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

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

The therapeutic benefit of antioxidants on the outcome of acute aluminum phosphide poisoning: a systemic review and meta-analysis.

This systematic review and meta-analysis pool evidence available from clinical trials to verify the effect of antioxidants on the outcome of acute aluminum phosphide (AlP) poisoning. A systematic review complied with "Preferred Reporting Items for Systematic Reviews and Meta-Analyses" (PRISMA) Protocols. Meta-analysis was conducted on 10 studies that fulfill eligibility criteria. Four antioxidants were implemented: N-Acetyl cysteine (NAC), L-Carnitine, Vitamin E, and Co-enzyme Q10 (Co Q10). Risk of bias, publication bias, and heterogeneity were assessed to ensure the results' reliability. Antioxidants significantly decrease mortality of acute AlP poisoning around three folds (OR = 2.684, 95% CI: 1.764-4.083; P < .001) and decrease the need for intubation and mechanical ventilation by two folds (OR = 2.391, 95% CI 1.480-3.863; P < .001) compared with control. Subgroup analysis revealed that NAC significantly decreases mortality by nearly three folds (OR = 2.752, 95% CI: 1.580-4.792; P < .001), and vitamin E significantly decreases mortality by nearly six folds (OR = 5.667, 95% CI: 1.178-27.254; P = .03) compared with control. L-Carnitine showed a borderline significance (P = .050). Co Q10 decreased the mortality compared with the control; however, the difference was not statistically significant (P = .263). This meta-analysis provides solid evidence regarding the efficacy of antioxidants in improving the outcome of acute AlP poisoning with reference to NAC. Wide confidence interval and small relative weight affect reliability regarding vitamin E efficacy. Future clinical trials and meta-analyses are recommended. To our knowledge, no previous meta-analysis was conducted to investigate the efficacy of treatment modalities for acute AlP poisoning.

Comparative Study Of Combined Co-Enzyme Q10 And Clomiphene Citrate Vs Clomiphene Citrate Alone For Ovulation Induction In Patients With Polycystic Ovarian Syndrome.

A total of 136 patients with PCOS were followed through the Department of the Obstetrics and Gynaecology, Unit-IV, Lady Aitchison Hospital, Lahore. Patients were randomly divided by lottery method into two groups i.e., Group-A (CoQ10 plus Clomiphene citrate) and Group-B (Clomiphene citrate alone). The selected patients in the study group (group-A) were given Clomiphene citrate 100mg/day from cycle days 2-6 for 45 days (2 cycles) and CoQ10 in a dose of 50mg soft gel capsules thrice per day starting at cycle day-2, until HCG administration. Patients in controlled group (group 21 B) received Clomiphene citrate 100mg/day twice a day cycle for 45 days. Data were analysed in SPSS v25.0. In group-A (CoQ10 plus Clomiphene citrate), successful ovulation induction was noted in 16 (23.5%) patients, showing that with the addition of CoQ10, the chances of ovulation induction increased.

Adjunctive role of Q10 with Ligilactobacillus salivarius, and Lactiplantibacillus plantarum probiotic Bacteria on the HEp-2 cells viability and adhesion of Streptococcus mutans.

Objective: Various studies have indicated the application of Coenzyme Q10 and probiotic bacteria such as Ligilactobacillus salivarius (L. salivarius) and Lactiplantibacillus plantarum (L. plantarum) in combating periodontal disease. Considering the positive effect of these two on oral health, and the destructive effect of S. mutans, in this study, we investigate the outcomes of the administration of probiotics and Q10 on infected HEp-2 cell viability and S. mutans adhesion in different settings. Methods: A 3-week-old human epidermoid laryngeal (HEp-2) cell line was cultured and exposed to two different probiotics and 3 different doses of Q10 doses. Samples were contaminated by S. mutans immediately (therapeutic setting) and after 3 hours (preventive setting). Eventually, the viability of HEp-2 cells was investigated by MTT. Also, the number of adhered S. mutans was explored by direct and indirect adhesion assays. Results: L. plantarum and L. salivarius protect epithelial cells against S. mutans in both therapeutic and preventive settings, albeit not fully. In contrast, Q10 completely preserves the viability of infected Her HEp-2 cells at all concentrations. The effects of the coexistence of Q10 and probiotics were not quite equal, among which L. salivarius and 5 µg of Q10 form the best results. The microscopic adherence assay of S. mutans revealed that samples containing Q10 had significantly lower adhesion of probiotics and S. mutans to HEp-2 cells. Similarly, plates containing L. salivarius with 5µg or L. plantarum with 1µg Q10 or sole presence of L. salivarius had the lowest S. mutans adherence among others. Also, L. salivarius with 5µg Q10 had one of the highest probiotic adherences. Conclusion: In conclusion, co-administration of Q10 and probiotics especially in presence of L. salivarius with 5µg Q10 could have remarkable effects on HEp-2 cell viability, S. mutans, and probiotic adherence. Nevertheless, our study, for the first time, showed that Q10 might have an anti-bacterial activity by suppressing the adhesion of tested bacteria to HEp-2 cells. This hypothesis, if correct, suggests that due to their different mechanisms, co-prescription of Q10 and probiotics may lead to better clinical responses, especially in the mentiond dose.

