Coenzyme Q10 in Male and Female Infertility

Infertility is a medical condition that can cause psychological, physical, mental, spiritual, and medical detriments to the patient. Infertility can also be a marker of an underlying chronic disease associated with infertility. It is currently affecting one out of six couples worldwide. The pathophysiology of male and female infertility is multifactorial and still not fully elucidated. Both are related to an imbalance between the production of Reactive Oxygen Species (ROS) and antioxidant defences. Antioxidants are biological and chemical compounds that are synthesized endogenously or exogenously, counteract oxidative stress and act as free radical scavengers. Coenzyme Q10 (CoQ10) is a lipidsoluble quinone acting as an effective antioxidant, which prevents lipid peroxidation and DNA oxidation. It empowers the body’s energy production cycle through Adenosine Triphosphate (ATP) synthesis and has long been used to ameliorate infertility outcomes. Evidence suggests that CoQ10 shows beneficial effects on semen quality, quantity, and mobility in male infertility. Moreover, the potential benefits of oral antioxidants on female infertility treatment are being increasingly investigated, including CoQ10. CoQ10 treatment significantly increases fertilization rate, the number of high-quality embryos, and higher clinical pregnancy and live birth rates. Furthermore, CoQ10 administration enhances ovarian response to stimulation and improves oocyte and embryo quality. Hence, available evidence and clinical studies suggest that CoQ10 supplementation could be considered an inexpensive, safe therapy to enhance infertility treatment in men and women of reproductive age

The efficacy and safety of coenzyme Q10 in preventing the progression of early Parkinson's disease: A meta-analysis

@#<p style="text-align: justify;"><strong>INTRODUCTION:</strong> Coenzyme Q10, also known as Ubiquinone, is a substance now being used as a dietary supplement in many countries including the Philippines. It has also been the focus of several researches as treatment for several diseases including Parkinson's Disease. Several studies have shown that Coenzyme Q10 inhibits mitochondrial dysfunction in Parkinson's Disease, hence delaying its progression.<br /><strong>OBJECTIVES:</strong> The objective of this study is to assess and summarize the available evidence on the efficacy and safety of Coenzyme Q10 administration in the prevention of the progression of early Parkinson's Disease.<br /><strong>METHODS:</strong> This is meta-analysis of randomized controlled trials on the use of Coenzyme Q10 in Parkinson's Disease. A literature search in several databases was conducted for relevant studies. Three randomized controlled trials met the inclusion criteria. The efficacy of Coenzyme Q10 were measured using the total and the component scores of the Unified Parkinson Disease Rating Scale on follow-up. On the other hand, safety were measured using the withdrawal rate and the associated adverse reactions during the therapy of CoQ10. The Review Manager Software was utilized for the meta-analysis.<br /><strong>RESULTS:</strong> Compared to Placebo, treatment of CoQ10 did not show any significant difference in the mean scores of the UPDRS mental and ADL scores. Interestingly, the UPDRS motor score showed a significant difference between Coenzyme Q10 and placebo, but no significant difference when a subgroup analysis between high-dose (-4.03 [-15.07-7.01], p-value 0.47, I2 67%, P for heterogeneity 0.08) and low-dose Coenzyme Q10 (0.53 [-0.89-1.94], p-value 0.47, I2 34%, P for heterogeneity 0.22) was done. Overall, there was no significant difference in the total UPDRS score (0.68 [-0.61-1.97], p-value 0.30, I2 0%, P for heterogeneity 0.70). The anxiety, back pain, headache, sore throat, nausea, dizziness and constipation.<br /><strong>CONCLUSION:</strong> Contrary to some animal and human studies, this meta-analysis showed that the use of CoQ10 results to non-significant improvement in all components of the UPDRS scores as opposed to placebo. However, the use of CoQ10 is tolerated and seems to be safe but further studies are needed to validate this finding.</p>

Effect of coenzyme Q10 supplementation on serum protein, mineral status, blood picture and immune status in broilers.

