Safety and efficacy indicators of guarana and Brazil nut extract carried in nanoparticles of coenzyme Q10: Evidence from human blood cells and red earthworm experimental model.

This study characterized a nanosupplement based on coenzyme Q10 containing guarana (Paullinia cupana) and Brazil nuts oil (Bertholetia excelsa) (G-Nut). Determined cytotoxic and oxi-immunomodulatory effects on human peripheral blood mononuclear cells (PBMCs) and its effect on mortality of red Californian earthworms (Eisenia fetida) and on the immune efficiency of its coelomocytes immune by in vitro exposure to yeast dead microorganism. The cytotoxic and immunomodulatory effects of G-Nut and the GN-Free extract (0.25-3 mg/mL) were determined in PBMC cultures. Apoptotic, oxidative, and inflammatory markers were determined using biochemical, immunological, and molecular protocols. The effects of G-Nut and GN-Free extracts on mortality and immune efficiency were investigated in earthworms. G-Nut and GN-Free did not induce cytotoxic events in PBMCs, triggering the decrease in apoptotic (caspases 3 and 8) gene expression, lipid and protein oxidation levels, or pro-inflammatory cytokine levels. G-Nut and GN-Free did not trigger earthworm mortality and improved coelomocyte immune efficiency by increasing Eisenia neutrophil extracellular DNA traps and brown body formation when exposed to dead yeasts. The G-Nut nanoformulation is safe and can be used as a new form of food supplement by oral or transdermal delivery.

The effect of coenzyme Q10 on cryotolerance of in vivo-derived mouse embryos.

OBJECTIVE: Cryopreservation has some adverse effects on embryos including cell metabolism reduction, mitochondria and plasma membrane damage, excess production of 'Reactive Oxygen Species' and damage to DNA. In the present study. In this study we assessed the effect of coenzyme Q10 as an exogenous antioxidant on mouse embryos following cryopreservation. METHODS: We collected mice embryos at the morula stage from uterine horns on the third day of gestation. The morulae were divided into 9 groups (1 control, 2 vehicles and 6 experimental), then vitrified. The culture and/or vitrification media of the experimental groups were supplemented by 10 or 30 µM of CoQ10. After one week, the embryos were warmed and then cultured. After 48 hours of embryo culture, the blastocyst rate, total cell number, viability; and after 72 hours of embryo culture, we assessed the hatching rate. RESULTS: Blastocyst rate and hatching rate were significantly reduced in the groups containing 30 µM CoQ10 supplemented culture media compared to other groups (p<0.05). The hatching rate in the groups containing 10 µM CoQ10 supplemented in both culture and vitrification media was significantly higher than in the other groups (p<0.05). In groups containing 10 µM CoQ10 supplemented culture media, the viability was higher than that in the other groups (p<0.05). CONCLUSIONS: It seems that CoQ10 in a dose-dependent manner is able to improve hatching rate and viability following cryopreservation through its antioxidant and anti-apoptotic properties, and through the production of ATP.

Novel approach over template molecule elimination in molecularly imprinted polymers by using heat activated persulfate.

This study proposes a new alternative for template removal from molecularly imprinted polymers by heat activated persulfate. It is known that trace amounts of template molecule remains in the polymer network after extraction by current methodologies leading to bleeding and incomplete removal of template which could compromise final determination of target analytes especially in trace analysis. A previously developed molecularly imprinted polymer specially designed for Coenzyme Q10 (CoQ10) extraction was employed as a model to test this template elimination approach. This polymer is based on methacrylic acid and ethylene glycol dimethylacrylate as monomers and Coenzyme Q0 as template. This coenzyme has the same quinone group as the CoQ10. Selectivity was analyzed comparing the recovery of CoQ10 and ubichromenol, a CoQ10 related substance. Chemical degradation using heat-activated persulfate allows the elimination of the template molecule with a high level of efficiency, being a simple and ecological methodology, yielding a polymer that exhibits comparable selectivity and imprinting effect with respect to traditional extraction methods.