Coenzyme Q10 treatment and diazinon exposure in parental male rats: effects of the exposure on their neonatal brains.

Prenatal acute and chronic exposure to organophosphorus pesticides may evoke physical and behavioral impairments in offspring development. However, the mechanism of antioxidant consumption repair to cure these impairments remains unclear. This study aimed to investigate the protective effects of COQ10 against DZN toxicity by measuring Malondialdehyde (MDA) level, superoxide dismutase (SOD) activity, the expression of MH2A, DNMT1, H2AZ, and HDAC3, and the histopathology in the brain of neonatal Wistar albino rats whose male parents were exposed to DZN and COQ10. The results showed that COQ10 could significantly decrease MDA level, histopathological alteration, and expression of DNMT1 and HDAC3 in the neonatal brain (P < 0.05). Also, an increase in SOD activity and expression of MH2A and H2AZ were observed in the neonatal brain of this group (P < 0.05). These investigations suggest that COQ10 can reduce the effects of DZN on neuronal oxidative stress and its damage to the neonatal brain.

The Effect of CoQ10 supplementation on ART treatment and oocyte quality in older women.

A significant problem associated with assisted reproductive technologies (ART) is recurrent treatment failure which can be attributed to the age-associated decline in oocyte quality. Co-enzyme Q10 (CoQ10) is an antioxidant and essential component of the mitochondrial electron transport chain. It is reported that de novo CoQ10 production declines with ageing and coincides with age-related decline in fertility, leading to CoQ10 supplementation being advocated to enhance response to ovarian stimulation and improve oocyte quality. CoQ10 supplementation was found to improve fertilization rates, embryo maturation rates and embryo quality when used before and during in vitro fertilization (IVF) and in vitro maturation (IVM) treatment in women aged 31 and over. Regarding oocyte quality, CoQ10 was able to reduce high rates of chromosomal abnormalities and oocyte fragmentation, as well as improve mitochondrial function. Proposed mechanisms of CoQ10 function include restoration of reactive oxygen species imbalance, preventing DNA damage and oocyte apoptosis, as well as restoration of Krebs cycle downregulation from ageing. In this literature review, we provide an overview of the use of CoQ10 in improving the success of IVF and IVM in older women, and additionally assess the impact of CoQ10 on oocyte quality and discuss potential mechanisms of action by CoQ10 on the oocyte.

Calcium voltage-gated channel subunit alpha 1 C and glial fibrillary acidic protein signaling pathways as a selective biomarker in predicting the efficacy of liposomal loaded co-enzyme Q in the autistic rat model.

