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A pilot clinical trial of the effects of coenzyme Q10 on chronic tinnitus aurium
Abstract
To determine the short-term effects of coenzyme Q10 (CoQ10) on the antioxidative status and tinnitus expression in patients with chronic tinnitus aurium.
A 16-week prospective nonrandomized clinical trial (n = 20). Tinnitus and Short Form-36 Questionnaires (TQ/SF-36) were evaluated together with the plasma concentrations of CoQ10, malondialdehyde, and the total antioxidant status.
The mean plasma CoQ10 concentration rose under external CoQ10 supply and remained elevated after medication stopped without overall effects on the tinnitus score. However, in a subgroup of 7 patients with low initial plasma CoQ10 concentration and significant increase in the plasma CoQ10 level, a clear decrease in the TQ score was observed.
In patients with a low plasma CoQ10 concentration, CoQ10 supply may decrease the tinnitus expression.
This is the first study to examine the effect of CoQ10 in chronic tinnitus aurium.
... In several studies mentioned above, short-term melatonin usage up to 3 months looked like safe for the majority of adults (1,2,4,(33)(34)(35)(36)(37)(38)(39)(40). But, it may cause nausea, headache, daytime sleepiness, short term feelings of depression, stomach cramps, dizziness, irritability and low body temperature [38]. ...
... To determine the effects of CoQ10 on the antioxidative status and tinnitus expression, Khan et al. [40] reported a prospective, nonrandomized clinical trial in which 20 patients were evaluated for plasma concentrations of CoQ10, malendialdehyde and antioxidant status with Tinnitus and Short Form-36 Questionnares (TQ/SF-36). They found that CoQ10 might decrease the tinnitus expression in patients with a low levels of plasma CoQ10 concentrations [40]. ...
... To determine the effects of CoQ10 on the antioxidative status and tinnitus expression, Khan et al. [40] reported a prospective, nonrandomized clinical trial in which 20 patients were evaluated for plasma concentrations of CoQ10, malendialdehyde and antioxidant status with Tinnitus and Short Form-36 Questionnares (TQ/SF-36). They found that CoQ10 might decrease the tinnitus expression in patients with a low levels of plasma CoQ10 concentrations [40]. ...
Oxidative stress and reactive oxygen species (ROS) have been working in the pathophysiology of various chronic diseases. Under normal circumstances, the human cochlea has some antioxidant molecules which can scavenge the oxidant substances and ROS to avoid the possible damage into the inner ear. In tinnitus therapy, several forms of complementary and alternative medicine (CAM) are increasingly popular but they are generally selected with or without professional guidance. Although several antioxidant agents like vitamin A, C, E and glutathione can be used in the treatment of tinnitus as CAM, melatonin, N-acetyl cysteine (NAC) and coenzyme Q10 (CoQ10) were especially used as alternative for classic antioxidants. According to the literature, it seems antioxidant therapy in patients with idiopathic tinnitus may reduce oxidative stress and damage to the inner ear. And also it can reduce the intensity and discomfort of tinnitus. Further clinical studies are necessary to determine antioxidants' protective role and to choose the appropriate therapeutic protocol.
... Treatment with CoQ10 was especially beneficial for tinnitus patients with a low plasma CoQ 10 concentration. 1 We hypothesized that tinnitus reduction seen in patients treated with CoQ 10 could be due to a direct effect of CoQ 10 on the auditory peripheral system. Therefore, we designed in vitro experiments that address the influence of CoQ 10 on hair cell survival. ...
... CoQ 10 was shown in vivo to prevent hearing loss in guinea pig 4 and had a partially curative effect in tinnitus patients. 1 The question remains as to the mechanism of protection or cure induced by this naturally occurring anti-oxidant. Our in vitro experiments presented here excluded the hypothetical possibility that CoQ 10 has a direct protective effect on the auditory sensory epithelium during ischemia. ...
To evaluate in vitro the effect of coenzyme Q10 (CoQ(10)) on ischemia-induced hair cell death.
Organotypic cochlear cultures of newborn rats were subjected to ischemia with and without CoQ(10).
Addition of CoQ(10) has not prevented HC loss.
CoQ(10) seems to protect against only certain modes of cell death.
... In addition, ROS can cause endothelial dysfunction, which is more obvious in the terminal microcirculation. Thus, the established hypothesis is that ROS might cause damage to the stria vascularis and the capillary networks of the planum semilunatum [144][145][146][147]. Khan et al. reported that the application of coenzyme Q10 (CoQ10) alone only reduced Tinnitus Questionnaire scores in those who lacked CoQ10 [148]. However, in another CoQ10 study, patients undergoing cisplatin chemotherapy retained stable concentrations of ROS and fewer instances of hearing impairment and tinnitus, but because the efficacy was from a mixture of several different compounds, it is difficult to discriminate the efficacy of CoQ10 alone [149]. ...
Tinnitus, which is the perception of sound in the absence of a corresponding external acoustic stimulus, including change of hearing and neural plasticity, has become an increasingly important ailment affecting the daily life of a considerable proportion of the population and causing significant burdens for both the affected individuals and society as a whole. Here, we briefly review the epidemiology and classification of tinnitus, and the currently available treatments are discussed in terms of the available evidence for their mechanisms and efficacy. The conclusion drawn from the available evidence is that there is no specific medication for tinnitus treatment at present, and tinnitus management might provide better solutions. Therapeutic interventions for tinnitus should be based on a comprehensive understanding of the etiology and features of individual cases of tinnitus, and more high quality and large-scale research studies are urgently needed to develop more efficacious medications.
... Since the negative effect of various drugs on mitochondria likely results in a damage of hearing, it is plausible that the mitochondria-supporting substances (such as coenzyme Q10, vitamin B12 with folic acid, sirtuin and many others) given as auxiliary therapy could protect the sense of hearing in patients with hepatitis, HIV, transplant patients or painkiller or PDE5 inhibitor users. In fact, targeting mitochondria is becoming increasingly popular [82], and there were some successful attempts in treatment of hearing conditions using mitochondrial supplements [83][84][85][86][87][88][89]. ...
Drug-induced ototoxicity has been known for centuries. Already in the seventeenth century, hearing loss was described to be a side effect of quinine. The post-World War II pharmaceutical industry boomed with the production of aminoglycoside antibiotics followed by diuretics and cytostatic drugs. Widespread and long-term usage of these medications brought the knowledge about their unwanted ototoxic effects. In the last decades, several new drugs appeared on the shelves of pharmacies and the hearing loss or tinnitus have been among the side effects of many of them. However, the awareness of community about new ototoxic medications is still not sufficient. New ototoxic drugs may belong to the class of phosphodiesterase-5 (PDE5) inhibitors, used to improve microcirculation and to treat erectile dysfunction. Moreover, interferons used for the therapy of hepatitis B and C, common painkiller paracetamol and hydrocodone, synthetic opioid methadone and the inhibitors of reverse transcriptase were demonstrated to induce adverse effects on hearing. Lastly, hearing loss linked to immunosuppres-sive drugs was documented in patients undergoing organ transplantation. Making the patients aware of adverse drug reactions and offering them audiological monitoring and intervention should be considered by respective therapists.
... No efficacy studies on dietary supplements, antioxidants, and drug combinations of appropriate methodological quality have been published. Relevant studies are either non-controlled, non-randomised, or inadequately designed [33, 65,95,119,132,146,159,168], have no tinnitusrelated criteria as primary or secondary endpoints [90], are not intervention studies [125], suffer from inadequate reporting (i.e., information on significance is missing, no information on study design) [126,127], or have no endpoint for describing tinnitus distress [189]. ...