In poultry, coenzyme Q10 (CoQ10) is widely used as a feed additive to control mortality due to ascites in broilers. Apart from its use the treatment of a variety of disorders viz., ischemic heart disease, diabetes mellitus, Parkinson’s disease, muscle fatigue and muscle weakness, its supplementation has been reported to be beneficial for cardiovascular disease, chronic heart failure, cancer, migraine, asthma and hypertension. In this study, we investigated the effect of CoQ10 supplementation on serum protein, serum minerals, blood parameters, ascites susceptibility and humoral immune status in broilers fed with different energy levels which influence their productivity, biochemical profile and ascites incidences. The treatment had three levels of CoQ10, namely 0, 20 and 40 mg/kg at normal (NE), low (LE) and high (HE) energy levels in which 2X3 factorial design was followed. The haemoglobin and packed cell volume were not affected (P >0.05) by either energy or CoQ10 levels but the erythrocyte osmotic fragility per cent (EOF %) and blood glucose levels were decreased by CoQ10 supplementation at both 20 and 40 mg/kg. The serum calcium level had significantly (P <0.01) increased with CoQ10 at 40 mg/kg (12.70 vs. 11.58 and 11.98 mg/dL) in NE diet group over the unsupplemented and 20 mg/kg supplemented birds. Compared to the respective unsupplemented groups, CoQ10 @40 mg/kg reduced (P <0.01) the serum total protein (4.69 vs. 5.23 g/dL) and serum albumin (2.46 vs. 2.78 g/dL) in NE group but increased (P <0.01) (4.70 vs. 4.08 g/dL) and (2.59 vs. 2.04 g/dL), respectively in LE group. High energy birds showed significantly (P <0.01) increased serum albumin (2.74 vs. 2.24 g/dL). The humoral immunity against Newcastle Disease (ND titre) was significantly (P <0.01) higher in 21 days of growth period at both the levels of supplementation but on 42 days no significant difference among the groups were observed. It can be concluded that CoQ10 supplementation at 20 mg/kg decreased blood glucose level and increased erythrocytes osmotic stability and hence, could reduce bird’s susceptibility to ascites.

Coenzyme Q10 defects may be associated with a deficiency of Q10-independent mitochondrial respiratory chain complexes

BACKGROUND: Coenzyme Q10 (CoQ10 or ubiquinone) deficiency can be due either to mutations in genes involved in CoQ10 biosynthesis pathway, or to mutations in genes unrelated to CoQ10 biosynthesis. CoQ10 defect is the only oxidative phosphorylation disorder that can be clinically improved after oral CoQ10 supplementation. Thus, early diagnosis, first evoked by mitochondrial respiratory chain (MRC) spectrophotometric analysis, then confirmed by direct measurement of CoQ10 levels, is of critical importance to prevent irreversible damage in organs such as the kidney and the central nervous system. It is widely reported that CoQ10 deficient patients present decreased quinone-dependent activities (segments I + III or G3P + III and II + III) while MRC activities of complexes I, II, III, IV and V are normal. We previously suggested that CoQ10 defect may be associated with a deficiency of CoQ10-independent MRC complexes. The aim of this study was to verify this hypothesis in order to improve the diagnosis of this disease. RESULTS: To determine whether CoQ10 defect could be associated with MRC deficiency, we quantified CoQ10 by LC-MSMS in a cohort of 18 patients presenting CoQ10-dependent deficiency associated with MRC defect. We found decreased levels of CoQ10 in eight patients out of 18 (45 %), thus confirming CoQ10 disease. CONCLUSIONS: Our study shows that CoQ10 defect can be associated with MRC deficiency. This could be of major importance in clinical practice for the diagnosis of a disease that can be improved by CoQ10 supplementation.

Coenzyme Q10 therapy in current clinical practice.

Coenzyme Q10 (CoQ10) is a naturally occurring, lipid soluble, essential compound and is also known as ubiquinone. CoQ10 acts as an intermediate of the electron transport chain situated in membrane of mitochondria and vital for ATP production and cellular respiration. CoQ10 also serves as an intercellular antioxidant. All the clinical use of CoQ10 are based upon these two functions. CoQ10 levels are altered in a number of oncological as well as non-oncological diseases. Furthermore, recent data indicate that CoQ10 has an impact on the expression of many genes involved in metabolism, cellular transport, transcription control, and cell signaling, making CoQ10 a potent gene regulator. CoQ10 supplementation is useful in diseases associated with CoQ10 deficiency which includes primary and secondary CoQ10 deficiencies, fibromyalgia, diabetes mellitus, mitochondrial diseases, neurodegenerative diseases, cardiovascular disease, cancer, male infertility and periodontal disease. Clinical presentations of severe CoQ10 deficiency include severe infantile multisystemic disease, encephalomyopathy, isolated myopathy cerebellar ataxia and Leigh syndrome with growth retardation. Oral CoQ10 administration can correct CoQ10 deficiency since it increases CoQ10 tissue levels. CoQ10 therapy has no serious side effects in humans and new formulations have been developed that increase CoQ10 absorption and tissue distribution. Future trends involving CoQ10 in many diseases needs more clinical trials for better understanding of CoQ10 efficacy.