Coenzyme Q10 prevents RANKL-induced osteoclastogenesis by promoting autophagy via inactivation of the PI3K/AKT/mTOR and MAPK pathways

Coenzyme Q10 (CoQ10) is a potent antioxidant that is implicated in the inhibition of osteoclastogenesis, but the underlying mechanism has not been determined. We explored the underlying molecular mechanisms involved in this process. RAW264.7 cells received receptor activator of NF-κB ligand (RANKL) and CoQ10, after which the differentiation and viability of osteoclasts were assessed. After the cells were treated with CoQ10 and/or H2O2 and RANKL, the levels of reactive oxygen species (ROS) and proteins involved in the PI3K/AKT/mTOR and MAPK pathways and autophagy were tested. Moreover, after the cells were pretreated with or without inhibitors of the two pathways or with the mitophagy agonist, the levels of autophagy-related proteins and osteoclast markers were measured. CoQ10 significantly decreased the number of TRAP-positive cells and the level of ROS but had no significant impact on cell viability. The relative phosphorylation levels of PI3K, AKT, mTOR, ERK, and p38 were significantly reduced, but the levels of FOXO3/LC3/Beclin1 were significantly augmented. Moreover, the levels of FOXO3/LC3/Beclin1 were significantly increased by the inhibitors and mitophagy agonist, while the levels of osteoclast markers showed the opposite results. Our data showed that CoQ10 prevented RANKL-induced osteoclastogenesis by promoting autophagy via inactivation of the PI3K/AKT/mTOR and MAPK pathways in RAW264.7 cells.

Combination Therapy of Cuban Policosanol (Raydel®, 20 mg) and Intensive Exercise for 12 Weeks Resulted in Improvements in Obesity, Hypertension, and Dyslipidemia without a Decrease in Serum Coenzyme Q10: Enhancement of Lipoproteins Quality and Antioxidant Functionality in Obese Participants.

Obesity and overweight, frequently caused by a lack of exercise, are associated with many metabolic diseases, such as hypertension, diabetes, and dyslipidemia. Aerobic exercise effectively increases the high-density lipoproteins-cholesterol (HDL-C) levels and alleviates the triglyceride (TG) levels. The consumption of Cuban policosanol (Raydel®) is also effective in enhancing the HDL-C quantity and HDL functionality to treat dyslipidemia and hypertension. On the other hand, no study has examined the effects of a combination of high-intensity exercise and policosanol consumption in obese subjects to improve metabolic disorders. In the current study, 17 obese subjects (average BMI 30.1 ± 1.1 kg/m2, eight male and nine female) were recruited to participate in a program combining exercise and policosanol (20 mg) consumption for 12 weeks. After completion, their BMI, waist circumference, total fat mass, systolic blood pressure (SBP), and diastolic blood pressure (DBP) reduced significantly up to around -15%, -13%, -33%, -11%, and -13%, respectively. In the serum lipid profile, at Week 12, a significant reduction was observed in the total cholesterol (TC) and triglyceride (TG) levels, up to -17% and -54% from the baseline, respectively. The serum HDL-C was elevated by approximately +12% from the baseline, as well as the percentage of HDL-C in TC, and HDL-C/TC (%), was enhanced by up to +32% at Week 12. The serum coenzyme Q10 (CoQ10) level was increased 1.2-fold from the baseline in all participants at Week 12. In particular, the male participants exhibited a 1.4-fold increase from the baseline. The larger rise in serum CoQ10 was correlated with the larger increase in the serum HDL-C (r = 0.621, p = 0.018). The hepatic function parameters were improved; the serum γ-glutamyl transferase decreased at Week 12 by up to -55% (p < 0.007), while the aspartate aminotransferase and alanine transaminase levels diminished within the normal range. In the lipoprotein level, the extent of oxidation and glycation were reduced significantly with the reduction in TG content. The antioxidant abilities of HDL, such as paraoxonase (PON) and ferric ion reduction ability (FRA), were enhanced significantly by up to 1.8-fold and 1.6-fold at Week 12. The particle size and number of HDL were elevated up to +10% during the 12 weeks, with a remarkable decline in the TG content, glycation extent, and oxidation. The improvements in HDL quality and functionality were linked to the higher survivability of adult zebrafish and their embryos, under the co-presence of carboxymethyllysine (CML), a pro-inflammatory molecule known to cause acute death. In conclusion, 12 weeks of Cuban policosanol (Raydel®, 20 mg) consumption with high-intensity exercise displayed a significant improvement in blood pressure, body fat mass, blood lipid profile without liver damage, CoQ10 metabolism, and renal impairment.