The majority of tinnitus patients are affected by chronic idiopathic tinnitus, and almost 60 different treatment modalities have been reported. The present study is a multidisciplinary systematic analysis of the evidence for the different forms of treatment for chronic tinnitus. The results are used to form the basis of an S3 guideline. A systematic search was carried out in PubMed and the Cochrane Library. The basis for presenting the level of evidence was the evidence classification of the Oxford Centre of Evidence-based Medicine. Whenever available, randomised controlled trials were given preference for discussing therapeutic issues. All systematic reviews and meta-analyses were assessed for their methodological quality, and effect size was taken into account. As the need for patient counselling is self-evident, specific tinnitus counselling should be performed. Due to the high level of evidence, validated tinnitus-specific, cognitive behavioural therapy is strongly recommended. In addition, auditory therapeutic measures can be recommended for the treatment of concomitant hearing loss and comorbidities; those should also be treated with drugs whenever appropriate. In particular, depression should be treated, with pharmacological support if necessary. If needed, psychiatric treatment should also be given on a case-by-case basis. With simultaneous deafness or hearing loss bordering on deafness, a CI can also be indicated. For auditory therapeutic measures, transcranial magnetic or direct current stimulation and specific forms of acoustic stimulation (noiser/masker, retraining therapy, music, and coordinated reset) for the treatment of chronic tinnitus the currently available evidence is not yet sufficient for supporting their recommendation.
... Coenzyme Q10 has been widely used for the treatment of mitochondrial and other neurodegenerative disorders. Potential treatment indications for the use of CoQ10 include migraine, [9,10] chronic tinnitus aurium, [11] hypertension, [12] heart failure and atherosclerosis [13] ; however, the role of CoQ10 in such conditions is still an open question. Despite the questions related to its therapeutic use, we cannot ignore the evidence that most patients with these deficiencies have shown clinical improvement with oral CoQ10 supplementation and, if deficiency is present, it appears that early administration of 10 mg/kg per day is highly beneficial, especially in infants. ...
Objectives:
Conduct a preliminary comparison of the bioavailability between two formulations: commercial grade coenzyme Q10 (CoQ10) powder (solid formulation) and a new oil-in-water liquid emulsion and their effect on other antioxidants.
Methods:
Six healthy individuals participated in a randomized, crossover, open, consecutive design, with a 2-week washout period. Pharmacokinetic parameters were assessed after a single and multiple intakes of 250 mg CoQ10 given daily for 1 week.
Key findings:
The differences in the pharmacokinetic parameters of maximum plasma concentration, area under the curve between 0-360 and 0-4 h, elimination half-life were statistically significant with a relative bioavailability of 489% increase over solid CoQ10 formulation. A multiple dose supplementation increased plasma CoQ10 levels in both formulations, liquid emulsion performing better (2.4- vs 3.9-fold for solid and liquid formulation, respectively) without modifications on other antioxidants. Furthermore, the plasma CoQ10 at 7th day was statistically different between formulations (P < 0.05).
Conclusions:
The results obtained showed that liquid emulsion improves the bioavailability of CoQ10 respect to solid form which not only facilitates the individualized administration for the child but in turn could increase the therapeutic efficacy, which should be confirmed by further studies.
... Coenzyme Q10 has been widely used for the treatment of mitochondrial and other neurodegenerative disorders. Potential treatment indications for the use of CoQ10 include migraine, [9,10] chronic tinnitus aurium, [11] hypertension, [12] heart failure and atherosclerosis [13] ; however, the role of CoQ10 in such conditions is still an open question. Despite the questions related to its therapeutic use, we cannot ignore the evidence that most patients with these deficiencies have shown clinical improvement with oral CoQ10 supplementation and, if deficiency is present, it appears that early administration of 10 mg/kg per day is highly beneficial, especially in infants. ...
Molecularly imprinted polymer nanoparticles (MIPNPs) with the ability to recognize coenzyme Q10 (CoQ10) were synthesised in order to be employed as sorbent in a dispersive micro-solid phase extraction (DMSPE) for the determination of CoQ10 in a liver extract. CoQ10 is a redox-active, lipophilic substance integrated in the mitochondrial respiratory chain which acts as an electron carrier, shuttling electrons from complex I (NADH-ubiquinone oxidoreductase) and II (succinate-ubiquinone oxidoreductase) to complex III (ubiquinol-cytochrome c reductase), for the production of cellular energy. The MIPNPs were synthesised by precipitation polymerization using coenzyme Q0 as the dummy template, methacrylic acid as the functional monomer, an acetonitrile: water mixture as the porogen, ethylene glycol dimethacrylate as the crosslinker and potassium persulfate as initiator. The nanoparticles were characterized by microscopy, capillary electrophoresis, dynamic light scattering, N2 adsorption–desorption isotherms, and infrared spectroscopy. The MIPNPs demonstrated the presence of selective cavities complementary to the quinone nucleus of CoQ10, leading to a specific recognition of CoQ10 compared with related compounds. In the liver extract the relative CoQ10 peak area (CoQ10 area/total peak area) increased from 4.6% to 25.4% after the DMSPE procedure. The recovery percentage of CoQ10 from the liver matrix was between 70.5% and 83.7% quantified against CoQ10 standard processed under the same conditions. The DMSPE procedure allows the elution of almost all the CoQ10 retained (99.4%) in a small volume (200 μL), allowing the sample to be concentrated 2.5 times (LOD: 1.1 μg g−1 and LOQ: 3.7 μg g−1 of tissue). The resulted clean up of the sample, the improvement in peak shape and baseline and the reduction of interferences, evidence that the MIPNPs could potentially be applied as sorbent in a DMSPE with satisfactory results and with a minimum amount of sorbent (1 mg).
... Im Tiermodell konnten mitochondriale Schäden und Hörverluste durch die orale und peritoneale Verabreichung des Coenzyms Q10 unmittelbar nach der Lärmbelastung wirksam verhindert werden [8,9]. Auch der klinische Befund von Tinnituspatienten, die an einem Coenzym Q10-Mangel litten, verbesserte sich deutlich nach der Gabe von Nanoquinon [10]. ...
Tinnitus tritt bei der Mehrzahl der Betroffenen mit Hörverlust kombiniert auf. Verschiedene Untersuchungen legen nahe, dass bei der Entstehung beider Störungen ein mitochondrialer Funktionsverlust im Innenohr oder im zentralen auditorischen Kortex eine Rolle spielt. Für die reduzierte Mitochondrienfunktion können u. a. ototoxische Substanzen und Nährstoffmangel verantwortlich sein.
... CoQ10 has been widely used for the treatment of mitochondrial disorders (MD) and other neurodegenerative disorders, as well as its analogue idebenone, which shares an identical modified parahydroxybenzoate ring with CoQ10, but has a short 10-carbon tail. Other potential treatment indications for the use of CoQ10 include migraine [3,4], chronic tinnitus [5], hypertension [6], heart failure and atherosclerosis [7]; however, the role of CoQ10 in such conditions is still an open question. CoQ10, which may ameliorate endothelial function, may be an independent predictor of mortality in chronic heart failure, and there is a rationale for controlled intervention studies with CoQ10 in such condition [8]. ...
Coenzyme Q10 (CoQ10, or ubiquinone) is a small electron carrier of the mitochondrial respiratory chain with antioxidant properties. CoQ10 supplementation has been widely used for mitochondrial disorders. The rationale for using CoQ10 is very powerful when this compound is primary decreased because of defective synthesis. Primary CoQ10 deficiency is a treatable condition, so heightened “clinical awareness” about this diagnosis is essential. CoQ10 and its analogue, idebenone, have also been widely used in the treatment of other neurodegenerative disorders. These compounds could potentially play a therapeutic role in Parkinson’s disease, Huntington’s disease, amyotrophic lateral sclerosis, Friedreich’s ataxia, and other conditions which have been linked to mitochondrial dysfunction. This article reviews the physiological roles of CoQ10, as well as the rationale and the role in clinical practice of CoQ10 supplementation in different neurological diseases, from primary CoQ10 deficiency to neurodegenerative disorders.