Effect of coenzyme Q10 and Ardisia japonica Blume on plasma and liver lipids, platelet aggregation, and erythrocyte Na efflux channels in simvastatin-treated guinea pigs

Forty guinea pigs were divided into four groups and fed 0.04% cholesterol based control diet, plus 0.05% simvastatin, and statin plus 0.1% CoQ10 or 10% Ardisia Japonica Blume (AJB) leave powder for 4 weeks. Plasma total cholesterol levels decreased significantly in all groups fed the statin-containing diet compared with that in guinea pigs fed the control diet (P < 0.01). Plasma and liver triglycerides decreased significantly in the statin plus CoQ10 group compared with those in the control (both P < 0.05). Maximum platelet aggregation was significantly higher in the statin plus CoQ10 group than that in the other groups (P < 0.05). Na-K ATPase activity increased in the statin group and decreased in the statin plus CoQ10 group (P < 0.01). Na-K co-transport and Na passive transport decreased significantly in the control group compared with those in the other groups (both P < 0.05). Intracellular Na was highest in the statin group and lowest in the statin plus CoQ10 group and was correlated with Na-K ATPase activity. Thiobarbituric acid reactive substance production in platelet-rich plasma and liver tended to decrease in the statin plus CoQ10 group compared with those in the other groups. Plasma glutamic-pyruvic transaminase and glutamic-oxaloacetic transaminase increased significantly in the statin group compared with those in the control (P < 0.05). These result suggest that antioxidant rich AJB did not have positive effects on cardiovascular disease parameters. The statin plus CoQ10 seemed to decrease cholesterol more efficiently than that of statin alone.

Antioxidant Effect of CoQ10 on N-nitrosodiethylamine-induced Oxidative Stress in Mice

The antioxidant effect of CoQ10 on N-nitrosodiethylamine (NDEA)-induced oxidative stress was investigated in mice. Food intake and body weight were similar in both CoQ10 and control groups during the 3-week experimental period. NDEA significantly increased the activities of typical marker enzymes of liver function (AST, ALT and ALP) both in control and CoQ10 groups. However, the increase of plasma aminotransferase activity was significantly reduced in the CoQ10 group. Lipid peroxidation in various tissues, such as heart, lung, liver, kidney, spleen and plasma, was significantly increased by NDEA, but this increase was significantly reduced by 100 mg/kg of CoQ10. Superoxide dismutase activity increased significantly upon NDEA-induced oxidative stress in both the control and CoQ10 groups with the effect being less in the CoQ10 group. Catalase activity decreased significantly in both the control and CoQ10 groups treated with NDEA, again with the effect being less in the CoQ10 group. The lesser effect on superoxide dismutase and catalase in the NDEA-treated CoQ10 group is indicative of the protective effect CoQ10. Thus, CoQ10 can offer useful protection against NDEA-induced oxidative stress.

Optimal Supply of Precursors for CoQ10 Production by Rhodopseudomonas Palustris / 现代生物医学进展

CoQ10 has been used not only as a medicine but also as food supplements because of its various physiological and biochemical activities. A full-factorial central composite design and response surface methodology were used for optimizing three precursors Solanesol, 4-hydroxybenzoic acid and methionine to maximize the production of CoQ10 by Rhodopseudomonas palustris J001. The optimization of the model predicted a maximum response 40.6 [(mg CoQ10)(g dried biomass)-1] CoQ10 production with 124.8 mg l-1 Solanesol, 267.7 mg l-14-hydroxybenzoic acid and 130.2 mg l-1 methionine, respectively. A new combination was prepared according to the result. The observed response was 40.5 ± 0.2 [(mg CoQ10)(g dried biomass)-1] and was 109.8%higher than in the control with no addition of the three precursors.

Optimal Supply of Precursors for CoQ10 Production by Rhodopseudomonas Palustris / 现代生物医学进展

CoQ10 has been used not only as a medicine but also as food supplements because of its various physiological and biochemical activities. A full-factorial central composite design and response surface methodology were used for optimizing three precursors Solanesol, 4-hydroxybenzoic acid and methionine to maximize the production of CoQ10 by Rhodopseudomonas palustris J001. The optimization of the model predicted a maximum response 40.6 [(mg CoQ10)(g dried biomass)-1] CoQ10 production with 124.8 mg l-1 Solanesol, 267.7 mg l-14-hydroxybenzoic acid and 130.2 mg l-1 methionine, respectively. A new combination was prepared according to the result. The observed response was 40.5 ± 0.2 [(mg CoQ10)(g dried biomass)-1] and was 109.8%higher than in the control with no addition of the three precursors.