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

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

Pharmacoinformatics studies of coenzyme Q10 and potassium polyacrylate on angiotensin-converting enzyme associated with hypertension.

Coenzyme Q10's (CoQ10) favorable impact on cardiovascular diseases risk factors like hypertension and atherosclerosis is linked to the antioxidant action of CoQ10 in these conditions. This study showed the possible effects of CoQ10, potassium polyacrylate (PCK), and valsartan, a reference drug, on the angiotensin-converting enzyme (ACE), a crucial component of the renin-angiotensin system. The Glide tool on Maestro 11.1 was used to calculate the respective binding affinity and binding energy of these compounds towards ACE. The Schrödinger suite was used to run molecular dynamic simulations for 100 ns. The pkCSM tool was used to forecast the pharmacokinetic characteristics and toxicological effects. The SwissADME server was used to estimate the drug-like properties of these compounds. Based on their corresponding scoring values and the negative values of the binding free energies, molecular docking analysis of CoQ10 and PCK revealed that both exhibited favorable binding affinities towards the ACE, with CoQ10 having the highest binding scores. The results showed that both CoQ10 and PCK and the reference drug, valsartan, have some amino acids in common (at the pocket site of ACE) as the key residues for binding to ACE. Both CoQ10 and PCK demonstrated drug-like qualities and were not harmful, according to the predicted pharmacokinetics and toxicology studies. The results of this study suggest that because of its inhibitory interactions with ACE, CoQ10 in particular could be useful in regulating and reducing hypertension.Communicated by Ramaswamy H. Sarma.

Lipid nanoparticles containing coenzyme Q10 for topical applications: An overview of their characterization.

The coenzyme Q10 is a compound widely used in pharmaceutical and cosmetic formulations because it is a potent eliminator of free radicals, giving it antioxidant and anti-aging properties. It is naturally synthesized by the human body, but its production wanes with age, leading to the formation of wrinkles. The efficacy of topical application of the coenzyme to counteract this process is subject to several difficulties, due to its instability in the presence of light, low solubility in water and high lipophilicity. Because of these drawbacks, many studies have been conducted of release systems. Lipid nanoparticles stand out in this sense due to the advantages of skin compatibility, protection of the active ingredient against degradation in the external medium, capacity to increase penetration of that ingredient in the skin, and its controlled and prolonged release. In this context, this article presents a review of the main studies of the coenzyme Q10 encapsulated in lipid nanoparticles for topical use, focusing on the analytic methods used to characterize the systems regarding morphology, zeta potential, release profile, Q10 content, encapsulation efficiency, crystalline organization and structure of the lipid matrix, rheology, antioxidant activity, skin penetration and efficacy, among other aspects. We also describe the main results of the different studies and discuss the critical aspects - the simplest, most reproducible, best, and most relevant - that characterize lipid nanoparticles with encapsulated Q10 for topical use.

Effect of Quinolinic Acid on Behavior, Morphology, and Expression of Inflammatory/oxidative Status in Rats' Striatum: Is Coenzyme Q10 a Good Protector?

Quinolinic acid (QUIN) is a toxic compound with pro-oxidant, pro-inflammatory, and pro-apoptotic actions found at high levels in the central nervous system (CNS) in several pathological conditions. Due to the toxicity of QUIN, it is important to evaluate strategies to protect against the damage caused by this metabolite in the brain. In this context, coenzyme Q10 (CoQ10) is a provitamin present in the mitochondria with a protective role in cells through several mechanisms of action. Based on these, the present study was aimed at evaluating the possible neuroprotective role of CoQ10 against damage caused by QUIN in the striatum of young Wistar rats. Twenty-one-day-old rats underwent a 10-day pretreatment with CoQ10 or saline (control) intraperitoneal injections and on the 30th day of life received QUIN intrastriatal or saline (control) administration. The animals were submitted to behavior tests or euthanized, and the striatum was dissected to neurochemical studies. Results showed that CoQ10 was able to prevent behavioral changes (the open field, object recognition, and pole test tasks) and neurochemical parameters (alteration in the gene expression of IL-1ß, IL-6, SOD, and GPx, as well as in the immunocontent of cytoplasmic Nrf2 and nuclear p-Nf-κß) caused by QUIN. These findings demonstrate the promising therapeutic effects of CoQ10 against QUIN toxicity.