... CoQ10 has been widely used for the treatment of mitochondrial disorders (MD) and other neurodegenerative disorders, as well as its synthetic analogue, idebenone [3]. Potential treatment indications for the use of CoQ10 include migraine [4,5], chronic tinnitus aurium [6], hypertension [7], heart failure and atherosclerosis [8], although the role of CoQ10 in such conditions is still an open question. CoQ10, which may ameliorate endothelial dysfunction [9], is an independent predictor of mortality in chronic heart failure, and there is a rationale for controlled intervention studies with CoQ10 in such condition [9,10]. ...
Coenzyme Q10 (CoQ10, or ubiquinone) is an electron carrier of the mitochondrial respiratory chain (electron transport chain) with antioxidant properties. In view of the involvement of CoQ10 in oxidative phosphorylation and cellular antioxidant protection a deficiency in this quinone would be expected to contribute to disease pathophysiology by causing a failure in energy metabolism and antioxidant status. Indeed, a deficit in CoQ10 status has been determined in a number of neuromuscular and neurodegenerative disorders. Primary disorders of CoQ10 biosynthesis are potentially treatable conditions and therefore a high degree of clinical awareness about this condition is essential. A secondary loss of CoQ10 status following HMG-Coa reductase inhibitor (statins) treatment has be implicated in the pathophysiology of the myotoxicity associated with this pharmacotherapy. CoQ10 and its analogue, idebenone, have been widely used in the treatment of neurodegenerative and neuromuscular disorders. These compounds could potentially play a role in the treatment of mitochondrial disorders, Parkinson's disease, Huntington's disease, amyotrophic lateral sclerosis, Friedreich's ataxia, and other conditions which have been linked to mitochondrial dysfunction. This article reviews the physiological roles of CoQ10, as well as the rationale and the role in clinical practice of CoQ10 supplementation in different neurological and muscular diseases, from primary CoQ10 deficiency to neurodegenerative disorders. We also briefly report a case of the myopathic form of CoQ10 deficiency.
... There is some evidence that severe psychological stress may cause oxidative damage in vivo (Liu et al.,1996;Sivonova et al., 2004). Indeed some author did explore the possibility that the severe emotional distress often perceived by tinnitus sufferers could lead to an increased production of reactive species, but their results are still uncertain at best (Neri et al., 2006;Khan et al., 2007). It could be tentatively concluded that although antioxidants may not be a therapy for tinnitus per se, their use may be considered as a supplemental treatment for patients undergoing therapy with ototoxic drugs; nevertheless clinical studies are needed to better assess antioxidants protective role. ...
The use of complementary and alternative medicine (CAM) is very popular in western countries and several CAM products are often used by individuals with tinnitus with or without medical guidance. CAM pharmacological approach to tinnitus today is mainly based on vitamins and minerals (dietary supplements), antioxidants, and herbal medications. Despite the popularity of CAM products, the evidence regarding their efficacy against tinnitus is in general scarce and their potential toxic effects are often underestimated or even neglected. In this paper the available literature on the efficacy of dietary supplements, antioxidants, and herbal medications against tinnitus is reviewed, and some of the major potential toxic effects are discussed. It is concluded that the use of CAM products in tinnitus therapy in general lack substantial scientific support, and that these substances are probably not clinically effective either. However, it is difficult to draw clear-cut conclusions regarding CAM pharmacological approach to tinnitus. In fact, the subjective nature of tinnitus and the reported variability in patient's response to therapy indicate that several non-pharmacological factors may be influencing drug effects, with the placebo effect playing a major role. Nevertheless, in view of the potential harm that may occur from inappropriate use of CAM products, physicians need to be aware of their principal characteristics with particular emphasis on toxicity and possibilities of interaction with prescription drugs.
ABSTRACT
Introduction: Dopamine is crucial in executive functions and motor system control. Its depletion appears to be
the patho-physiological hallmark of several neurodegenerative diseases including but not limited to Parkinson’s,
schizophrenia, addiction and attention deficit disorders. This study examined the effects of Co-enzyme Q10
(CQ10) and omega-3 fatty acid co-supplementation in haloperidol induced dopamine depletion in mice. Materials
and Method: Adult male mice weighing 30-35g each were grouped into six (A-F) of 10animals each. Group A
control, fed standard diet, Group B, ip haloperidol (HAL) while groups C, oral Levodopa Cabidopa (LD), D and
E, CQ1O diet (120 mg/kg of feed) and omega-3 fatty acid (500 mg/kg of feed) diet respectively, following ip
haloperidol. Group F co-administered CQ10 and omega-3 fatty acid diet with ip haloperidol. All administrations
were daily and lasted 28 days. Behaviours of mice in the open field apparatus, radial arm maze and anxiety related
elevated plus maze were assessed, following which animals were sacrificed. Prefrontal cortex sections were
homogenized for malondialdehyde (MDA), Interleukin -10 (IL-10), caspase-3 and dopamine and also processed
for histological and immunohistochemical studies. Results: Result showed a significant [F (9, 90) = 21.9, p <
0.001] decrease in locomotor activity with HAL, HAL&LD and a significant increase with HAL&CQ10&Ώ-3F
compared to control. An increase in radial arm maze spatial working memory with HAL&CQ10, HAL&Ώ-3 and a
decrease with HAL and HAL&LD compared to control. Compared to HAL&LD, there was an increase in open
arm with HAL&CQ10, HAL&Ώ-3F and HAL&CQ10&Ώ-3F and a decrease in closed arm with HAL&Ώ-3F and
HAL&CQ10&Ώ-3F. Lipid peroxidation measured as MDA concentration [F (9, 90) = 22.10, p < 0.001] increased
significantly with HAL, HAL&LD, and decreased with HAL&CQ10, HAL&Ώ-3F, HAL&CQ10&Ώ-3F compared
to control. Compared to HAL&LD, there was an increase in the IL-10levels with HAL&CQ10, HAL&Ώ-3F and
HAL&CQ10&Ώ-3F respectively. Compared to HAL, dopamine increases significantly with HAL&LD,
HAL&CQ10, HAL&Ώ-3F and HAL&CQ10&Ώ-3F. Compared to HAL&LD, there was a decrease in the Caspase-
3activity with HAL&CQ10and HAL&CQ10&Ώ-3F respectively. Normal pyramidal cells with normal cytoplasmic
distribution of nissl bodies were seen in HAL&CQ10&Ώ-3F, while groups HAL and HAL&LD showed
comparatively reduced staining intensities with poor distribution of nissl bodies within their cytoplasm.
Bielschowsky silver staining revealed neuritic plaques and argyrophilic structures in the HAL treated group. These
fibrillary amyloid deposits were absent in the supplemented groups. Neuron Specific Enolase immunoreactivity is
present HAL and HAL&LD while absent in HAL&CQ10and HAL&CQ10&Ώ-3F. Nil astrocytic reaction to
dopamine depletion also seen in the prefrontal cortex of HAL&Ώ-3F, HAL&CQ10 and HAL&CQ10&Ώ-3F.
Conclusion: The study concluded that CQ10 and omega3 fatty acid co-supplementation ameliorates
neuroinflammation, lipid peroxidation, neutritic plaque and apoptosis in haloperidol induced dopamine depletion
in mice.
KEYWORDS: Dopamine depletion; Neuroinflammation; CoQ10; Omega3 fatty- acid.
Migraine headaches frequently coexist with vestibular symptoms such as vertigo, motion sickness, and gait instability. Migraine-related vasospasm can also damage the inner ear, which results in symptoms such as sudden sensorineural hearing loss and resultant tinnitus. The pathophysiology of these symptoms is not yet fully understood, and despite their prevalence, there is no universally approved management. This review summarizes the data on complementary and integrative medicine in treating patients with migrainous ear disorders.