Autism spectrum disorder (ASD) is an extreme neuropsychotic disturbance with both environmental and genetic origins. Sodium propionate (PPA) a metabolic bioproduct of gut microbiota is well-thought-out as a successful autism animal model. Nevertheless, Liposomal drug delivery system possess the advantagous of biocompatibility, targeting organs, ability to carry large drug payloads and skipping macrophages for this purpose the current study was carried out to investigate the hypothesis that Calcium Voltage-Gated channel subunit alpha 1 C (CACNA1C) and glial fibrillary acidic protein (GFAP) signaling pathways crosstalk with the efficacy of Co-enzyme Q10 (Co-Q10) and liposomal loaded Co-enzyme Q10 (L Co-Q10) in PPA mediated autistic rat model. Autism was conducted by buffered PPA (500 mg/Kg b.wt) daily for 5 consecutive days subsequently treatment via Co-Q10 in a dose of (10 mg/kg b.wt) and L Co-Q10 (2 mg/kg b.wt) for four weeks then the autistic model was followed for signs of autism at different time intervals of (one, two and four weeks). The control, PPA intoxicated, and treated groups were subjected to behavioral tests (Y-Maze and open field), antioxidant analysis, gene expression analysis, and histological examination at different time intervals of the study. The results revealed that Co-Q10 and L Co-Q10 significantly elevated antioxidative stress biomarkers, comprising superoxide dismutase (SOD), glutathione (GSH), and total antioxidant capacity (TAC). In addition, they significantly ameliorated the oxidative stress biomarker malondialdehyde (MDA). Meanwhile, they significantly downregulated GFAP and CACNA1C mRNA gene expressions, Co-Q10 and LCo-Q10 showed improvement in almost brain regions post PPA histopathological alterations, even better results were manifested via LCo-Q10 groups. These results showed the superiority of LCo-Q10 over Co-Q10 in competing autism. In conclusion: The administration of anti-inflammatory and antioxidant agents such as Co-Q10 and L Co-Q10 may represent a promising strategy to counteract pathological behaviors in ASD model via targeting organs, increasing retention time, and reducing side effects.

Recent Advancements in In Vitro Fertilisation.

The field of assisted reproductive technologies has witnessed many new developments over the past 10 years. This review examines new stimulation techniques that might increase the number of fully developed oocytes derived during the in vitro fertilisation (IVF) cycle in addition to strategies for enhancing oocyte quality in older women. Before moving on to several fresh methods for determining endometrial receptivity, we talk about how preimplantation genetic screening (PGS) is currently being utilised. The main goal of this review is to highlight technological fields that might be debatable or are still sufficiently novel to require rigorous controlled trials for recognition. The use of IVF has been on the rise recently, mostly as a result of deferred childbearing, and there is no reason to believe that this trend will alter. Infertility therapies have advanced significantly thanks to the methods and techniques that were established via studies on animals and, more recently, people. Some technical discoveries in reproductive medicine have had a significant impact on innovations and treatment choices in other fields of medicine as well. The objective of this succinct review article is to quickly summarise and explain the advancements made in this intriguing area of medicine over the past 40 years.

Rosuvastatin and co-enzyme Q10 improve high-fat and high-fructose diet-induced metabolic syndrome in rats via ameliorating inflammatory and oxidative burden.

The prevalence of metabolic syndrome (MetS) has been rising alarmingly and it has now become a global concern causing an enormous economic burden on the health care system. MetS is generally linked to complications in lipid metabolism, oxidative stress and low grade inflammation. The aim of the current study was to evaluate the effect of rosuvastatin, co-enzyme Q10 (CoQ10), and their combination on blood pressure, blood sugar, dyslipidemia, and liver function in rats with MetS induced by high fructose and high fat diet (HF-HFD) and the possible underlying mechanism. Oral administration of rosuvastatin (10 mg/kg/day), CoQ10 (10 mg/kg/day) and their combination for 4 weeks in HF-HFD-fed rats elevated serum high density lipoprotein and reduced glutathione. On the other hand, treatment with rosuvastatin, CoQ10 or their combination decreased the serum levels of malondialdehyde, triglycerides, total cholesterol, and low density lipoprotein-cholesterol as well as systolic blood pressure, body weight and fasting blood glucose level. In addition, the drugs or their combination declined serum pro-inflammatory cytokines, namely tumor necrosis factor-α and interleukin-1ß. In conclusion, our results showed that rosuvastatin or CoQ10 protected against HF-HFD-induced MetS through the regulation of dyslipidemia, elevated blood glucose, elevated blood pressure, antioxidant defenses and inflammatory response. Rosuvastatin or CoQ10 also alleviated the impairment of liver function that was induced by HF-HFD. Interestingly, CoQ10 augmented rosuvastatin's effect in ameliorating MetS, via exerting synergistic modulatory effects on oxidative stress and inflammation. Thus, rosuvastatin and CoQ10 combination therapy may have possible applications in ameliorating metabolic disorders.