Beneficial in vitro effect of N-acetylcysteine and coenzyme Q10 on DNA damage in neurodegenerative Niemann-Pick type C 1 disease: preliminary results.

Niemann-Pick type C1 (NP-C1) is a lysosomal storage disease (LSD) caused by mutations in NPC1 gene that lead to defective synthesis of the respective lysosomal transporter protein and cholesterol accumulation in late endosomes/lysosomes (LE/L) compartments, as well as glycosphingolipids GM2 and GM3 in the central nervous system (CNS). Clinical presentation varies according to the age of onset and includes visceral and neurological symptoms, such as hepatosplenomegaly and psychiatric disorders. Studies have been associating the pathophysiology of NP-C1 with oxidative damage to lipids and proteins, as well as evaluating the benefits of adjuvant therapy with antioxidants for this disease. In this work, we evaluated the DNA damage in fibroblasts culture from patients with NP-C1 treated with miglustat, as well as the in vitro effect of the antioxidant compounds N-acetylcysteine (NAC) and Coenzyme Q10 (CoQ10), using the alkaline comet assay. Our preliminary results demonstrate that NP-C1 patients have increased DNA damage compared to healthy individuals and that the treatments with antioxidants can mitigate it. DNA damage may be due to an increase in reactive species since it has been described that NP-C1 patients have increased peripheral markers of damage to other biomolecules. Our study suggests that NP-C1 patients could benefit from the use of adjuvant therapy with NAC and CoQ10, which should be better evaluated in a future clinical trial.

Evaluation of oxidative stress and mitochondrial function in a type II mucopolysaccharidosis cellular model: in vitro effects of genistein and coenzyme Q10.

Mucopolysaccharidosis type II (MPS II or Hunter Syndrome) is a lysosomal disease caused by deficient degradation of glycosaminoglycans (GAGs) heparan sulfate and dermatan sulfate due to the deficiency of the enzyme iduronate-2-sulfatase. The main treatment for MPS II is the administration of the recombinant form of the enzyme, in a process known as enzyme replacement therapy (ERT). Oxidative damage can contribute to the pathophysiology of MPS II and treatment with ERT can reduce the effects of oxidative stress. For a better understanding of pathophysiology of MPS II, we evaluated biomarkers of mitochondrial dysfunction, DNA (Deoxyribonucleic acid) damage, antioxidant defenses, reactive species production and lysosomal size in IDS-deficient HEK 293 cells and investigate the in vitro effect of genistein and coenzyme Q10 (CoQ) on these biomarkers. An increase in the production of reactive species was demonstrated, as well as an increase in the activities of the antioxidant enzymes superoxide dismutase (SOD) and catalase (CAT). Also, an increase in lysosomal volume and oxidative damage to DNA were verified. There was no evidence of a change in mitochondrial function in this cell model. In the HEK 293 (human embryonic kidney 293) knockout (KO) HP10 cell model we found that genistein at concentrations of 25 and 50 µm decreased in vitro the production of reactive species and the activity of the SOD enzyme, showing an antioxidant protective effect. Still, in these cells we verified that the coenzyme Q10 in the concentrations of 5 and 10 µm decreased in vitro the activity of the SOD enzyme and in the concentration of 10 µm decreased in vitro the DNA damage, also demonstrating antioxidant protection. In conclusion, MPS II knockout cells demonstrated oxidative stress and DNA damage and genistein, as well as coenzyme Q10, have been shown to have an important protective effect in vitro against these oxidative damages.

In vitro approaches to antioxidant screening for the development of a sunscreen formulation

Abstract The incorporation of antioxidants into sunscreens may provide additional skin photoprotection against the harmful photobiological effects of ultraviolet radiation. The present study evaluated the applicability of a screening approach to the assessment of the antioxidant and photoprotective properties of vitamin C, vitamin E, and coenzyme Q10 and then determined the performance of the most effective antioxidant in a sunscreen formulation. Antioxidant activity was assessed by the 2,2-diphenyl-1-picrylhydrazyl (DPPH) assay, 2,2`-azino-bis (3-ethylbenzothiazoline-6-sulfonic acid) (ABTS) assay, and oxygen radical absorbance capacity (ORAC) assay, and the photoprotective potential was investigated by the yeast photoprotection assay. The antioxidant with the best effect was incorporated into sunscreen formulations which were evaluated for 120 days regarding their in vitro photoprotective parameters. Vitamin C showed high antioxidant capacity as well as a photoprotective potential against simulated solar irradiation applied for times longer than 1 h. Although the Sun Protection Factor, UVA/UVB ratio and critical wavelength did not differed significantly (p<0.05) between the formulation blank and the formulations containing 0.5% or 1% vitamin C, formulations with vitamin C kept their photostability for 6 months. Consequently, the proposed screening approach seems to be promising for the development of an antisolar photostable formulation containing vitamin C as an antioxidant.