"Because Western medicine has remained largely unsuccessful at treating tinnitus symptoms, many physicians as well as patients have turned to alternative treatment options to decrease patients' suffering and improve their quality of life. Although research in complementary/integrative medicine continues to be scarce and inconclusive, studies are pointing toward the positive effects of acupuncture, herbal remedies, dietary supplements, antioxidants, melatonin, and hypnosis on tinnitus. Although the efficacies of these treatments are inconsistent and may depend on a patient's unique circumstances, studies acknowledge that each treatment is worth trying in light of the potential benefits while being both noninvasive and well tolerated."
Tinnitus is a frequent symptom, which, particularly in combination with comorbidities, can result in a severe disease-related burden. Chronic idiopathic tinnitus (CIT) is the most frequent type of tinnitus. A considerable number of treatment strategies are used to treat CIT-for many of which there is no evidence of efficacy. In order to enable scientific evidence-based treatment of CIT, German interdisciplinary S3 guidelines have recently been constructed for the first time. Here we present a short form of these S3 guidelines.
The guidelines were constructed based on a meta-analysis of the treatment of chronic tinnitus performed by the authors. Additionally, a systematic literature search was performed in the PubMed and Cochrane Library databases. Furthermore, a systematic search for international guidelines was performed in Google, as well as in the Guidelines International Network and National Guideline Clearinghouse (USA) database. Evidence was classified according to the Oxford Centre for Evidence-Based Medicine system.
According to the guidelines, alongside counselling, manualized structured tinnitus-specific cognitive behavioral therapy (tCBT) with a validated treatment manual is available as evidence-based therapy. In addition, the guidelines recommend concurrent treatment of comorbidities, including drug-based treatment, where appropriate. Particularly important is treatment of anxiety and depression. Where a psychic or psychiatric comorbidity is suspected, further diagnosis and treatment should be performed by an appropriately qualified specialist (psychiatrist, neurologist, psychosomatic medicine consultant) or psychological psychotherapist. In cases accompanied by deafness or hearing loss bordering on deafness, cochlear implants may be indicated.
No recommendations can be made for drug-based treatment of CIT, audiotherapy, transcranial magnetic or electrical stimulation, specific forms of acoustic stimulation or music therapy; or such recommendations must remain open due to the lack of available evidence. Polypragmatic tinnitus treatment with therapeutic strategies for which there is no evidence of efficacy from controlled studies is to be refused.
Coenzyme Q10 (Q10) has a poor bioavailability due to its very low aqueous solubility and high molecular weight. The purpose of this review is to discuss the different types of Q10 drug delivery systems (DDS) ranging from the simple oily dispersions to the nanotechnology-oriented systems such as nanocrystals, self-nanoemulsified drug delivery systems, etc. to overcome the solubility issue. The basics of these approaches were discussed in relationship to the effect of Q10 absorption. For that purpose, the percentage of the drug absorbed to the blood stream out of the administered dose was calculated as the fraction absorbed (Fa%). The Fa% for the nanoemulsions discussed in this article did not correlate with droplet size. In human studies most of the delivery systems had a low Fa% being in the range from 1.53 to 12.48 %. The highest Fa% value was found to be for the self-emulsified drug delivery systems (SEDDS). In dogs studies, the Fa% values ranged between 0.28 (cyclodextrin complex) and 4.8 %. In rat studies, some other DDS like emulsions and solubilized formulations showed Fa% of around 0.22 %. The relationship between the average Fa% in rats, dogs and humans was found to be 1:15:20. One recent study applied both oral and intravenous delivery of Q10; the orally tested SEDDS formulation had an absolute bioavailability of 2.2 % corresponding to Fa% = 0.04 %. The studies with Q10 formulations based only on in vitro data were also discussed and assessed regarding the influence of formulation on solubility, release and/or uptake.
1.
Several different complementary therapies have been attempted, but few studies have been published regarding the efficacy of complementary treatments for tinnitus.
2.
Acupuncture seems to be mostly effective in acute and recent tinnitus as well as in somatic tinnitus. Other therapies that are in the area of musculoskeletal therapies, such as electrical stimulation applied to skin, the use of manipulations, or exercising, have been studied for somatic tinnitus.
3.
There are strong indications that a metabolic component is involved in a subgroup of individuals with tinnitus, but only few studies have been performed of this aspect of tinnitus.
4.
Training in mindfulness (including awareness), breathing techniques, meditation, and hypnosis are useful as complementary therapies for tinnitus that can reduce annoyance and fixation on the presence of tinnitus, improving sleep, anxiety, and the perceived quality of life.
5.
Methodologies and study design for studies of efficacy of treatment are critical for the interpretation of the results. Difficulty to reach significance is not only an issue for complementary therapies, but also for drug trials or other kinds of therapies.
Reactive oxygen species (ROS) not only play an important role in cell signaling and metabolic processes but are also thought to be implicated in the pathogenesis of a variety of inflammatory disorders. Indeed, novel therapies are being developed, specifically aimed at reducing oxidative stress at the tissue and cellular level . Oxidative stress arises within tissues when the normal balance between ROS generation and antioxidant defence shifts in favour of the former, a situation arising from either an excess of ROS and/or a depletion of antioxidants . Periodontitis is a term used to describe an inflammatory process, initiated by the plaque biofilm, that leads to loss of periodontal attachment to the root surface and adjacent alveolar bone and which ultimately results in tooth loss. Periodontal pathogens can induce ROS overproduction and thus may cause collagen and periodontal cell breakdown. When ROS are scavenged by antioxidants, there can be a reduction of collagen degradation. Coenzyme Q10 serves as an endogenous antioxidant which increases the concentration of CoQ10 in the diseased gingiva and effectively suppresses advanced periodontal inflammation. Antioxidants, such as CoQ10, can neutralize free radicals and may reduce or even help prevent some of the damage [3,4] they cause. Although CoQ10 can be synthesized in body, situation may arise in which the body's synthetic capacity is insufficient t o m e e t C o Q 1 0 r e q u i r e m e n t s . Susceptibility to CoQ10 deficiency appear to be greatest in cell that are metabolically active (such as heart, immune system, gingiva and gastric mucosa), since these cells presumably have the highest requirements for [3] CoQ10. Tissue deficiencies of CoQ10 have been occur in the wide range of medical and dental conditions, including cardiovascular diseases, periodontal diseases, gastric ulcer, cancer and acquired immunodeficiency syndrome (AIDS). A deficiency may result from: i) impaired synthesis due to nutritional deficiencies ii) genetic or acquired defect in synthesis or utilization iii) increased tissue needs resulting from illness iv) CoQ10 levels decline with advancing [5] age. Historical context C o e n z y m e Q -1 0 (C o Q -1 0 o r Ubiquinone) is a naturally occurring quinone that is found in most aerobic organisms from bacteria to mammals. It was first identified in 1940 and isolated from the mitochondria of beef heart in [6] 1957. In 1961 Peter Mitchel proposed the electron transport chain (which includes the vital proton-motive role of CoQ10). In 1972, Gian Paolo Littarru and Karl Folkers separately demonstrated a deficiency of CoQ10 in human heart disease. The antioxidant role of the molecule as a free radical scavenger was [1] widely studied by Lars Ernster. Common Names Coenzyme Q10 is also known as Coenzyme Q, CoQ, CoQ10, Ubiquinone, Ubiquinone-Q10, Ubidecarenone, and Vitamin Q10. Biochemistry Normal blood levels of CoQ10 are 0.7 -1 [7] mcg/ml4 . CoQ10 is another name for 2,3-dimethoxy-5-methylbenzoquinone to which a terpenoid side chain (consisting of ten monounsaturated trans-isoprenoid units) is attached. It is a fat soluble quinone, structurally similar [8] to vitamin K2. Quinones with six to 10 side chains (CoQ6 -CoQ10) are found in mammals. Human cells synthesize CoQ10 in an eight-step cascade starting Introduction Coenzyme Q10 (CoQ10) is a compound found naturally in the energy-producing center of the cell known as the mitochondria. Because of its ubiquitous presence in the nature and its quinone structure (similar to that of vitamin K),
This work evaluates trials on drug treatment of tinnitus. Tinnitus is a subjective complaint and there are no objective outcome measures. The rationale of treating tinnitus is based on two major therapeutic models: 1) cochlear origin of tinnitus in that tinnitus is alleviated by cochlear mechanisms reducing the cytotoxicity induced by the metabolic stress, influencing neural transmission and restoring the cochlear homeostasis. 2) central origin of tinnitus that involves similar mechanisms to neuropathic pain. In controlled studies there are no convincing results that any treatment will be beneficial for tinnitus. There are some exceptions with drugs that antagonize neurotransmission in glutaminergic receptors, and also possibly melatonin when sleep disorders are associated with tinnitus. The central neurotransmitter agonists and antagonists seem not to be effective. Finally, novel nano-technological advances in targeted drug carrier technology that can administer growth factors and gene machinery may be useful in future treatment of tinnitus.