A Comparative Study on the Efficacy of Coenzyme Q10 and Amitriptyline in the Prophylactic Treatment of Migraine Headaches in Children: A Randomized Controlled Trial.

Background: Migraine, one of the most common headaches in children, has a significant impact on children and their family's quality of life (QoL). There are two approaches for controlling migraine headaches preventative and controlling acute attacks. Several drugs have been used for this purpose, and tricyclic antidepressants were at the top. Amitriptyline has shown not only a desirable effect on controlling the headaches but also some adverse side effects. Recently, finding effective drugs with fewer side effects, become more critical. Among them, nutraceuticals were one of the promising ones. Materials and Methods: In this randomized clinical trial on 72 patients aged 5-15 years old with diagnosis of migraine based on the International Headache Society criteria, we compare the effectiveness of coenzyme Qten on frequency, duration, and severity of childhood migraine. For comparing the QoL, we used the International PedMIDAS questionnaire. Results: Coenzyme Qten showed good therapeutic effects in children, especially in long-term use; however, amitriptyline showed more rapid response. After 3 months of treatment, clinical outcomes in the two groups did not significantly differ from each other. Similarly, Children's QoL increased in the same way. There are more reported side effects in children using amitriptyline compared to coenzyme Qten. Conclusions: According to results, Co-enzyme Q10, with fewer side effects and comparable therapeutic effects, especially in the long term, could be a good drug for prophylactic treatment of migraine headaches.

Acetyl-L-carnitine and/or liposomal co-enzyme Q10 prevent propionic acid-induced neurotoxicity by modulating oxidative tissue injury, inflammation, and ALDH1A1-RA-RARα signaling in rats.

Propionic acid (PPA) is a short-chain fatty acid produced endogenously by gut microbiota and found in foodstuffs and pharmaceutical products as an additive. Exposure to PPA has been associated with the development of autism spectrum disorder (ASD). The purpose of this study was to investigate the protective effect of acetyl-L-carnitine (ALCAR) and liposomal Co-enzyme Q10 (CoQ10) against cerebral and cerebellar oxidative injury, inflammation, and cell death, and alterations in ALDH1A1-RA-RARα signaling in an autism-like rat model induced by PPA. The rats were treated with PPA and concurrently received ALCAR and/or CoQ10 for 5 days. The animals were sacrificed, and the cerebral cortex and cerebellum were collected for analysis. PPA caused histopathological alterations along with increased malondialdehyde (MDA), NF-κB p65, TNF-α, and IL-6 in the cerebrum and cerebellum of rats. Reduced glutathione (GSH) and antioxidant enzymes were declined in the brain of rats that received PPA. Concurrent treatment with ALCAR and/or CoQ10 prevented tissue injury, decreased MDA, NF-κB p65, and pro-inflammatory cytokines, and enhanced cellular antioxidants in PPA-administered rats. ALCAR and/or CoQ10 upregulated Bcl-2 and decreased Bax and caspase-3 in the brain of rats. In addition, ALCAR and/or CoQ10 upregulated cerebral and cerebellar ALDH1A1 and RARα in PPA-treated rats. The combination of ALCAR and CoQ10 showed more potent effects when compared with the individual treatments. In conclusion, ALCAR and/or CoQ10 prevented tissue injury, ameliorated oxidative stress, inflammatory response, and apoptosis, and upregulated ALDH1A1-RA-RARα signaling in the brain of autistic rats.

Screening and engineering of high-activity promoter elements through transcriptomics and red fluorescent protein visualization in Rhodobacter sphaeroides.