Biomolecules resveratrol + coenzyme Q10 recover the cell state of human mesenchymal stem cells after 1-methyl-4-phenylpyridinium-induced damage and improve proliferation and neural differentiation.

Neurodegenerative disorders are a critical affection with a high incidence around the world. Currently, there are no effective treatments to solve this problem. However, the application of mesenchymal stem cells (MSCs) and antioxidants in neurodegenerative diseases has shown to be a promising tool due to their multiple therapeutic effects. This work aimed to evaluate the effects of a combination of resveratrol (RSV) and coenzyme Q10 (CoQ10) on the proliferation and differentiation of MSC and the protector effects in induced damage. To characterize the MSCs, we performed flow cytometry, protocols of cellular differentiation, and immunocytochemistry analysis. The impact of RSV + CoQ10 in proliferation was evaluated by supplementing 2.5 and 10 µM of RSV + CoQ10 in a cellular kinetic for 14 days. Cell viability and lactate dehydrogenase levels (LDH) were also analyzed. The protective effect of RSV + CoQ10 was assessed by supplementing the treatment to damaged MSCs by 1-methyl-4-phenylpyridinium (MPP+); cellular viability, LDH, and reactive oxygen species (ROS) were evaluated.. MSCs expressed the surface markers CD44, CD73, CD90, and CD105 and showed multipotential ability. The combination of RSV + CoQ10 increased the proliferation potential and cell viability and decreased LDH levels. In addition, it reverted the effect of MPP+-induced damage in MSCs to enhance cell viability and decrease LDH and ROS. Finally, RSV + CoQ10 promoted the differentiation of neural progenitors. The combination of RSV + CoQ10 represents a potential treatment to improve MSCs capacities and protect against neurodegenerative damage.

Antioxidant Effect of Coenzyme Q10 in the Prevention of Oxidative Stress in Arsenic-Treated CHO-K1 Cells and Possible Participation of Zinc as a Pro-Oxidant Agent.

Oxidative stress is an imbalance between levels of reactive oxygen species (ROS) and antioxidant enzymes. Compounds with antioxidant properties, such as coenzyme Q10 (CoQ10), can reduce cellular imbalance caused by an increase in ROS. CoQ10 participates in modulating redox homeostasis due to its antioxidant activity and its preserving mitochondrial functions. Thus, the present study demonstrated the protective effects of CoQ10 against oxidative stress and cytotoxicity induced by arsenic (As). Antioxidant capacity, formation of hydroperoxides, generation of ROS, and the effect on cellular viability of CoQ10, were investigated to determine the protective effect of CoQ10 against As and pro-oxidant compounds, such as zinc. Cell viability assays showed that CoQ10 is cytoprotective under cellular stress conditions, with potent antioxidant activity, regardless of the concentration tested. Zn, when used at higher concentrations, can increase ROS and show a pro-oxidant effect causing cell damage. The cytotoxic effect observed for As, Zn, or the combination of both could be prevented by CoQ10, without any decrease in its activity at cellular levels when combined with Zn.

Quinolinic Acid Impairs Redox Homeostasis, Bioenergetic, and Cell Signaling in Rat Striatum Slices: Prevention by Coenzyme Q10.