As one of the most important neurochemicals in biological systems, ascorbate plays vital roles in many physiological and pathological processes. In order to understand the roles of ascorbate in the pathological process of tinnitus, this study demonstrates an in vivo method for real time monitoring of the changes of ascorbate level in the cochlear perilymph of guinea pigs during the acute period of tinnitus induced by local microinfusion of salicylate with carbon fiber microelectrodes (CFMEs) modified with multiwalled carbon nanotubes (MWNTs). To accomplish in vivo electrochemical monitoring of ascorbate in the microenvironment of the cochlear perilymph, the MWNT-modified CFME is used as working electrode, a microsized Ag/AgCl is used as reference electrode, and Pt wire is used as counter electrode. Three electrodes are combined together around a capillary to form integrated capillary-electrodes. The integrated capillary-electrode is carefully implanted into the cochlear perilymph of guinea pigs and used both for externally microinfusing of salicylate into the cochlear perilymph and for real time monitoring of the change of ascorbate levels. The in vivo voltammetric method based on the integrated capillary-electrodes possesses a high selectivity and a good linearity for ascorbate determination in the cochlear perilymph of guinea pigs. With such a method, the basal level of cochlear perilymph ascorbate is determined to be 45.0 ± 5.1 μM (n = 6). The microinfusion of 10 mM salicylate (1 μL/min, 5 min) into the cochlear decreases the ascorbate level to 28 ± 10% of the basal level (n = 6) with a statistical significance (P < 0.05), implying that the decrease in ascorbate level in the cochlear may be associated with salicylate-induced tinnitus. This study essentially offers a new method for in vivo monitoring of the cochlear perilymph ascorbate following the salicylate-induced tinnitus and can thus be useful for investigation on chemical essences involved in tinnitus.
Die Ätiologie des akuten Tinnitus ist wie die des Hörsturzes in der Mehrzahl der Fälle als idiopathisch anzusehen; wesentlich
seltener sind infektiöse oder vaskuläre Ursachen. In einer umfassenden Literaturrecherche werden Studien und Metaanalysen
zur Pharmakotherapie ausgewertet: Für den chronischen Tinnitus sind medikamentöse Therapien nicht indiziert, allenfalls werden
begleitende, etwa psychosomatische Komorbidiäten mit Psychopharmaka behandelt. Beim akuten Tinnitus wird analog der Hörsturzbehandlung
trotz schwacher Evidenz nach ausbleibender Spontanerholung eine Behandlung mit Glukokortikoiden und initial mit Volumenersatzmitteln
empfohlen. Als Reservetherapie eignet sich, jedenfalls bei starkem Hörverlust und akutem Tinnitus, eine intratympanale Steroidbehandlung.
The aetiology of acute hearing loss is mostly idiopathic like sudden sensorineural hearing loss and rarely infectious or vascular.
Several studies and meta-analyses of pharmacotherapy are reviewed: In chronic tinnitus there is no indication for pharmacotherapy;
sometimes a possible psychosomatic comorbidity has to be treated with psychopharmaceutical agents. Despite a low level of
evidence treatment with steroids and initially plasma expanding infusions is recommended for acute tinnitus if there is no
spontaneous remission. Intratympanic steroid therapy can be used as an alternative if there is severe hearing loss together
with tinnitus.
SchlüsselwörterTinnitus-Hörsturz-Hörminderung, sensorineurale-Pharmakotherapie-Intratympanale Steroidbehandlung
KeywordsTinnitus-Hearing loss, sudden-Hearing loss, sensorineural-Pharmacotherapy-Intratympanic steroidal therapy
Coenzyme Q10 (ubiquinone) is a mitochondrial coenzyme which is essential for the production of ATP. Being at the core of cellular energy processes it assumes importance in cells with high energy requirements like the cardiac cells which are extremely sensitive to CoQ10 deficiency produced by cardiac diseases. CoQ10 has thus a potential role for prevention and treatment of heart ailments by improving cellular bioenergetics. In addition it has an antioxidant, a free radical scavenging and a vasodilator effect which may be helpful in these conditions. It inhibits LDL oxidation and thus the progression of atherosclerosis. It decreases proinflammatory cytokines and decreases blood viscosity which is helpful in patients of heart failure and coronary artery disease. It also improves ischemia and reperfusion injury of coronary revascularisation. Significant improvement has been observed in clinical and hemodynamic parameters and in exercise tolerance in patients given adjunctive CoQ10 in doses from 60 to 200 mg daily in the various trials conducted in patients of heart failure, hypertension, ischemic heart disease and other cardiac illnesses. Recently it has been found to be an independent predictor of mortality in congestive heart failure. It has also been found to be helpful in vertigo and Meniere-like syndrome by improving the immune system. Further research is going on to establish firmly its role in the therapy of cardiovascular diseases.
Cisplatin causes both acute and chronic forms of tinnitus as well as increases in spontaneous neural activity (hyperactivity) in the dorsal cochlear nucleus (DCN) of hamsters. It has been hypothesized that the induction of hyperactivity in the DCN may be a consequence of cisplatin's effects on cochlear outer hair cells (OHCs); however, systematic studies testing this hypothesis have yet to appear in the literature. In the present investigation, the relationship between hyperactivity and OHC loss, induced by cisplatin, was examined in detail. Hamsters received five treatments of cisplatin at doses ranging from 1.5 to 3 mg · kg ⁻¹ · day ⁻¹ , every other day. Beginning 1 mo after initiation of treatment, electrophysiological recordings were carried out on the surface of the DCN to measure spontaneous multiunit activity along a set of coordinates spanning the medial-lateral (tonotopic) axis of the DCN. After recordings, cochleas were removed and studied histologically using a scanning electron microscope. The results revealed that cisplatin-treated animals with little or no loss of OHCs displayed levels of activity similar to those seen in saline-treated controls. In contrast, the majority (75%) of cisplatin-treated animals with severe OHC loss displayed well-developed hyperactivity in the DCN. The induced hyperactivity was seen mainly in the medial (high-frequency) half of the DCN of treated animals. This pattern was consistent with the observation that OHC loss was distributed mainly in the basal half of the cochlea. In several of the animals with severe OHC loss and hyperactivity, there was no significant damage to IHC stereocilia nor any observable irregularities of the reticular lamina that might have interfered with normal IHC function. Hyperactivity was also observed in the DCN of animals showing severe losses of OHCs accompanied by damage to IHCs, although the degree of hyperactivity in these animals was less than in animals with severe OHC loss but intact IHCs. These results support the view that loss of OHC function may be a trigger of tinnitus-related hyperactivity in the DCN and suggest that this hyperactivity may be somewhat offset by damage to IHCs.
A 36-item short-form (SF-36) was constructed to survey health status in the Medical Outcomes Study. The SF-36 was designed for use in clinical practice and research, health policy evaluations, and general population surveys. The SF-36 includes one multi-item scale that assesses eight health concepts: 1) limitations in physical activities because of health problems; 2) limitations in social activities because of physical or emotional problems; 3) limitations in usual role activities because of physical health problems; 4) bodily pain; 5) general mental health (psychological distress and well-being); 6) limitations in usual role activities because of emotional problems; 7) vitality (energy and fatigue); and 8) general health perceptions. The survey was constructed for self-administration by persons 14 years of age and older, and for administration by a trained interviewer in person or by telephone. The history of the development of the SF-36, the origin of specific items, and the logic underlying their selection are summarized. The content and features of the SF-36 are compared with the 20-item Medical Outcomes Study short-form.
