposome gels), 48 h after preparation and in predetermined time intervals during 6 months storage at different temperatures in order to predict their long term stability. Results: Liposomes were of small particle size, homogeneous, negatively charged, and their incorporation into gel did not significantly change (p > .05) their particle size and PDI. All gels revealed non-Newtonian, shear-thinning plastic flow behavior during storage with no marked changes in rheological parameters. Storage of gels did not significantly influence the pH value (p > .05), while it significantly decreased Q10-content (p < .05). Q10 was significantly more (p < .05) stable in liposome gel containing unsaturated lecithin liposomes (G1) than in gel containing saturated lecithin liposomes (G2) and liposome-free gel (G3). Conclusions: Q10-loaded liposome gel G1 was the optimal formulation, since during storage at different temperatures, it did not show significant increase in liposome size and PDI, it provided significantly higher stability for Q10 than other gels and its pH value was suitable for skin application. Due to limited Q10-stability it should be stored at 4 °C. [ABSTRACT FROM AUTHOR]

Multiple acyl-CoA dehydrogenase deficiency (MADD), an autosomal recessive metabolic disorder of fatty acid metabolism, is mostly caused by mutations in the ETFA, ETFB or ETFDH genes that result in dysfunctions in electron transfer flavoprotein (ETF) or electron transfer flavoprotein-ubiquinone dehydrogenase (ETFDH). In β-oxidation, fatty acids are processed to generate acyl-CoA, which is oxidised by flavin adenine dinucleotide and transfers an electron to ETF and, through ETFDH, to mitochondrial respiratory complex III to trigger ATP synthesis. Coenzyme Q10 (CoQ10) is believed to be a potential treatment that produces symptom relief in some MADD patients. CoQ10 acts as a key regulator linking ETFDH and mitochondrial respiratory complex III. Our aim is to investigate the effectiveness of CoQ10 in serving in the ETF/ETFDH system to improve mitochondrial function and to reduce lipotoxicity. In this study, we used lymphoblastoid cells with an ETFDH mutation from MADD patients. ETFDH dysfunction caused insufficient β-oxidation, leading to increasing lipid droplet and lipid peroxide accumulation. In contrast, supplementation with CoQ10 significantly recovered mitochondrial function and concurrently decreased the generation of reactive oxygen species and lipid peroxides, inhibited the accumulation of lipid droplets and the formation of the NOD-like receptor family pyrin domain-containing three (NLRP3) inflammasome, and reduced interleukin-1β release and cell death. These results clarify the causal role of CoQ10 in coupling the electron transport chain with β-oxidation, which may promote the development of CoQ10-directed therapies for MADD patients. [ABSTRACT FROM AUTHOR]

Patients with type 2 diabetes mellitus (T2DM) have been known to be suffering from coenzyme Q10 (CoQ10) deficiency which results in some complications in them. The purpose of this clinical trial study was to evaluate the effects of CoQ10 supplementation on serum values of adiponectin (A), leptin (L), 8-isoprostane, malondialdehyde (MDA), the A/L ratio in women with T2DM. Sixty-eight women with T2DM were enrolled in the current study and were randomly divided into drug (n = 34) and placebo (n = 34) groups who were consuming 100 mg CoQ10 and 100 mg cellulose acetate per day for 12 weeks, respectively. Measurements were performed at the beginning and after the intervention. Serum values of adiponectin (p = .001) and the A/L ratio (p = .001) were increased while values of leptin (p = .041), MDA (p = .023), 8-isoprostane (p = .004) were decreased significantly in drug group after intervention. This study had shown that CoQ10 supplementation in women with T2DM was effective in elevation of adiponectin and the A/L ratio and reduction of leptin, MDA and 8-isoprostane which could result in improving insulin resistance and modulating oxidative stress situation. [ABSTRACT FROM AUTHOR]