Optimal Supply of Precursors for CoQ10 Production by Rhodopseudomonas Palustris / 现代生物医学进展

CoQ10 has been used not only as a medicine but also as food supplements because of its various physiological and biochemical activities. A full-factorial central composite design and response surface methodology were used for optimizing three precursors Solanesol, 4-hydroxybenzoic acid and methionine to maximize the production of CoQ10 by Rhodopseudomonas palustris J001. The optimization of the model predicted a maximum response 40.6 [(mg CoQ10)(g dried biomass)-1] CoQ10 production with 124.8 mg l-1 Solanesol, 267.7 mg l-14-hydroxybenzoic acid and 130.2 mg l-1 methionine, respectively. A new combination was prepared according to the result. The observed response was 40.5 ± 0.2 [(mg CoQ10)(g dried biomass)-1] and was 109.8%higher than in the control with no addition of the three precursors.

Effect of Coenzyme Q10 and green tea on plasma and liver lipids, platelet aggregation, TBARS production and erythrocyte Na leak in simvastatin treated hypercholesterolmic rats

This study was conducted to investigate the hypocholesterolemic effect of simvastatin (30 mg/kg BW) and antioxidant effect of coenzyme Q10 (CoQ10, 15 mg/kg BW) or green tea (5%) on erythrocyte Na leak, platelet aggregation and TBARS production in hypercholesterolemic rats treated with statin. Food efficiency ratio (FER, ADG/ADFI) was decreased in statin group and increased in green tea group, and the difference between these two groups was significant (p<0.05). Plasma total cholesterol was somewhat increased in all groups with statin compared with control. Plasma triglyceride was decreased in statin group and increased in groups of CoQ10 and green tea, and the difference between groups of statin and green tea was significant (p<0.05). Liver total cholesterol was not different between the control and statin group, but was significantly decreased in the group with green tea compared with other groups (p<0.05). Liver triglyceride was decreased in groups of statin and green tea compared with the control, and the difference between groups of the control and green tea was significant (p<0.05). Platelet aggregation of both the initial slope and the maximum was not significantly different, but the group with green tea tended to be higher in initial slope and lower in the maximum. Intracellular Na of group with green tea was significantly higher than the control or statin group (p<0.05). Na leak in intact cells was significantly decreased in the statin group compared with the control (p<0.05). Na leak in AAPH treated cells was also significantly reduced in the statin group compared with groups of the control and CoQ10 (p<0.05). TBARS production in platelet rich plasma was significantly decreased in the groups with CoQ10 and green tea compared with the control and statin groups (p<0.05). TBARS of liver was significantly decreased in the group with green tea compared with the statin group (p<0.05). In the present study, even a high dose of statin did not show a cholesterol lowering effect, therefore depletion of CoQ10 following statin treatment in rats is not clear. More clinical studies are needed for therapeutic use of CoQ10 as an antioxidant in prevention of degenerative diseases independent of statin therapy.

Advance in Parkinson's Disease(review) / 中国康复理论与实践

@#Parkinson's disease (PD) is one of the prevalent neurodegenerative diseases in human being, which is characterized by the selective degeneration and death of dopaminergic neurons in the substantia negra. The etiology of PD is not illuminated yet. Currently this disease is thought to be the result of the co-operation of multiple factors. So far, PD can't be cured, and all the treatments are to control its symptoms. DA, PDI, Parkin gene, PINK1 gene and α-synuclein are all related to PD. Apoptosis may play a role in the degeneration and death of dopaminergic neurons. Disfunction of mitochondria appears to play a role in the pathogenesis of PD. The levels of CoQ10 from PD patients have been reported to be lower than that from normal people, and the supplement of CoQ10 favors the assistant treatment of PD.

Space Mutation Effects of Rhodobacter Sphaeroides / 航天医学与医学工程

Objective To study mutagenic effects of spaceflight on physiological and biochemical parameters of Rhodobacter sphaeroides and select high-yield mutants in co-enzyme Q10(CoQ10) production for providing the experimental and theoretical basis for industrial production through mutagenic effects of spaceflight.Methods Variations in stress resistance and CoQ10 production of isolated strains were studied,the strain Rhodobacter sphaeroides was taken back by a recoverable satellite after 15 d flight in space.Results Compared to the control,the strain was characterized by highter NaCl tolerance and higher stress resistance,as well as with broader scope in growth temperature and pH value after spaceflight.The mutant colonies appeared white or pink which was different from their original red.The CoQ10 production of mutant 10 strain was increased by 73.13% much higher than that of control.Conclusion Spaceflight mutagenic effects on Rhodobacter sphaeroides shows to be multi-factor compared to the traditional single-factor mutagenesis methods.It can enhance stress resistance and increase CoQ10 production of isolated strains,and can be utilized in industrial microbial mutagenesis and breeding in the future.