Effect of coenzyme Q10 on endotoxin shock in dogs

We studied the effects of coenzyme Q10 pretreatment on both pulmonary function and chemical mediators during endotoxin shock in dogs. Coenzyme Q10 pretreatment inhibited disturbances in peak airway pressure, total compliance of lung plus chest wall, lung clearance index, plasma histamine, base excess, and lactate; however, it had little effect on the circulation. The mechanism of coenzyme Q10's significant effects on pulmonary function during endotoxin shock is presently unknown.     

Effects of coenzyme Q10 on salivary secretion

ObjectivesDry mouth is a condition associated with reduced salivary secretion and is thought to be related to aging. This study was conducted to test whether reduced (ubiquinol) or oxidized (ubiquinone) forms of CoQ10 affect salivary secretion and salivary CoQ10 content before and after treatment.Design and methodsSixty-six patients were given either ubiquinol or ubiquinone orally at a dosage of 100 mg/day, or a placebo for 1 month, and salivary secretion and salivary CoQ10 content were analyzed before and after treatment.ResultsBoth parameters were significantly improved following treatment with either form of CoQ10, suggesting the effectiveness of CoQ10 in attenuating dry mouth symptoms.ConclusionCoQ10 was locally detected in salivary glands, suggesting that orally administered CoQ10 was transported to the salivary glands via the blood stream and exerted its activity, improving salivary secretion.     

Effects of pentoxifylline and coenzyme Q10 in hepatic ischemia/reperfusion injury

OBJECTIVES: We examined whether pentoxifylline (PTX) and coenzyme Q10 (Q) pretreatment affect ischemia-reperfusion damage in the rat liver. DESIGN AND METHODS: Twenty minutes of reflow following 30 min of ischemia was performed. Before the experiment, rats were treated PTX 50 mg/kg, IP or PTX 50 mg/kg IP + Q10 mg/kg, intragastric, or untreated. Rats were divided into four groups: control (C), ischemia-reperfusion (IR), PTX-treated (P), and Q+PTX-treated (QP) groups. Hepatic glutathione (GSH) and malondialdehyde (MDA) levels and catalase, superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and reductase (GSSGR) activities were measured. RESULTS: In IR group GSH levels decreased (p<0.01), conversely MDA levels increased (p<0.01). PTX pretreatment did not affect GSH and MDA values, but Q+PTX pretreatment improved of those (p<0.01). It was shown that catalase and GSH-Px activities increased during ischemia-reperfusion (p<0.01, both of), but PTX pretreatment did not significantly ameliorate those activities. GSSGR activity was higher in IR group than in basal levels (p<0.01). The decrease GSSGR activity that was observed in P group was not significant compared to IR group. During ischemia/reperfusion also SOD activity increased as compared with controls (p<0.05). In PTX-treated group, SOD activity was significantly higher than control and ischemia/reperfusion groups (p<0.01, both of). Q+PTX treatment ameliorated those enzyme activities to the control values. CONCLUSIONS: Short-term hepatic ischemia-reperfusion diminished GSH, increased MDA levels and induced some antioxidant enzyme activities. Q+PTX pretreatment was useful in hepatic ischemia-reperfusion injury, but treatment of PTX alone did not cause beneficial effect in the present study.     

The role of coenzyme Q10 in heart failure

OBJECTIVE: To review the clinical data demonstrating the safety and efficacy of coenzyme Q10 (CoQ10) in heart failure (HF). DATA SOURCES: Pertinent literature was identified through MEDLINE (1966-January 2005) using the search terms coenzyme Q10, heart failure, antioxidants, and oxidative stress. Only articles written in the English language and evaluating human subjects were used. DATA SYNTHESIS: HF impairs the ability of the heart to maintain its normal cardiac output. Following an initial insult, cardiac remodeling ensues, resulting in left ventricular dilation and hypertrophy. Oxidative stress is also increased, while CoQ10 levels are decreased in patients with HF. This has led to the hypothesis that CoQ10, an antioxidant, may decrease oxidative stress, impair remodeling, and improve cardiac function. CONCLUSIONS: Large, well-designed studies on this topic are lacking. The limited data from well-designed trials indicate there may be some minor benefits with CoQ10 therapy in ejection fraction and end diastolic volume. CoQ10 therapy has been shown to be relatively safe with a low incidence of adverse effects.     