The objective of the study was to develop a self-microemulsifying drug delivery system (SMEDDS), also known as microemulsion preconcentrate, for oral delivery of five poorly water-soluble nutraceuticals or bioactive agents, namely, vitamin A, vitamin K2, coenzyme Q10, quercetin and trans-resveratrol. The SMEDDS contained a 1:1 mixture (w/w) of Capmul MCM NF (a medium chain monoglyceride) and Captex 355 EP/NF (a medium chain triglyceride) as the hydrophobic lipid and Tween 80 (polysorbate 80) as the hydrophilic surfactant. The lipid and surfactant were mixed at 50:50 w/w ratio. All three of the SMEDDS components have GRAS or safe food additive status. The solubility of nutraceuticals was determined in Capmul MCM, Captex 355, Tween 80, and the SMEDDS (microemulsion preconcentrate mixture). The solubility values of vitamin A palmitate, vitamin K2, coenzyme Q10, quercetin, and trans-resveratrol per g of SMEDDS were, respectively, 500, 12, 8, 56, and 87 mg. Appropriate formulations of nutraceuticals were prepared and filled into hard gelatin capsules. They were then subjected to in vitro dispersion testing using 250 mL of 0.01 N HCl in USP dissolution apparatus II. The dispersion test showed that all SMEDDS containing nutraceuticals dispersed spontaneously to form microemulsions after disintegration of capsule shells with globule size in the range of 25 to 200 nm. From all formulations, except that of vitamin K2, >80-90% nutraceuticals dispersed in 5-10 min and there was no precipitation of compounds during the test period of 120 min. Some variation in dispersion of vitamin K2 was observed due to the nature of the material used (vitamin K2 pre-adsorbed onto calcium phosphate). The present report provides a simple and organic cosolvent-free lipid-based SMEDDS for the oral delivery of poorly water-soluble nutraceuticals. Although a 50:50 w/w mixture of lipid to surfactant was used, the lipid content may be increased to 70:30 without compromising the formation of microemulsion. [ABSTRACT FROM AUTHOR]

This study depicts coenzyme Q10 (CoQ10) and retinaldehyde (RAL) co-loaded nanostructured lipid carriers (NLCs); having activity on different targets of photoageing, which can overcome deficits of conventional topical dosage forms. The developed NLCs were characterised for particle size, polydispersity index and percent entrapment efficiency (%EE), followed by their incorporation into Carbopol®934 P-NF gel.In vitrocellular uptake and cytotoxicity assay was performed to evaluate NLCs andin vivostudy on ultraviolet- (UV) induced wrinkle model to determine efficacy of NLCs. The developed stable, homogenous and spherical NLCs with size range of 200–230 nm and more than 80 %EE, showed prolonged, biphasicin vitrorelease pattern for CoQ10 and RAL.Ex vivostudy portrayed negligible permeation through skin but appreciable penetration and distribution in skin layers. This has shown good uptake of both drugs with least cytotoxicity in cell culture studies.In vivoirritation study on Sprague Dawley (SD) rats and pharmacodynamic study on female Swiss albino mice proved it less irritant and efficacious. The developed NLCs thus hold promise in the efficient management of wrinkle and their reduction as indicated by the data obtained. [ABSTRACT FROM PUBLISHER]

The present study showed the development of nanocapsules containing the association of the coenzyme Q10 and vitamin E acetate and the evaluation of their effect on in vitro cells culture of malignant glioma and melanoma. In order to investigate if nanocapsules are able to protect coenzyme Q10 from degradation under UVC radiation, a photostability study was carried out. For this, three concentrations of vitamin E acetate were evaluated (1%, 2%, or 3%). Nanocapsules presented suitable physicochemical characteristics and were able to protect coenzyme Q10 from photodegradation. In addition, this protection was influenced by higher vitamin E acetate concentrations, attributing to this oil an important role on coenzyme Q10 photostabilization. Regarding to in vitro citotoxicity assay, nanocapsules containing coenzyme Q10 and 2% vitamin E significantly reduced glioma and melanoma cell viability in 61% and 66%, respectively. In this sense, these formulations represent interesting platforms for the delivery of coenzyme Q10 and vitamin E acetate, presenting effect on the reduction of malignant cells viability. [ABSTRACT FROM AUTHOR]

Objective:In this study, solid dispersion (SD) for oral delivery of a poorly water-soluble drug, coenzyme Q10 was developed by supercritical fluid technology and characterizedin vitroandin vivo. Methods:Dissolution was used to optimize the formulations of CoQ10-SD. The physicochemical properties of SD were investigated by differential scanning calorimetry (DSC), powder X-ray diffraction (PXRD), and scanning electron microscopy (SEM). The supercritical fluid chromatography–electrospray ionization tandem mass spectrometry (SFC–ESI-MS/MS) was used for thein vivostudy. Results:The results of DSC and PXRD indicated that the drug in SD was in amorphous state.In vitrodrug release, the dissolution of coenzyme Q10 in solid dispersion improved to 78.8% compared with commercial tablets of 0.16%. The area underc–tcurve (AUC0–72h) and mean maximum concentrations (Cmax) of CoQ10-SD were 2.43-fold and 3.0-fold, respectively higher than that of commercial tablets in rats, confirming improved bioavailability. Conclusion:Supercritical fluid technology was successfully used for the preparation and analysis of CoQ10-SD for the first time and significantly improved the dissolution and bioavailability of coenzyme Q10. [ABSTRACT FROM PUBLISHER]