A 36-item short-form (SF-36) was constructed to survey health status in the Medical Outcomes Study. The SF-36 was designed for use in clinical practice and research, health policy evaluations, and general population surveys. The SF-36 includes one multi-item scale that assesses eight health concepts: 1) limitations in physical activities because of health problems; 2) limitations in social activities because of physical or emotional problems; 3) limitations in usual role activities because of physical health problems; 4) bodily pain; 5) general mental health (psychological distress and well-being); 6) limitations in usual role activities because of emotional problems; 7) vitality (energy and fatigue); and 8) general health perceptions. The survey was constructed for self-administration by persons 14 years of age and older, and for administration by a trained interviewer in person or by telephone. The history of the development of the SF-36, the origin of specific items, and the logic underlying their selection are summarized. The content and features of the SF-36 are compared with the 20-item Medical Outcomes Study short-form.
Immobilization stress of male Sprague-Dawley rats induces oxidative damage to lipid, protein, and DNA in the brain. Significant increases in lipid peroxidation were found in the cerebral cortex, cerebellum, hippocampus, and midbrain compared to the unstressed controls. Significant increases in levels of protein oxidation were also found in the cortex, hypothalamus, striatum, and medulla oblongata. Oxidative nuclear DNA damage increased after stress in all brain regions, although only the cerebral cortex showed a significant increase. Depletion of glutathione showed some stimulation to oxidative damage in the unstressed control and stressed animals. Further studies of the mitochondrial and cytosol fractions of cerebral cortex demonstrated that mitochondria showed a significantly greater increase in lipid peroxidation and protein oxidation than cytosol. Data from plasma and liver showed oxidative damage similar to that of the brain. These findings provide evidence to support the idea that stress produces oxidants, and that the oxidative damage in stress could contribute to the degenerative diseases of aging, including brain dysfunction.
Coenzyme Q is well defined as a crucial component of the oxidative phosphorylation process in mitochondria which converts the energy in carbohydrates and fatty acids into ATP to drive cellular machinery and synthesis. New roles for coenzyme Q in other cellular functions are only becoming recognized. The new aspects have developed from the recognition that coenzyme Q can undergo oxidation/reduction reactions in other cell membranes such as lysosomes. Golgi or plasma membranes. In mitochondria and lysosomes, coenzyme Q undergoes reduction/oxidation cycles during which it transfers protons across the membrane to form a proton gradient. The presence of high concentrations of quinol in all membranes provides a basis for antioxidant action either by direct reaction with radicals or by regeneration of tocopherol and ascorbate. Evidence for a function in redox control of cell signaling and gene expression is developing from studies on coenzyme Q stimulation of cell growth, inhibition of apoptosis, control of thiol groups, formation of hydrogen peroxide and control of membrane channels. Deficiency of coenzyme Q has been described based on failure of biosynthesis caused by gene mutation, inhibition of biosynthesis by HMG coA reductase inhibitors (statins) or for unknown reasons in ageing and cancer. Correction of deficiency requires supplementation with higher levels of coenzyme Q than are available in the diet.
Cisplatin causes both acute and chronic forms of tinnitus as well as increases in spontaneous neural activity (hyperactivity) in the dorsal cochlear nucleus (DCN) of hamsters. It has been hypothesized that the induction of hyperactivity in the DCN may be a consequence of cisplatin's effects on cochlear outer hair cells (OHCs); however, systematic studies testing this hypothesis have yet to appear in the literature. In the present investigation, the relationship between hyperactivity and OHC loss, induced by cisplatin, was examined in detail. Hamsters received five treatments of cisplatin at doses ranging from 1.5 to 3 mg. kg(-1). day(-1), every other day. Beginning 1 mo after initiation of treatment, electrophysiological recordings were carried out on the surface of the DCN to measure spontaneous multiunit activity along a set of coordinates spanning the medial-lateral (tonotopic) axis of the DCN. After recordings, cochleas were removed and studied histologically using a scanning electron microscope. The results revealed that cisplatin-treated animals with little or no loss of OHCs displayed levels of activity similar to those seen in saline-treated controls. In contrast, the majority (75%) of cisplatin-treated animals with severe OHC loss displayed well-developed hyperactivity in the DCN. The induced hyperactivity was seen mainly in the medial (high-frequency) half of the DCN of treated animals. This pattern was consistent with the observation that OHC loss was distributed mainly in the basal half of the cochlea. In several of the animals with severe OHC loss and hyperactivity, there was no significant damage to IHC stereocilia nor any observable irregularities of the reticular lamina that might have interfered with normal IHC function. Hyperactivity was also observed in the DCN of animals showing severe losses of OHCs accompanied by damage to IHCs, although the degree of hyperactivity in these animals was less than in animals with severe OHC loss but intact IHCs. These results support the view that loss of OHC function may be a trigger of tinnitus-related hyperactivity in the DCN and suggest that this hyperactivity may be somewhat offset by damage to IHCs.
Mental stress in psychiatric disease and in daily life contributes to oxidative stress in the body. In this study we investigated a connection between possible psychological stress caused by university undergraduate examinations and oxidative stress experienced by our test subjects. Some parameters of oxidative stress (single strand breaks of DNA in lymphocytes, sensitivity to lipid oxidation and antioxidant status) were studied in medical students on the day of the examination (stress condition) and compared with the same parameters obtained from the same students during the term between two examination periods (non-stress condition). The results show that in the stress condition oxidative damage to DNA and sensitivity to lipid oxidation were significantly increased (p<0.05) when compared with the same parameters in "non-stress" conditions. A significant decrease in plasma antioxidant activity (p<0.05) in students that were under stress was observed. These results suggest that during university examinations students are under increased oxidative stress.
Background and purpose: Ischaemia/reperfusion generates free oxygen radicals, that react with the unsaturated lipids of biomembranes resulting in the generation of products such as malondialdehyde (MDA). MDA could be a sensor for tissue damage and reperfusion. Nitric oxide (NO), released due to the early arrival of leukocytes to the brain parenchyma, could be a sensor for non-flow phenomenon. Thereby, the purpose of this research was to evaluate the behavior of MDA and NO within the first 24 hours after the stroke onset.
Objectives
Cognitive-behavioural treatment of chronic tinnitus needs active cooperation and motivation in patients. The transtheoretical model (TTM) defines the behavioural change using six different stages of change (SoC). In this study, we examined SoC in patients with tinnitus via a new self-rating instrument.
Sample and methods
An item-pool, consisting of 48 questions, was administered to 125 tinnitus sufferers in a cross-sectional study. In addition to data on tinnitus history, the tinnitus strain (THI, German: TB-12), scores of anxiety and depression (HADS-D), and life quality (SF-12) were assessed.
Results
Four SoC could be identified empirically: (1) precontemplation, (2) contemplation/preparation, (3) action/maintenance, and (4) termination. Associations of the SoC with socio-demographic and tinnitus related data, as well as with the instruments applied, conformed with the theory.
Conclusions
The results confirm the transfer of SoC theory to patients with tinnitus.
Dimensions of psychological complaints due to chronic and disabling tinnitus were investigated by means of the Tinnitus Questionnaire (TQ), administered to a sample of 138 tinnitus sufferers who had been admitted to a psychosomatic hospital. Factor analysis revealed that tinnitus-related patterns of emotional and cognitive distress, intrusiveness, auditory perceptual difficulties, sleep disturbances, and somatic complaints can be differentiated. Cognitive distortions and inappropriate attitudes towards the tinnitus and it's personal consequences were found to be highly intercorrelated forming a subgroup within a broader and more general distress factor. The stability of the factor solution obtained was examined by systematically varying the number of factors to be extracted. Based on the results of this method, scales are proposed for the questionnaire which can be used in clinical and scientific work to specifically assess major areas of tinnitus-related distress and their degree of severity. Implications for a further evaluation of the instrument are discussed.