Therapeutic role of coenzyme Q(10) in Parkinson's disease

Mitochondrial dysfunction has been well established to occur in Parkinson's disease (PD) and appears to play a role in the pathogenesis of the disorder. A key component of the mitochondrial electron transport chain (ETC) is coenzyme Q(10), which not only serves as the electron acceptor for complexes I and II of the ETC but is also an antioxidant. In addition to being crucial to the bioenergetics of the cell, mitochondria play a central role in apoptotic cell death through a number of mechanisms, and coenzyme Q(10) can affect certain of these processes. Levels of coenzyme Q(10) have been reported to be decreased in blood and platelet mitochondria from PD patients. A number of preclinical studies in in vitro and in vivo models of PD have demonstrated that coenzyme Q(10) can protect the nigrostriatal dopaminergic system. A phase II trial of coenzyme Q(10) in patients with early, untreated PD demonstrated a positive trend for coenzyme Q(10) to slow progressive disability that occurs in PD.     

阿托伐他汀与辅酶Q10联合应用对冠脉介入术后血清超敏C反应蛋白的影响

[目的]探讨阿托伐他汀与辅酶Q10联合应用对经皮冠脉介入（PCI）术后血清超敏C反应蛋白（hs-CRP）的影响。[方法]158例PCI患者随机分为A组（29例,阿托伐他汀10mg每晚一次联合辅酶Q1010mg每日3次口服,30d）和B组（29例,阿托伐他汀10mg每晚一次,30d）,测定两组患者术前、术后24h及术后30 d hs-CRP的变化。[结果]术前、术后24h及术后30d,A组hs—CRP水平分别为（10．04±4．46）、（4．11±4．67）及（13．45±4．07）mg／L,B组则水平分别为（9．34±4．56）、（3．24±5．46）及（16．13±3．86）mg／L,两组患者PCI术后hs-CRP水平明显高于术前（P〈0．01）;两组术后24h及术后30d比较,hs—CRP下降程度有显著差异性（P〈0．01）;两组术后30d比较,A组hs-CRP水平较B组下降更明显,差异达到统计学意义（P〈0．05）。[结论]PCI增加血清hs—CRP水平;阿托伐他汀与辅酶Q10联合应用能够增强其抗炎作用,有利于预防再狭窄。     

Measurement of reduced and oxidized coenzyme Q9 and coenzyme Q10 levels in mouse tissues by HPLC with coulometric detection

BACKGROUND: Ubiquinone-responsive multiple respiratory chain dysfunction due to coenzyme Q(10) (CoQ(10)) deficiency has been previously identified in muscle biopsies. However, previous methods are unreliable for estimating CoQ(10) redox status in tissue. We developed an accurate method for measuring tissue concentrations of reduced and oxidized coenzyme Q (CoQ). METHODS: Mouse tissues were weighed in the frozen state and homogenized with cold 1-propanol on ice. After solvent extraction, centrifugation and filtration, the filtrate was subsequently analyzed by reversed-phase HPLC with coulometric detection. RESULTS: Reference calibration curves were used to determine reduced and oxidized coenzyme Q(9) (CoQ(9)) and CoQ(10) concentrations in tissues. The method is sensitive ( approximately 15 microg/l), reproducible (6% CV) for CoQ(9) and CoQ(10), and linear up to 20 mg/l for CoQ(9) and CoQ(10). Analytical recoveries were 90-104%. In mouse tissues the amounts of total CoQ (TQ) ranged from 261 to 1737 nmol/g of protein. Total CoQ(9) levels are comparable with the values of those previously reported. CoQ is found to be mostly in the reduced form in mouse liver ( approximately 87%), heart ( approximately 60%), and muscle tissues ( approximately 58%); in the brain, most of the CoQ is in the oxidized state ( approximately 65%). CONCLUSION: This procedure provides a precise, sensitive, and direct assay method for the determination of reduced and oxidized CoQ(9) and CoQ(10) in mouse hindleg muscle, heart, brain, and liver tissues.     

Molecular diagnosis of coenzyme Q10 deficiency: an update

Introduction: Coenzyme Q₁₀ (CoQ) deficiency syndromes comprise a growing number of genetic disorders. While primary CoQ deficiency syndromes are rare diseases, secondary deficiencies have been related to both genetic and environmental conditions, which are the main causes of biochemical CoQ deficiency. The diagnosis is the essential first step for planning future treatment strategies, as the potential treatability of CoQ deficiency is the most critical issue for the patients.

Areas covered: While the quickest and most effective tool to define a CoQ-deficient status is its biochemical determination in biological fluids or tissues, this quantification does not provide a definite diagnosis of a CoQ-deficient status nor insight about the genetic etiology of the disease. The different laboratory tests to check for CoQ deficiency are evaluated in order to choose the best diagnostic pathway for the patient.