Coenzyme Q10 (CoQ10) is an insoluble, poorly permeable antioxidant with great biological value which acts as anti-aging and anti-wrinkle agent. To improve its permeability through topical application, the current study aimed at formulating oil/water (o/w) nanoemulsion (NE) as an efficient vehicle for delivering (CoQ10) through the skin barriers. The solubility of (CoQ10) was tested for various oils, surfactants (S), and co-surfactants (CoS). The NE region was determined by constructing pseudoternary phase diagrams. NE formulae containing 1, 2, and 3% w/w drug have been subjected to thermodynamic stability test. The formulae that passed thermodynamic stability tests were characterized by physical properties as pH, viscosity, refractive index, droplet size, zeta-potential, TEM, electroconductivity,in vitrorelease, andex vivopermeation. The formula ‘F2’ containing 10% w/w isopropyl myristate (oil phase), 60% w/w of Tween 80: Transcutol HP mixture (S/CoSmix) at ratio 2:1, 30% w/w water and 2% w/w drug was evaluated for its anti-wrinkle efficiency using an animal model. The ‘F2’ formula showed 11.76 ± 1.1 nm droplet size, 1.4260 ± 0.0016 refractive index, 0.228 PDI, −14.7 ± 1.23 mv zeta potential, 7.06 ± 0.051 pH, 199.05 ± 0.35 cp viscosity, and the highest percentage of drug release in the selected dissolution media. About 47.21% of the drug was released in phosphate buffer 7.4 containing 5% w/v Labrasol and 5% w/v isopropyl alcohol through 24 h. It also showed the highest drug flux (Jss = 3.164 µg/cm2/h), enhancement ratio (Er = 8.32), and permeability coefficient (Kp = 22.14 × 10−4cm2/h). CoQ10 NE reduced the skin wrinkles and gave the skin smooth appearance. Our investigation suggests the potential use of NE as a vehicle for enhancing solubility and permeability of CoQ10 and thus improving its anti-wrinkle efficiency. [ABSTRACT FROM PUBLISHER]

Purpose: To evaluate protective effect of coenzyme Q10 (CoQ10) in lacrimal glands against high-dose radioactive iodine (RAI)-associated oxidative damage. Materials and Methods: Thirty Wistar albino rats were randomly divided into three groups. Group 1 was the control group. Group 2 received 3 mCi/kg RAI via gastric gavage but no medication. Group 3 received 3 mCi/kg RAI via gastric gavage and 30 mg/kg/day CoQ10 intraperitoneally. CoQ10 was started at day one just before RAI administration and continued for five days. Seven days after RAI therapy, the animals were anesthetized and decapitated. Intraorbital (IG), extraorbital (EG), and Harderian (HG) lacrimal glands were removed bilaterally for histopathological and tissue cytokine level assessments. Results: Abnormal lobular pattern, acinar fibrosis, lipofuscin-like accumulations, perivascular infiltration, cell size variation, abnormal cell outlines, irregular nucleus shapes in all lacrimal gland types (p < 0.05 for each), periductal fibrosis, periductal and periacinar fibrosis in EG (p = 0.01, 0.044, respectively) and in HG (p = 0.036, 0.044, respectively), periductal infiltration in HG (p = 0.039) and IG (p = 0.029), acinar atrophy in EG (p = 0.044), and cell shape variation in IG (p = 0.036) were observed more frequently in group 2 than in other groups. RAI caused significant increase in TNF-α, IL-6, nuclear factor kappa B, and total oxidant status, and decrease in IL-2, IL-10, and total antioxidant status levels (p < 0.05 for each). Addition of CoQ10 decreased all cytokine levels, increased nuclear factor kappa B levels more, and increased total antioxidant status levels significantly (p < 0.05 for each). Conclusions: RAI administration causes prominent inflammatory response in lacrimal glands. Addition of CoQ10 ameliorates the oxidative damage and protects lacrimal glands both in histopathological and tissue cytokine level assessments. Protection of lacrimal glands against oxidative damage may become a new era of CoQ10 use in the future. [ABSTRACT FROM AUTHOR]