The versatile photosynthetic α-proteobacterium Rhodobacter sphaeroides, has recently been extensively engineered as a novel microbial cell factory (MCF) to produce pharmaceuticals, nutraceuticals, commodity chemicals and even hydrogen. However, there are no well-characterized high-activity promoters to modulate gene transcription during the engineering of R. sphaeroides. In this study, several native promoters from R. sphaeroides JDW-710 (JDW-710), an industrial strain producing high levels of co-enzyme Q10 (Q10) were selected on the basis of transcriptomic analysis. These candidate promoters were then characterized by using gusA as a reporter gene. Two native promoters, P rsp _ 7571 and P rsp _ 6124 , showed 620% and 800% higher activity, respectively, than the tac promoter, which has previously been used for gene overexpression in R. sphaeroides. In addition, a P rsp _ 7571 -derived synthetic promoter library with strengths ranging from 54% to 3200% of that of the tac promoter, was created on the basis of visualization of red fluorescent protein (RFP) expression in R. sphaeroides. Finally, as a demonstration, the synthetic pathway of Q10 was modulated by the selected promoter T334* in JDW-710; the Q10 yield in shake-flasks increased 28% and the production reached 226 mg/L. These well-characterized promoters should be highly useful in current synthetic biology platforms for refactoring the biosynthetic pathway in R. sphaeroides-derived MCFs.

Combination of Omega 3 and Coenzyme Q10 Exerts Neuroprotective Potential Against Hypercholesterolemia-Induced Alzheimer's-Like Disease in Rats.

Alzheimer's disease (AD) is the most common form of dementia that progressively disrupts neurocognitive function, which has neither cure nor effective treatment. Hypercholesterolemia might be involved in brain alterations that could evolve into AD. The present study aims to evaluate the potential of omega-3, Co-enzyme Q10 (Co-Q10), as well as their combination in ameliorating hypercholesterolemia-initiated AD-like disease. We adapted a hypercholesterolemic (HC) rat model, a model of oxidative stress-mediated neurodegeneration, to study AD-like pathology. Hypercholesterolemia resulted in increased lipid peroxidation coupled with declined nitric oxide production, reduced glutathione levels, and decreased antioxidant activities of glutathione-s-transferase (GST) and glutathione peroxidase (GSH-Px) in the brain. Moreover, hypercholesterolemia resulted in decreased acetylcholine (ACh) levels and increased acetylcholine-esterase (AChE) activity, along with an increment of tumor necrosis factor and amyloid-ß 42. Behaviorally, HC-rats demonstrated depressive-like behavior and declined memory. Treatment of HC-rats with omega-3 and Co-Q10 (alone or in combination) alleviated the brain oxidative stress and inflammation, regulated cholinergic functioning, and enhanced the functional outcome. These findings were verified by the histopathological investigation of brain tissues. This neuroprotective potential of omega-3 and Co-Q10 was achieved through anti-oxidative, anti-inflammatory, anti-amyloidogenic, pro-cholinergic, and memory-enhancing activities against HC-induced AD-like disease; suggesting that they may be useful as prophylactic and therapeutic agents against the neurotoxic effects of hypercholesterolemia.

Co-enzyme Q10 protects primary chicken myocardial cells from heat stress by upregulating autophagy and suppressing the PI3K/AKT/mTOR pathway.

In this study, we investigated the function of co-enzyme Q10 (Q10) in autophagy of primary chicken myocardial cells during heat stress. Cells were treated with Q10 (1 µΜ, 10 µΜ, and 20 µM) before exposure to heat stress. Pretreatment of chicken myocardial cells with Q10 suppressed the decline in cell viability during heat stress and suppressed the increase in apoptosis during heat stress. Treatment with 20 µM Q10 upregulated autophagy-associated genes during heat stress. The expression of LC3-II was highest in cells treated with 20 µM Q10. Pretreatment with Q10 decreased reactive oxygen species (ROS) levels during heat stress. The number of autophagosomes was significantly increased by 20 µM Q10 treatment, as demonstrated by electron microscopy or monodansylcadaverine (MDC) fluorescence. SQSTM1 accumulation was diminished by Q10 treatment during heat stress, and the number of LC3II puncta was increased. Treatment with 20 µM Q10 also decreased the activation of the PI3K/Akt/mTOR pathway. Our results showed that co-enzyme Q10 can protect primary chicken myocardial cells by upregulating autophagy and suppressing the PI3K/Akt/mTOR pathway during heat stress.

Neuroprotective Methodologies of Co-Enzyme Q10 Mediated Brain Hemorrhagic Treatment: Clinical and Pre-Clinical Findings.