Expert commentary: New insights are being discovered about the implication of new proteins in the intricate CoQ biosynthetic pathway. These insights reinforce the idea that next generation sequencing diagnostic strategies are the unique alternative in terms of rapid and accurate molecular diagnosis of CoQ deficiency.     

Considerations for supplementing with coenzyme Q10 during statin therapy

OBJECTIVE: To review the literature concerning the effects of statin use on coenzyme (Co) Q10 concentrations and explain the rationale behind considering CoQ10 supplementation. DATA SOURCES: A MEDLINE search was conducted through January 2006. Search terms included ubiquinone, coenzyme Q10, HMG-CoA reductase inhibitors, statins, myotoxicity, and clinical trials. DATA SYNTHESIS: Statin therapy reduces blood CoQ10 concentrations. Studies exploring how this affects the development of myotoxicity have been small and dissimilar, thus limiting the ability to draw strong conclusions. Isolated studies suggested that statins induce mitochondrial dysfunction, but the clinical implications of this effect are limited. Limited data suggest that patients with familial hypercholesterolemia, heart failure, or who are over 65 years of age might represent at-risk populations who would benefit from CoQ10 supplementation. CONCLUSIONS: Routine CoQ10 supplementation for all patients taking statins to prevent myotoxicity is not recommended. However, certain subpopulations might be at risk and warrant further study.     

辅酶Q10对多巴胺损伤的PC12细胞凋亡的影响

目的：观察辅酶Q10在以PC12细胞建立的多巴胺神经元凋亡细胞模型中的作用。 方法：实验于2003-04／2004-04在锦州医学院科技试验中心进行。取体外培养的Pcl2细胞分为3组：①辅酶Q10组：加450μmol／L辅酶Q10和0．3mmol／L多巴胺。②多巴胺组：加0．3mmol／L多巴胺。③空白对照组：只加等量RPM11640。24h后进行流式细胞仪测试DNA含量，检测细胞凋亡率。 结果：多巴胺组细胞凋亡率明显高于空白对照组[（30．66&;#177;1．90）％，（0．82&;#177;0．07）％，P〈0．011，辅酶Q10组细胞凋亡率[（16．05&;#177;2．16）％1明显低于多巴胺组（P〈0．01）。 结论：辅酶Q10能显著降低多巴胺引起的PC12细胞凋亡，提示辅酶Q10作为神经保护性药物对保护多巴胺能神经元，防治帕金森病可能有实际应用价值。     

Open label trial of coenzyme Q10 as a migraine preventive

The objective was to assess the efficacy of coenzyme Q10 as a preventive treatment for migraine headaches. Thirty-two patients (26 women, 6 men) with a history of episodic migraine with or without aura were treated with coenzyme Q10 at a dose of 150 mg per day. Thirty-one of 32 patients completed the study; 61.3% of patients had a greater than 50% reduction in number of days with migraine headache. The average number of days with migraine during the baseline period was 7.34 and this decreased to 2.95 after 3 months of therapy, which was a statistically significant response (P < 0.0001). Mean reduction in migraine frequency after 1 month of treatment was 13.1% and this increased to 55.3% by the end of 3 months. Mean migraine attack frequency was 4.85 during the baseline period and this decreased to 2.81 attacks by the end of the study period, which was a statistically significant response (P < 0.001). There were no side-effects noted with coenzyme Q10. From this open label investigation coenzyme Q10 appears to be a good migraine preventive. Placebo-controlled trials are now necessary to determine the true efficacy of coenzyme Q10 in migraine prevention.     

Effects of sodium bicarbonate in canine hemorrhagic shock

We studied the use of sodium bicarbonate administration in a canine model of hemorrhagic shock to determine its effect on hemodynamics, arterial and venous blood gases, respiratory gases, and blood lactate levels. Thirteen dogs were anesthetized, paralyzed, mechanically ventilated, and hemodynamically monitored. Hypotension was induced and maintained at a mean arterial pressure of 40 to 45 mm Hg using controlled hemorrhage and reinfusion. After 2.5 h of shock, the dogs were randomized into two groups: one group (n = 6) received NaCl infusion; the other (n = 7) received sodium bicarbonate (1 mEq/kg followed by a continuous infusion of 2.5 mEq/kg.h for 2.5 h). CO2 production was increased in the alkali group, but there was no statistically significant difference between groups in any measured hemodynamic, blood gas, or respiratory gas variable. These included heart rate, BP, cardiac output, arterial and venous pH, CO2 production, and bicarbonate levels. Blood lactate levels, however, in the bicarbonate treated animals were significantly (p less than .01) higher than in the group treated with NaCl alone (10.1 +/- 3.2 vs. 5.1 +/- 1.2 mEq/L). These results are similar to the effects of bicarbonate found in other models of lactic acidosis, and suggest that bicarbonate therapy may have limited usefulness in the treatment of lactic acidosis.     