Introduction: Friedreich ataxia (FRDA) is a progressive, inherited, neurodegenerative disease for which there is currently no cure or approved treatment. FRDA is caused by deficits in the production and expression of frataxin, a protein found in the mitochondria that is most likely responsible for regulating iron-sulfur cluster enzymes within the cell. A decrease in frataxin causes dysfunction of adenosine triphosphate synthesis, accumulation of mitochondrial iron, and other events leading to downstream cellular dysfunction. Areas covered: Therapeutic development for FRDA currently focuses on improving mitochondrial function and finding ways to increase frataxin expression. Additionally, the authors will review potential approaches aimed at iron modulation and genetic modulation. Finally, gene therapy is progressing rapidly and is being explored as a treatment for FRDA. Expert commentary: The collection of multiple therapeutic approaches provides many possible ways to treat FRDA. Although the mitochondrial approaches are not thought to be curative, as the primary frataxin deficit will remain, they may still produce improvements in quality of life and slowing of progression. Therapies aimed at frataxin restoration are more likely to truly modify the disease, with gene therapy as the best possibility to alter the course of the disease from both a cardiac and neurological perspective. [ABSTRACT FROM PUBLISHER]

The present study evaluates the prophylactic efficacy of α-tocopherol (α-TOH), resveratrol (RES), and coenzyme Q10 (CoQ10) co-loaded self-nanoemulsifying drug delivery system (α-TOH-RES-CoQ10 SNEDDS) in 7,12-Dimethylbenz[a]anthracene (DMBA) induced breast cancer model. SNEDDS formulation components were rationally selected and optimized for maximum drug loading by applying the design of experiments and further evaluated for stability in simulated gastrointestinal fluids, functional stability of antioxidants,in vitrorelease, Caco-2 cell uptake, oral bioavailability and prophylactic anticancer activity. The SNEDDS demonstrated excellent stability in stimulated gastrointestinal fluids. The functional activity of antioxidants was confirmed by 2,2-diphenylpicrylhydrazyl (DPPH) scavenging assay wherein significantly (p > .05) higher antioxidant activity was observed in case of SNEDDS as compared with free antioxidants. Coumarin 6 (C-6)-loaded SNEDDS formulation demonstrated remarkably higher Caco-2 cell uptake in comparison with free C-6, indicative of efficient internalization of sub-micron SNEDDS droplets by Caco-2 cells. In line with Caco-2 cell uptake observations, α-TOH-RES-CoQ10-SNEDDS showed ∼2.30- and ∼3.64-fold increase in the AUC0−∞values of RES and CoQ10 in comparison with free antioxidants. Significantly lower (p < .001) tumor volume (∼327 mm3) was found in case of animals treated with α-TOH-RES-CoQ10-SNEDDS in comparison with free antioxidant combination (∼1070 mm3) and DMBA control (∼1540 mm3) groups. Conclusively, the proposed strategy posed great potential in improving the prophylactic activity of antioxidants and hold promise for further exploration. [ABSTRACT FROM PUBLISHER]

This study was aimed to investigate the therapeutic potential of coenzyme Q10 and its combination with sitagliptin in experimentally induced diabetic nephropathy. The diabetic rats were treated with coenzyme Q10 or sitagliptin and their concomitant administration. Various parameters of renal function like serum creatinine, urea, uric acid and markers of oxidative stress such as renal malondialdehyde content (MDA), glutathione (GSH) level and superoxide dismutase (SOD), catalase activities were measured. TNF-α, TGF-β, MPO activity and nitrite content were estimated in renal tissue with histopathological observation. Diabetic rats showed a significant reduction in renal function, which was reflected with an increase in serum creatinine, urea and uric acid levels. Streptozotocin-nicotinamide caused renal tubular damage with a higher MDA level, depletion of SOD and CAT activity and GSH level. In addition, TNF-α, TGF- β, MPO activity and nitrite content were significantly increased in diabetic rats. Treatment with coenzyme Q10 or sitagliptin and their co-administration ameliorated STZ-nicotinamide-induced renal damage which was reflected by decreased oxidative stress, TNF-α, TGF-β, MPO activity, nitrite content along with histopathological changes. To conclude, concomitant administration of coenzyme Q10 and sitagliptin showed a better renoprotective effect than coenzyme Q10 or sitagliptin when given alone. [ABSTRACT FROM PUBLISHER]