Tinnitus often entails severe psychological distress. Reversely, tinnitus may be considered as a chronic stressor. Based on this hypothesis, we investigated whether improving stress-managing capabilities would influence psychological and stress-related immunological parameters in chronic tinnitus sufferers.
Tinnitus (TPs, n=26) and non-tinnitus participants (NTPs, n=13) took part in a standardised 10-week relaxation program. An additional group of tinnitus sufferers (n=18), randomly assigned to a waiting list, served as control (TC) subjects. Mood, perceived stress, global quality of life, and tinnitus disturbance were assessed before and after the intervention. The stress-sensitive immunological parameters TNF-alpha, IL-6, and IL-10 were measured before, during, and at the end of the intervention.
The program resulted in a significantly decreased perception of stress, anxious depression, anger, and tinnitus disturbance, paralleled by a reduction of TNF-alpha. No alterations were noted for IL-6 or IL-10. For the NTPs and TCs, no relevant psychological or immune changes could be observed.
The data suggest that (1) the training offered improved stress-managing capabilities in chronic tinnitus sufferers, and (2) TNF-alpha may be conceived as a stress marker.
Coenzyme Q (CoQ(10)) is a component of the mitochondrial electron transport chain and also a constituent of various cellular membranes. It acts as an important in vivo antioxidant, but is also a primary source of O(2)(-*)/H(2)O(2) generation in cells. CoQ has been widely advocated to be a beneficial dietary adjuvant. However, it remains controversial whether oral administration of CoQ can significantly enhance its tissue levels and/or can modulate the level of oxidative stress in vivo. The objective of this study was to determine the effect of dietary CoQ supplementation on its content in various tissues and their mitochondria, and the resultant effect on the in vivo level of oxidative stress. Rats were administered CoQ(10) (150 mg/kg/d) in their diets for 4 and 13 weeks; thereafter, the amounts of CoQ(10) and CoQ(9) were determined by HPLC in the plasma, homogenates of the liver, kidney, heart, skeletal muscle, brain, and mitochondria of these tissues. Administration of CoQ(10) increased plasma and mitochondria levels of CoQ(10) as well as its predominant homologue CoQ(9). Generally, the magnitude of the increases was greater after 13 weeks than 4 weeks. The level of antioxidative defense enzymes in liver and skeletal muscle homogenates and the rate of hydrogen peroxide generation in heart, brain, and skeletal muscle mitochondria were not affected by CoQ supplementation. However, a reductive shift in plasma aminothiol status and a decrease in skeletal muscle mitochondrial protein carbonyls were apparent after 13 weeks of supplementation. Thus, CoQ supplementation resulted in an elevation of CoQ homologues in tissues and their mitochondria, a selective decrease in protein oxidative damage, and an increase in antioxidative potential in the rat.
Features of Parkinson's disease (PD) include oxidative stress, nigral mitochondrial complex I deficiency and visual dysfunction, all of which are also associated with coenzyme Q(10) (CoQ(10)) deficiency. The objective of this monocenter, parallel group, placebo controlled, double-blind trial was to determine the symptomatic response of daily oral application of 360 mg CoQ(10) lasting 4 weeks on scored PD symptoms and visual function, measured with the Farnsworth-Munsell 100 Hue test (FMT), in 28 treated and stable PD patients. CoQ(10) supplementation provided a significant (P=0.01) mild symptomatic benefit on PD symptoms and a significantly (F((1,24))=8.48, P=0.008) better improvement of FMT performance compared with placebo. Our results indicate a moderate beneficial effect of oral CoQ(10) supplementation in PD patients.
Assuming that superoxide anion radicals (O(2)-) may play a role in damage to the inner ear, the authors investigated the possible benefit of vitamin E as an antioxidant in the treatment of idiopathic sudden hearing loss.
Prospective, double-blind study.
The Department of Otolaryngology of Rambam Medical Center serves as a tertiary referral center for a population of 1.2 million people.
A total of 66 patients, aged 15 to 70 years, with diagnoses of idiopathic sudden hearing loss of less than 7 days' duration during 1998 to 2001, were included in the study. All were treated with bed rest, steroids, magnesium, and carbogen inhalation. The study group received vitamin E in addition.
The recovery rate, calculated as hearing gain divided by the difference in hearing level between the affected and unaffected ear, was better than 75% in 41 of 66 (62.12%) patients. This rate was achieved in 26 (78.78%) patients in the study group treated with vitamin E, compared with 15 (45.45%) patients in the control group.
Patients treated with the addition of vitamin E achieved better recovery than did the control patients. Further studies should be directed toward a better understanding of the role of antioxidants in idiopathic sudden hearing loss.
Ischemia/reperfusion generates free oxygen radicals, which react with the unsaturated lipids of biomembranes resulting in the generation products such as malondialdehyde. Malondialdehyde could be a sensor for tissue damage and reperfusion. Nitric oxide, released due to the early arrival of leukocytes in the brain parenchyma, could be a sensor for nonflow phenomenon. Thereby, the purpose of this research was to evaluate the behavior of malondialdehyde and nitric oxide within the 24 hours after the stroke onset.
Fifteen patients up to an age of 49 years, admitted to the emergency of University Hospital and Chiquinquirá Hospital in Maracaibo, Venezuela, were examined by a neurologist and underwent 12-lead electrocardiograms and computed tomography for the diagnosis of thrombotic stroke. Serum malondialdehyde and nitric oxide were measured as thiobarbituric acid adducts and total nitrites. Data were collected within the 24 hours after the stroke onset.
Malondialdehyde for patients with stroke had a significant increase (P<0.001) when compared with healthy controls (47.9 +/- 7.1 vs. 1.7 +/- 0.2 micromol/L). Conversely, serum nitric oxide for patients with stroke had a significant decrease (P<0.001) when compared with the control group (14.5 +/- 1.4 vs. 41.3 +/- 3.7 micromol/L). The lowest values of malondialdehyde and the highest values of nitric oxide were observed in two patients, who died.
Serum levels of malondialdehyde increase, and serum levels of nitric oxide diminish within 24 hours after the onset of thrombotic stroke onset. This suggests that serum malondialdehyde level could be used as potentially reliable and sensitive marker for reperfusion, whereas nitric oxide levels could acts as potential biochemical sensor for nonreflow phenomenon.
Coenzyme Q10 (CoQ10) originates from food intake as well as from endogenous synthesis. While plasma concentrations may be influenced by dietary uptake, little is known whether concentrations in plasma reflect or influence intracellular concentrations.
For clinical routine investigation of intracellular CoQ10 contents, blood erythrocytes and platelets were isolated by Ficoll separating solution and CoQ10 analysed using HPLC. The intracellular concentrations were compared to environmental plasma concentrations of 50 clinically healthy infants and additionally after exogenous pharmaceutical supplementation of CoQ10 (3 mg/kg/day) to 12 adult probands for 14 days.
In healthy children, no correlation between plasma concentration and content in blood cells was found. A negative correlation exists between the year of life of the infants and CoQ10 concentrations in plasma correlated to cholesterol content. Probands supplemented with CoQ10 showed a distinct response in plasma concentrations after 14 days. While excessive environmental supplementation was without influence on erythrocyte concentrations, a positive correlation exists between plasma content and concentrations in platelets as mitochondria containing cell lines.
Under physiologically normal conditions, blood cells or organs may regulate their CoQ10 content independently from environmental supply. Effects may be expected in situations of deficiency or excessive supply. Erythrocyte concentration of CoQ10 keeps independent from environmental supply. Thus incorporation into outer cell membranes may be limited. However, an excessive environmental supply may influence inner compartments like mitochondrial membranes.