Cerebral brain hemorrhage is associated with the highest mortality and morbidity despite only constituting approximately 10-15% of all strokes classified into intracerebral and intraventricular hemorrhage where most of the patients suffer from impairment in memory, weakness or paralysis in arms or legs, headache, fatigue, gait abnormality and cognitive dysfunctions. Understanding molecular pathology and finding the worsening cause of hemorrhage will lead to explore the therapeutic interventions that could prevent and cure the disease. Mitochondrial ETC-complexes dysfunction has been found to increase neuroinflammatory cytokines, oxidative free radicals, excitotoxicity, neurotransmitter and energy imbalance that are the key neuropathological hallmarks of cerebral hemorrhage. Coenzyme Q10 (CoQ10), as a part of the mitochondrial respiratory chain can effectively restore these neuronal dysfunctions by preventing the opening of mitochondrial membrane transition pore, thereby counteracting cell death events as well as exerts an anti-inflammatory effect by influencing the expression of NF-kB1 dependent genes thus preventing the neuroinflammation and energy restoration. Due to behavior and biochemical heterogeneity in post cerebral brain hemorrhagic pattern different preclinical autologous blood injection models are required to precisely investigate the forthcoming therapeutic strategies. Despite emerging pre-clinical research and resultant large clinical trials for promising symptomatic treatments, there are very less pharmacological interventions demonstrated to improve post operative condition of patients where intensive care is required. Therefore, in current review, we explore the disease pattern, clinical and pre-clinical interventions under investigation and neuroprotective methodologies of CoQ10 precursors to ameliorate post brain hemorrhagic conditions.

Co-enzyme Q10 protects chicken hearts from in vivo heat stress via inducing HSF1 binding activity and Hsp70 expression.

In this report, we investigated the protective function of co-enzyme Q10 on chicken hearts during in vivo heat stress (HS) and the relationship with Hsp70 expression. The concentration of co-enzyme Q10 (Q10) in the serum indicated that Q10 exogenously added prior HS was fully absorbed by chickens and is maintained at high levels during HS. The level of heart and oxidative damage-associated enzymes in the serum revealed that treatment with Q10 decreased the activity of CK-MB, CK, and LDH compared with the HS group; moreover, oxidative injury was also alleviated by Q10 according to the level of SOD, MDA, and T-AOC in the serum compared with HS group during heat stress. A pathological examination indicated that the chicken hearts suffered serious damage during HS, including hemorrhage, granular changes, karyopyknosis, and cardiac muscle fiber disorder; however, the extent of heart damage was reduced in HS + Q10 group. Our results indicated that the addition of Q10 could upregulate the expression of Hsp70 during HS compared with the HS group. Compared with the HS group, the addition of Q10 significantly increased the gene expression of hsf1 during HS and hsf3 at 5 h of HS. The expression of hsf2 and hsf4 was not influenced by HS. Q10 could only accelerate the trimerization of HSF1 as well binding activities to Hsp70 HSE according to native page and ChIP assays. These findings suggest that co-enzyme Q10 can protect chicken hearts from in vivo HS by inducing HSF1 binding activity and Hsp70 expression.

Systematic review of antioxidant types and doses in male infertility: Benefits on semen parameters, advanced sperm function, assisted reproduction and live-birth rate.

OBJECTIVE: To explore the current evidence concerning the effect of oral antioxidant supplementation on various male fertility outcomes, as antioxidants are widely available compounds that are commonly used for the treatment of male infertility. MATERIALS AND METHODS: PubMed, Medline and Cochrane electronic databases were searched according to a modified Preferred Reporting Items for Systemic Reviews and Meta-Analyses (PRISMA) guidelines looking for studies investigating the effect of antioxidant therapy on infertile men. The studies were explored looking for antioxidants: (i) types and doses; (ii) mechanism of action and rationale for use; and (iii) effect on the different outcome measures reported. RESULTS: In all, 26 studies reported a significant positive effect of antioxidant therapy on basic semen parameters, advanced sperm function, outcomes of assisted reproductive therapy, and live-birth rate. Vitamin E, vitamin C, carnitines, N-acetyl cysteine, co-enzyme Q10, zinc, selenium, folic acid and lycopene were most commonly used. The vitamins' mechanism of action and reported doses is presented in Table 1, Table 2. CONCLUSION: Antioxidants generally have a favourable effect on male fertility. Further studies are needed to identify the optimal antioxidant regimen that can be used safely and efficiently in clinical practice.