Comparison of coenzyme Q10 plasma levels in obese and normal weight children

BACKGROUND: Childhood obesity is associated with lower plasma levels of lipophilic antioxidants which may contribute to a deficient protection of low-density lipoproteins (LDL). An increased plasma level of oxidized LDL in obese people with insulin resistance has been demonstrated. The lipophilic antioxidant coenzyme Q10 (CoQ10) is known as an effective inhibitor of oxidative damage in LDL as well. The aim of the present study was to compare the CoQ10 levels in obese and normal weight children. METHODS: The CoQ10 plasma concentrations were measured in 67 obese children (BMI>97th percentile) and related to their degree of insulin resistance. Homeostasis model assessment (HOMA) was used to detect the degree of insulin resistance. The results were compared to a control group of 50 normal weight and apparently healthy children. The results of the CoQ10 levels were related to the plasma cholesterol concentrations. RESULTS: After adjustment to plasma cholesterol, no significant difference in the CoQ10 levels between obese and normal weight children could be demonstrated. Furthermore, there was no difference between insulin-resistant and non-insulin-resistant obese children. CONCLUSION: CoQ10 plasma levels are not reduced in obese children and are not related to insulin resistance.     

The clinical and hemodynamic effects of coenzyme Q10 in congestive cardiomyopathy.

Despite major advances in treatment congestive heart failure (CHF) is still one of the major causes of morbidity and mortality. Coenzyme Q(10) is a naturally occurring substance that has antioxidant and membrane stabilizing properties. Administration of coenzyme Q(10) in conjunction with standard medical therapy has been reported to augment myocardial kinetics, increase cardiac output, elevate the ischemic threshold, and enhance functional capacity in patients with congestive heart failure. The aim of this study was to investigate some of these claims. Seventeen patients (mean New York Heart Association functional class 3.0 +/- 0.4) were enrolled in an open-label study. After 4 months of coenzyme Q ( 10 ) therapy, functional class improved 20% (3.0 +/- 0.4 to 2.4 +/- 0.6, p < 0.001) and there was a 27% improvement in mean CHF score (2.8 +/- 0.4 to 2.2 +/- 0.4, p < 0.001). Percent change in the resting variables included the following: left ventricular ejection fraction (LVEF), +34.8%; cardiac output, +15.7%; stroke volume index, +18.9%; end-diastolic volume area, -8.4%; systolic blood pressure (SBP), -4. 4%; and E (max), (SBP / end-systolic volume index [ESVI]) +11.7%. MVo ( 2 ) decreased by 5.3% (31.9 +/- 2.6 to 30.2 +/- 2.4, p = NS). Therapy with coenzyme Q(10) was associated with a mean 25.4% increase in exercise duration and a 14.3% increase in workload. Percent changes after therapy include the following: exercise LVEF, +24.6%; cardiac output, +19.1%; stroke volume index, +13.2%; heart rate, +6.5%; SBP, -4.3%; SBP / ESVI, +18.6%; end-diastolic volume (EDV) area, -6.0%; MVo (2), -7.0%; and ventricular compliance (%Delta SV / EDV) improved >100%. In summary, coenzyme Q(10) therapy is associated with significant functional, clinical, and hemodynamic improvements within the context of an extremely favorable benefit-to-risk ratio. Coenzyme Q(10) enhances cardiac output by exerting a positive inotropic effect upon the myocardium as well as mild vasodilatation.     

辅酶Q10对多巴胺损伤的PC12细胞凋亡的影响

目的:观察辅酶Q10在以PC12细胞建立的多巴胺神经元凋亡细胞模型中的作用。方法:实验于2003-04/2004-04在锦州医学院科技试验中心进行。取体外培养的PC12细胞分为3组:①辅酶Q10组:加450μmol/L辅酶Q10和0.3mmol/L多巴胺。②多巴胺组:加0.3mmol/L多巴胺。③空白对照组:只加等量RPMI1640。24h后进行流式细胞仪测试DNA含量,检测细胞凋亡率。结果:多巴胺组细胞凋亡率明显高于空白对照组[(30.66±1.90)%,(0.82±0.07)%,P<0.01],辅酶Q10组细胞凋亡率[(16.05±2.16)%]明显低于多巴胺组(P<0.01)。结论:辅酶Q10能显著降低多巴胺引起的PC12细胞凋亡,提示辅酶Q10作为神经保护性药物对保护多巴胺能神经元,防治帕金森病可能有实际应用价值。