This study explored effects of ubiquinol-10 and ubiquinone-10, two different forms of coenzyme Q10, in diabetic rats. Oxidative stress is characterized by the depletion of antioxidant defenses and overproduction of free radicals that might contribute to, and even accelerate, the development of diabetes mellitus (DM) complications. Coenzyme Q10 was administered orally to diabetic rats and oxidative stress markers were then assessed. Bioavailability in normal rats was additionally assessed in various tissues and subcellular fractions after short-term and long-term coenzyme Q10 supplementation. Elevated nonfasting blood glucose and blood pressure in diabetic rats were decreased by ubiquinone-10. Both ubiquinol-10 and ubiquinone-10 ameliorated oxidative stress, based on assays for reactive oxygen metabolites and malondialdehyde. Coenzyme Q10 levels increased with both treatments and liver nicotinamide adenine dinucleotide phosphate (NADPH) coenzyme Q reductase with ubiquinone-10. Ubiquinol-10 was better absorbed in the liver and pancreas than ubiquinone-10, though both were similarly effective. In bioavailability study, a longer period of coenzyme Q10 supplementation did not lead to its accumulation in tissues or organelles. Both forms of coenzyme Q10 reduced oxidative stress in diabetic rats. Long-term supplementation of coenzyme Q10 appeared to be safe. [ABSTRACT FROM AUTHOR]

Cryopreservation-induced oxidative stress (OS) may lead to lipid peroxidation, which may be responsible for decreased cell survival rate. Coenzyme Q10 (CoQ10) as a potent antioxidant may improve cell viability by neutralizing OS. In this study, oxidative lipid injury following the vitrification of preantral follicles was investigated. The effects of CoQ10 treatment on the malondialdehyde (MDA) levels, lipid peroxidation products, and activities of enzymatic and nonenzymatic antioxidants of vitrified preantral follicles were also studied. Preantral follicles were isolated from immature mouse ovaries and were vitrified. After warming, these follicles were cultured with or without CoQ10 for four days. The levels of total antioxidant capacity (TAC) and MDA, as well as the activities of superoxide dismutase (SOD), glutathione peroxidase (GPX), and catalase (CAT), were assessed at 0, 24, 48, 72, and 96 hours of culture period. The MDA level in the vitrified preantral follicles was higher than that in the fresh groups. By contrast, the MDA level was significantly lower in the groups with CoQ10 treatment than in those without this treatment during cultivation. The TAC level was higher in the fresh preantral follicles than in the vitrified groups. The rates were also higher in the CoQ10-treated groups than in those without this treatment. The activities of SOD, GPX, and CAT were also significantly higher in the fresh groups than in the vitrified groups, especially in the groups with CoQ10 treatment than in those without this treatment. Lowering the vitrification-induced lipid peroxidation of preantral follicles by CoQ10-supplemented maturation medium may be mediated by increasing SOD, GPX, and CAT activities and TAC level during cultivation. [ABSTRACT FROM AUTHOR]

To improve the oral bioavailability of nanocrystalline drug preparations, the cationic 12-3-12 quaternary ammonium surfactant gemini was introduced into nanocrystals as a novel gastrointestinal bioadhesive material. Coenzyme Q10 (CoQ10), a typical Biopharmaceutics Classification System (BCS) class II drug, was used as a model drug. The 12-3-12 gemini surfactant was added to the preparation at a low concentration and imbued the particles with abundant positive charges.In vitroandin vivogastrointestinal adhesion tests confirmed that the gemini-modified nanocrystals were prone to adhere to the upper gastrointestinal tract (GIT), thereby prolonging retention time in the GIT and enhancing absorption. In the distribution study in rats, the use of nanocrystals modified with gemini led to greater drug distribution to the heart and the liver than that achieved with the naked nanocrystals. A pharmacokinetic study in beagle dogs showed that the gemini-modified CoQ10 nanocrystals improved the oral bioavailability of CoQ10 in a dose-dependent manner, and the smaller size produced a much better effect with the same gemini modification. These results demonstrate that the cationic surfactant gemini is a promising oral bioadhesive material with applications in nanoscale drug delivery systems. [ABSTRACT FROM AUTHOR]