Co-enzyme Q10 upregulates Hsp70 and protects chicken primary myocardial cells under in vitro heat stress via PKC/MAPK.

In this report, we investigate the protective mechanism of co-enzyme Q10 on chicken primary myocardial cells during heat stress. Morphological observations indicate that addition of co-enzyme Q10 protects myocardial cells from heat stress, reduces the damage of mitochondria and nucleus, and decreases the mean number of vacuolated mitochondria. We have previously shown that co-enzyme Q10 can protect myocardial cells by upregulating the expression of Hsp70. Therefore, signaling pathways involved in this process were explored. No changes of total MAPK protein (P38MAPK, JNK, ERK) expression in the experimental groups were detected, with the exception of total JNK1. Co-enzyme Q10 failed to increase the expression of JNK1 compared to the HS group which was treated with heat stress only. Addition of Q10 upregulated the expression of p-P38MAPK, p-JNK, and p-ERK1. Inhibitors of P38MAPK and JNK, SB203580 and SP600125, respectively, weakened the upregulation of Hsp70 by co-enzyme Q10, indicating that MAPK pathways participate in the Hsp70 upregulation by co-enzyme Q10. Co-enzyme Q10 upregulates the expression of p-MEK3/6 and p-MEK4, but not p-MEK7 during heat stress. Expression of p-PKCα and p-PKCß1 was also elevated following the addition of co-enzyme Q10 during heat stress, and addition of PKC inhibitors decreased the expression of Hsp70 induced by co-enzyme Q10. This confirms that PKC is also associated with the upregulation of Hsp70. In HS+Q10 group, addition of SP600125 or SB203580 could increase cell apoptosis under heat stress. Our results suggest that co-enzyme Q10 upregulates the expression of Hsp70 during heat stress to protect chicken primary myocardial cells via the PKC-MEK3/4/6-P38MAPK/JNK pathways.

The potential benefit of combined versus monotherapy of coenzyme Q10 and fluoxetine on depressive-like behaviors and intermediates coupled to Gsk-3ß in rats.

As a part of the serotoninergic dysfunction implicated in neurobiology of depression, evidence has focused on serotonin (5-HT) receptors downstream signaling intermediates including glycogen synthase kinase-3ß (GSK-3ß), cAMP response element binding protein (CREB) and brain derived neurotrophic factor (BDNF). Our team previously reported that coenzyme Q10 (CoQ10) exerted antidepressant-like effect in rats exposed to chronic unpredictable mid stress (CUMS) via elevating serotonin levels. However, the effect of CoQ10 has not been elucidated in downstream signaling molecules mediating 5HT receptors' effect involved in depressive disorder hitherto. In the present study, we focused on 5-HT1A and 5-HT2A receptors (activation of 5-HT1A receptor and inhibition of 5-HT2A receptors reduce depressive like-behaviors). We investigated the role of these 5-HT receptors and their linked GSK-3ß signaling intermediates as an underlying mechanism of CoQ10 as monotherapy or combined with fluoxetine, a selective serotonin reuptake inhibitor, to alleviate depressive-like phenotype. Effects of CoQ10 (100mg/kg/day) or/and fluoxetine (10mg/kg/day) were determined on 5-HT1A, 5-HT2A receptors mRNA expression, GSK-3ß and phosphorylated (p)GSK-3ß, CREB, pCREB and BDNF protein expression in rats subjected to CUMS for 6weeks. CUMS rats exhibited obvious depressive-like behaviors (anhedonia-like behavior, negative alterations in social interaction, open field and forced swimming tests) with increased corticosterone and adrenal glands weight, decreased hippocampal levels of pGSK-3ß, pCREB and BDNF protein expressions. Additionally, they exhibited decreased hippocampal 5-HT1A and increased 5-HT2A receptor mRNA expression. CoQ10 or fluoxetine significantly attenuated the behavioral and neurochemical alterations in stressed rats with more significance with combined treatment. These findings imply that CoQ10 or/and fluoxetine attenuated CUMS-induced depressive-like behavior partly through modulating dysfunctional regulation of post-serotonergic receptor signaling pathway focusing on GSK-3ß, CREB and BDNF.