Quinolinic acid (QUIN) is an important agonist of NMDA receptors that are found at high levels in cases of brain injury and neuroinflammation. Therefore, it is necessary to investigate neuroprotection strategies capable of neutralizing the effects of the QUIN on the brain. Coenzyme Q10 (CoQ10) is a provitamin that has an important antioxidant and anti-inflammatory action. This work aims to evaluate the possible neuroprotective effect of CoQ10 against the toxicity caused by QUIN. Striatal slices from 30-day-old Wistar rats were preincubated with CoQ10 25-100 µM for 15 min; then, QUIN 100 µM was added to the incubation medium for 30 min. A dose-response curve was used to select the CoQ10 concentration to be used in the study. Results showed that QUIN caused changes in the production of ROS, nitrite levels, activities of antioxidant enzymes, glutathione content, and damage to proteins and lipids. CoQ10 was able to prevent the effects caused by QUIN, totally or partially, except for damage to proteins. QUIN also altered the activities of electron transport chain complexes and ATP levels, and CoQ10 prevented totally and partially these effects, respectively. CoQ10 prevented the increase in acetylcholinesterase activity, but not the decrease in the activity of Na+,K+-ATPase caused by QUIN. We also observed that QUIN caused changes in the total ERK and phospho-Akt content, and these effects were partially prevented by CoQ10. These findings suggest that CoQ10 may be a promising therapeutic alternative for neuroprotection against QUIN neurotoxicity.

Avaliação dos efeitos da coenzima Q10 utilizada como coadjuvante local e/ou sistêmica ao tratamento mecânico da periodontite experimental em ratos tratados com nicotina / Evaluation of the effects of coenzyme Q10 as local and/or systemic adjuvant to mechanical treatment of experimental periodontitis in rats treated ith nicotine

O propósito do estudo foi avaliar a efetividade da raspagem e alisamento radicular (RAR) associado à coenzima Q10 (CQ10) administrada localmente e/ou sistemicamente no tratamento da periodontite experimental (PE) em ratos tratados sistemicamente com nicotina (NIC). 128 ratos (Wistar) foram divididos em oito grupos (n=16). Durante todo o período experimental, os animais receberam duas injeções subcutâneas diárias de 3mg/kg de hemissulfato de nicotina ou solução salina (SS) na região dorsal, com 12 horas de intervalo entre elas, começando nos 30 dias que antecederam à indução da PE. Após 15 dias da indução da PE, o protocolo de RAR foi realizado bem como o tratamento coadjuvante local e/ou sistêmico com CQ10, com e sem tratamento com a NIC, sendo: SS-PE-RAR e NIC-PE-RAR: irrigação subgengival com SS; SS-PE-RAR/Q10L e NIC-PE-RAR/Q10L: irrigação subgengival com 1ml solução de CQ10; SS-PE-RAR/Q10S e NIC-PE-RAR/Q10S: gavagem gástrica diária com 120 mg de CQ10; SS-PE-RAR/Q10LS e NIC-PE-RAR/Q10LS: irrigação subgengival com 1ml solução de CQ10 e gavagem gástrica diária com 120 mg de CQ10. As eutanásias foram realizadas 7 e 28 dias após tratamento. As peças coletadas foram processadas com desmineralização para as análises histopatológica, histométrica e imunoistoquímica para detecção de TRAP. Os dados foram submetidos ao teste paramétrico Anova two-way e pós-teste de Tukey. O nível de significância adotado foi de 5% (p≤0,05). Na análise histopatológica, pode-se observar que os grupos NIC-PE-RAR-Q10L E NIC-PE-RAR-Q10LS apresentaram tecidos periodontais com aspecto de normalidade, com preservação da inserção conjuntiva e de região de furca preservada aos 7 e 28 dias, de modo distinto do grupo NIC-PE-RAR e NIC-PE-RAR-Q10S em ambos os períodos. Na análise histométrica, pode-se observar maior porcentagem de osso na furca (POF) (p≤0,05) nos grupos NIC-PE-RAR-Q10L, NIC-PE-RAR-Q10S e NIC-PERAR-Q10LS em comparação com o grupo NIC-PE-RAR em ambos os períodos e também com o grupo SS-PE-RAR aos 28 dias. Pode-se observar menor número de células TRAP positivas (p≤0,05) no grupo NIC-PE-RAR-Q10L quando comparado aos grupos SS-PE-RAR E NIC-PE-RAR aos 7 dias e no grupo NIC-PE-RAR-Q10LS quando comparado aos mesmos grupos aos 28 dias. Conclui-se que RAR associado à CQ10 utilizada local e local/sistemicamente no tratamento da PE em ratos tratados sistemicamente com nicotina foram efetivas mostrando resultados favoráveis nas análises histopatológica, histométrica e imunoistoquímica(AU)