The hepatotoxic effects of the antipsychotic agent, risperidone (RIS) were investigated for better understanding the pathogenesis of RIS in liver toxicityin vivoand inin vitro. Isolated rat hepatocytes were obtained by collagenase perfusion technique and were then incubated with RIS, different antioxidants in particular coenzyme Q10 (CoQ10), N-acetyl cysteine (NAC). Our results showed that RIS could induce cytotoxicity via rising reactive oxygen species (ROS), mitochondrial potential collapse, lysosomal membrane leakiness, GSH depletion and lipid peroxidation. All of these effects were significantly (p < 0.05) inhibited by ROS scavengers, antioxidants, endocytosis inhibitors and adenosine triphosphate (ATP) generators. Similar outcomes were obtained from thein vivoexperiments. Liver function enzyme test and histopathological evaluation confirmed RIS-(6 mg/kg) induced damage. Based on these results, it is suggested that RIS-induced liver toxicity is associated with mitochondrial/lysosomal cross-talk following the initiation of oxidative stress. Thus, the use of CoQ10 and/or NAC seems to be a safe therapeutic option in this context. [ABSTRACT FROM AUTHOR]

Coenzyme Q10 (CoQ10), also known as ubiquinone or ubidecarenone, is a powerful, endogenously produced, intracellularly existing lipophilic antioxidant. It combats reactive oxygen species (ROS) known to be responsible for a variety of human pathological conditions. Its target site is the inner mitochondrial membrane (IMM) of each cell. In case of deficiency and/or aging, CoQ10 oral supplementation is warranted. However, CoQ10 has low oral bioavailability due to its lipophilic nature, large molecular weight, regional differences in its gastrointestinal permeability and involvement of multitransporters. Intracellular delivery and mitochondrial target ability issues pose additional hurdles. To maximize CoQ10 delivery to its biopharmaceutical target, numerous approaches have been undertaken. The review summaries the current research on CoQ10 bioavailability and highlights the headways to obtain a satisfactory intracellular and targeted mitochondrial delivery. Unresolved questions and research gaps were identified to bring this promising natural product to the forefront of therapeutic agents for treatment of different pathologies. [ABSTRACT FROM PUBLISHER]

Background: Coenzyme Q10 (CoQ10) deficiency has been associated with statin-induced myopathy, and supplementation with CoQ10 may reduce inflammation markers. The effects of statins on CoQ10 and its anti-inflammatory properties have not been investigated in HIV-positive patients. Objective: The objectives of this study were to examine the effect of rosuvastatin on CoQ10 and CoQ10/LDL ratio over 24-week SATURN-HIV trial, explore the associations between CoQ10 levels and markers of vascular disease, inflammation, and immune activation, and assess whether changes in CoQ10 affected the anti-inflammatory effects of statin therapy or were associated with myalgia symptoms. Methods: This was a secondary analysis of the SATURN-HIV trial, a 96-week randomized clinical trial of 10 mg daily rosuvastatin vs. placebo in HIV-infected patients on antiretroviral therapy. We assessed the statin treatment effect on CoQ10 levels and CoQ10/LDL ratios and whether changes in these markers were related to myalgias. Relationships between CoQ10, subclinical vascular disease, and biomarkers of inflammation and immune activation were explored using Spearman correlations and multivariable regression models. Results: Overall, 147 patients were included. Median age was 46 years; 78% were male and 68% African American. At baseline, CoQ10 levels and CoQ10/LDL ratio were modestly correlated with markers of HIV disease, immune activation, and carotid distensibility. After 24 weeks of statin therapy, CoQ10 levels decreased (p = 0.002 for between group difference) and CoQ10/LDL ratio increased (p = 0.036). In the statin treatment arm, we did not find evidence of a relationship between changes in CoQ10 or CoQ10/LDL ration and changes in markers of inflammation or immune activation. There was a borderline statistically significant association between changes in CoQ10 and myalgia symptoms [OR 4.0 per 0.1 mg/L decrease in CoQ10,p = 0.07]. Conclusion: Twenty-four weeks of 10 mg daily rosuvastatin decreases CoQ10 concentration and increases CoQ10/LDL ratio in HIV-infected patients on antiretroviral therapy. [ABSTRACT FROM PUBLISHER]