Oxidative stress is caused by a higher production of reactive oxygen and reactive nitrogen species or a decrease in endogenous protective antioxidative capacity. In all types of critical illness, such as sepsis, trauma, burn injury, acute pancreatitis, liver injury, severe diabetes, acute respiratory distress syndrome, AIDS and kidney failure, the occurrence of increased oxidative stress or a reduced antioxidative status is described. Whereas in the past, reactive oxygen and reactive nitrogen species were mainly known as harmful agents, recent investigations have given a new insight into the (patho)physiological importance of these substances as powerful messenger molecules involved in gene regulation, thereby enabling the synthesis of cytokines or adhesion molecules necessary for defending inflammatory processes. As shown in this review, there are numerous possibilities for the quantification of oxidative stress.
Several investigations showed a close association of single or multiple parameters, such as total antioxidative capacity, lipid peroxidation, vitamins C and E, the activation of nuclear factor kappa B, and respiratory burst, with the patient's outcome. However, no recommendation for a single parameter to be measured can be given because the assays described do not allow the definition of an overall "antioxidative status" for patients.
The occurrence of oxidative stress in critically ill patients is associated with a poor prognosis. The measurement of a cluster of assays representative of the quantification of reactive species or of antioxidants may improve the usefulness of therapeutic intervention and increase knowledge of pathophysiological alterations.
Oxidative stress is suggested to play an important role in the pathogenesis of Parkinson's disease (PD). However, no elevation of plasma oxidative stress marker has been reported. We measured percent content of the oxidized form of coenzyme Q10 in total coenzyme Q10 (%CoQ-10) because %CoQ-10 has been shown to be a sensitive marker of oxidative stress. A slight but significant elevation in %CoQ-10 was observed in PD patients when compared with age/gender-matched normal subjects, suggesting elevated systemic oxidative stress in PD patients.
There is substantial evidence that mitochondrial dysfunction and oxidative damage may play a key role in the pathogenesis of neurodegenerative disease. Evidence supporting this in both Alzheimer's and Parkinson's diseases is continuing to accumulate. This review discusses the increasing evidence for a role of both mitochondrial dysfunction and oxidative damage in contributing to beta-amyloid deposition in Alzheimer's disease. I also discuss the increasing evidence that Parkinson's disease is associated with abnormalities in the electron transport gene as well as oxidative damage. Lastly, I reviewed the potential efficacy of coenzyme Q as well as a number of other antioxidants in the treatment of both Parkinson's and Alzheimer's diseases.
Cognitive-behavioural treatment of chronic tinnitus needs active cooperation and motivation in patients. The transtheoretical model (TTM) defines the behavioural change using six different stages of change (SoC). In this study, we examined SoC in patients with tinnitus via a new self-rating instrument.
An item-pool, consisting of 48 questions, was administered to 125 tinnitus sufferers in a cross-sectional study. In addition to data on tinnitus history, the tinnitus strain (THI, German: TB-12), scores of anxiety and depression (HADS-D), and life quality (SF-12) were assessed.
Four SoC could be identified empirically: (1) precontemplation, (2) contemplation/preparation, (3) action/maintenance, and (4) termination. Associations of the SoC with socio-demographic and tinnitus related data, as well as with the instruments applied, conformed with the theory.
The results confirm the transfer of SoC theory to patients with tinnitus.
Neuronal cells depend on mitochondrial oxidative phosphorylation for most of their energy needs and therefore are at a particular risk for oxidative stress. Mitochondria play an important role in energy production and oxidative stress-induced apoptosis. In the present study, we have demonstrated that external oxidative stress induces mitochondrial dysfunction leading to increased ROS generation and ultimately apoptotic cell death in neuronal cells. Furthermore, we have investigated the role of Coenzyme Q10 as a neuroprotective agent. Coenzyme Q10 is a component of the mitochondrial respiratory chain and a potent anti-oxidant. Our results indicate that total cellular ROS generation was inhibited by Coenzyme Q10. Further, pre-treatment with Coenzyme Q10 maintained mitochondrial membrane potential during oxidative stress and reduced the amount of mitochondrial ROS generation. Our study suggests that water-soluble Coenzyme Q10 acts by stabilizing the mitochondrial membrane when neuronal cells are subjected to oxidative stress. Therefore, Coenzyme Q10 has the potential to be used as a therapeutic intervention for neurodegenerative diseases.
According to the free radical theory, aging can be considered as a progressive, inevitable process partially related to the accumulation of oxidative damage into biomolecules -- nucleic acids, lipids, proteins or carbohydrates -- due to an imbalance between prooxidants and antioxidants in favor of the former. More recently also the pathogenesis of several diseases has been linked to a condition of oxidative stress. In this review we focus our attention on the evidence of oxidative stress in aging brain, some of the most important neurodegenerative diseases -- Alzheimer's disease (AD), mild cognitive impairment (MCI), Parkinson's disease (PD), amyotrophic lateral sclerosis (ALS) and Huntington's disease (HD) -- and in two common and highly disabling vascular pathologies--stroke and cardiac failure. Particular attention will be given to the current knowledge about the biomarkers of oxidative stress that can be possibly used to monitor their severity and outcome.
Brain imaging studies suggest that the functional connectivity of various limbic, prefrontal, and temporal brain structures can be understood as the basis for particularly intense experiences of impairment and many secondary symptoms of decompensated tinnitus. Results to date suggest cortical plasticity as a likely mechanism to be involved in the chronic progression of tinnitus. Relationships between the processing of auditory signals and neural networks associated with somatosensory, attentional, cognitive and emotional processes are relevant for the genesis of the pathology. However, the neural bases of subjective impairment in tinnitus patients are unknown. An integrative model of developing tinnitus is presented here, based on the most recent neurophysiological data in current discussion. We assume the involvement of altered brain functions in the development and maintenance of perceptions of tinnitus and outline various possibilities which could contribute to decompensation and chronic progression. The discussions surrounding present models of the generation of tinnitus and its reinforcement to the point of decompensation make it clear that a unidimensional approach in clinical interventions is insufficient. Patients with decompensated tinnitus suffer from a complex somatic and psychological disorder. The interactive processes involving emotions, behaviour and symptoms, as well as the high co-morbidity with affective and psychosomatic illnesses and the important influence of psychosocial factors (distress), make the use of stage-appropriate interdisciplinary treatments necessary.
Ein Instrument zur Erfassung von Belastung und Schweregrad bei Tinnitus, Handanweisung Göttingen: Hogrefe, 1998. (Grade B). 12 The MOS 36-item short-form health survey (SF-36). I. Conceptual framework and item selection
- G Goebel
- W Hiller
- Tinnitus-Fragebogen
- Ware
- Jr
- Sherbourne
Goebel G, Hiller W. Tinnitus-Fragebogen (TF)-Ein Instrument zur Erfassung von Belastung und Schweregrad bei Tinnitus, Handanweisung. Göttingen: Hogrefe, 1998. (Grade B). 12. Ware JE Jr, Sherbourne CD. The MOS 36-item short-form health survey (SF-36). I. Conceptual framework and item selection. Med Care 1992;30:473– 83. (Grade B).
Tinnitus-Fragebogen (TF)-Ein Instrument zur Erfassung von Belastung und Schweregrad bei Tinnitus, Handanweisung
- G Goebel
- W Hiller
Goebel G, Hiller W. Tinnitus-Fragebogen (TF)-Ein Instrument zur
Erfassung von Belastung und Schweregrad bei Tinnitus, Handanweisung. Göttingen: Hogrefe, 1998. (Grade B).
Not significant Not significant Not significant the antioxidant level in blood cells and their environment in healthy children and after oral supplementation in adults
P 0.05
Not significant
Not significant
Not significant
the antioxidant level in blood cells and their environment in healthy
children and after oral supplementation in adults. Clin Chim Acta
2004;342:219-26. (Grade B).