The aim of this study was to evaluate the effectiveness of scaling and root planing (SRP) combined with adjunctive local and/or systemic administration of coenzyme Q10 (CQ10) for the treatment of experimental periodontitis (EP) in rats systemically treated with nicotine (NIC). 128 Wistar rats were divided into 8 groups (n=16). Throughout the experiment, animals received two subcutaneous injections of either 3mg/kg nicotine hemissulfate or physiological saline solution (PSS) with 12 h interval between them. These injections were initiated 30 days prior EP induction. 15 days after EP induction, the protocol for SRP was performed together (or not) with local and/or systemic adjunctive CQ10 administration in animals treat with either NIC or PSS, as described: PSS-EP-SRP and NIC-EP-SRP: subgingival irrigation with PSS; PSS-EP-SRP/Q10L and NIC-EP-SRP/Q10L: subgingival irrigation with 1ml of CQ10 solution; PSS-EP-SRP/Q10S and NIC-EP-SRP/Q10S: daily gastric gavage with 120 mg of CQ10; PSS-EP-SRP/Q10LS and NIC-EP-SRP/Q10LS: subgingival irrigation with 1ml of CQ10 solution and daily gastric gavage with 120 mg of CQ10. The euthanasia was performed at 7 and 28 days after treatment. The specimens were collected and processed for histopathologic, histometric and immunochemical for of TRAP analyzes. The data were submitted to the two-way ANOVA and Tukey's post-test. The level of significance adopted was 5% (p≤0.05). In the histopathological analysis, it can be observed that the NIC-PE-RAR-Q10L and NIC-PE-RAR-Q10LS groups presented periodontal tissues with normal aspect, preserving the conjunctival insertion and furca region preserved at 7 and 28 days, differently from the NIC-PE-RAR and NIC-PE-RAR-Q10S groups in both periods. In histometric analysis, a higher percentage of bone in furca (PBF) (p≤0.05) can be observed in the NIC-PE-RAR-Q10L, NIC-PE-RAR-Q10S and NIC-PE-RAR-Q10LS groups compared to the NIC-PE-RAR group in both periods and also with the SS-PE-RAR group at 28 days. A lower number of TRAPpositive cells (p≤0.05) can be observed in the NIC-PE-RAR-Q10L group when compared to the SS-PE-RAR and NIC-PE-RAR groups at 7 days and in the NIC-PE-RAR-Q10LS group when compared to the same groups at 28 days. It was concluded that RAR associated with CQ10 used locally and locally/systemically in the treatment of EP in rats treated systemically with NIC were effective, showing favorable results in histopathological, histometric and immunohistochemical analyses(AU)

Genotoxic risk in humans and acute toxicity in rats of a novel oral high-dose coenzyme Q10 oleogel.

Coenzyme Q10 (CoQ10) supplementation has demonstrated to be safe and effective in primary and secondary CoQ10 deficiencies. Previously, we have designed a high-dose CoQ10 oleogel (1 g/disk) with excipients used in quantities that do not represent any toxic risk. However, it was necessary to demonstrate their safety in the final formulation. Following this purpose, an acute toxicity study of the oleogel in rats was performed. Furthermore, the genotoxic risk was evaluated in human volunteers after CoQ10 supplementation with oleogel and compared to the solid form (1 g/three 00-size-capsules). In addition, the general health status and possible biochemical changes of the participants were determined using serum parameters. Results suggested the absence of adverse effects caused by the interaction of the components in the oleogel formulation. Therefore, we conclude that the designed novel high-dose CoQ10 oleogel was safe for oral consumption.

An Overview on Topical Administration of Carotenoids and Coenzyme Q10 Loaded in Lipid Nanoparticles.

Carotenoids and coenzyme Q10 are naturally occurring antioxidant compounds that are also found in human skin. These bioactive compounds have been the focus of considerable research due to their antioxidant, anti-inflammatory, and photoprotective properties. In this review, the current state of the art in the encapsulation of carotenoids and coenzyme Q10 in lipid nanoparticles to improve their bioavailability, chemical stability, and skin absorption is discussed. Additionally, the main findings are highlighted on the cytotoxic and photoprotective effects of these systems in the skin.

Protection of coenzyme Q10 against contrast-induced acute kidney injury in male diabetic rats.

BACKGROUND: Diabetes mellitus (DM) is a major risk factor for contrast-induced acute kidney injury (CI-AKI). DM and CI-AKI result in oxidative damage and inflammation that can be reduced when treated with the coenzyme Q-10 (CoQ10). The aim of this study was to investigate the therapeutic potential of CoQ10 in renal function, renal hemodynamics, oxidative profile and renal histology in diabetic rats subjected to CI-AKI. METHODS: Wistar rats, male, randomized into five groups: citrate: control animals received citrate buffer (streptozotocin vehicle, 0.4 mL); Tween: control animals of CoQ10 treatment received 1% Tween 80 (CoQ10 vehicle, 0.5 mL); DM: animals that received streptozotocin (60 mg/kg); DM + IC: DM animals treated with iodinated contrast (IC, 6 mL/kg); DM + IC + CoQ10: DM animals treated with CoQ10 (10 mg/kg) and that received IC (6 mL/kg). The protocols lasted 4 weeks. An evaluation was made to measure renal function, inulin clearance and serum creatinine, renal hemodynamics by renal blood flow (RBF) and renal vascular resistance (RVR), markers of oxidative stress such as urinary peroxides and nitrate, lipid peroxidation, thiols in renal tissue and renal histological analysis. RESULTS: DM animals showed reduced renal function, which was followed by an increase inserum creatinine and significant reduction of inulin clearance and RBF. It was noticed an increase in RVR and redox imbalance with higher urinary peroxides and nitrate lipid peroxidation levels with depletion of thiols in renal tissue. IC treatment exacerbated these changes in DM + IC. CoQ10 administration ameliorated renal function, prevented hemodynamic changes and neutralized oxidative damage and progression of the histologic damage in the DM + IC + CoQ10 group. CONCLUSION: This study demonstrated the renoprotection properties of CoQ10 in an experimental model of risk factor of DM for CI-AKI. CoQ10 presented an antioxidant effect on the CI-AKI in male diabetic rats by improving renal function and renal hemodynamics, preserving morphology and reducing oxidative stress.

Coenzyme Q10 deficiency in patients with hereditary hemochromatosis.

AIM: Hereditary hemochromatosis (HH) is a group of inherited disorders that causes a slow and progressive iron deposition in diverse organs, particularly in the liver. Iron overload induces oxidative stress and tissue damage. Coenzyme Q10 (CoQ10) is a cofactor in the electron-transport chain of the mitochondria, but it is also a potent endogenous antioxidant. CoQ10 interest has recently grown since various studies show that CoQ10 supplementation may provide protective and safe benefits in mitochondrial diseases and oxidative stress disorders. In the present study we sought to determine CoQ10 plasma level in patients recently diagnosed with HH and to correlate it with biochemical, genetic, and histological features of the disease. METHODS: Plasma levels of CoQ10, iron, ferritin, transferrin and vitamins (A, C and E), liver tests (transaminases, alkaline phosphatase and bilirubin), and histology, as well as three HFE gene mutations (H63D, S654C and C282Y), were assessed in thirty-eight patients (32 males, 6 females) newly diagnosed with HH without treatment and in twenty-five age-matched normolipidemic healthy subjects with no HFE gene mutations (22 males, 3 females) and without clinical or biochemical signs of iron overload or liver diseases. RESULTS: Patients with HH showed a significant decrease in CoQ10 levels respect to control subjects (0.31 ±â€¯0.03 µM vs 0.70 ±â€¯0.06 µM, p < 0.001, respectively) independently of the genetic mutation, cirrhosis, transferrin saturation, ferritin level or markers of hepatic dysfunction. Although a decreasing trend in CoQ10 levels was observed in patients with elevated iron levels, no correlation was found between both parameters in patients with HH. Vitamins C and A levels showed no changes in HH patients. Vitamin E was significantly decreased in HH patients (21.1 ±â€¯1.3 µM vs 29.9 ±â€¯2.5 µM, p < 0.001, respectively), but no correlation was observed with CoQ10 levels. CONCLUSION: The decrease in CoQ10 levels found in HH patients suggests that CoQ10 supplementation could be a safe intervention strategy complementary to the traditional therapy to ameliorate oxidative stress and further tissue damage induced by iron overload.