107 research outputs found
Effect of Ambrotose AO® on resting and exercise-induced antioxidant capacity and oxidative stress in healthy adults
<p>Abstract</p> <p>Background</p> <p>The purpose of this investigation was to determine the effects of a dietary supplement (Ambrotose AO<sup>®</sup>) on resting and exercise-induced blood antioxidant capacity and oxidative stress in exercise-trained and untrained men and women.</p> <p>Methods</p> <p>25 individuals (7 trained and 5 untrained men; 7 trained and 6 untrained women) received Ambrotose AO<sup>® </sup>(4 capsules per day = 2 grams per day) or a placebo for 3 weeks in a random order, double blind cross-over design (with a 3 week washout period). Blood samples were collected at rest, and at 0 and 30 minutes following a graded exercise treadmill test (GXT) performed to exhaustion, both before and after each 3 week supplementation period. Samples were analyzed for Trolox Equivalent Antioxidant Capacity (TEAC), Oxygen Radical Absorbance Capacity (ORAC), malondialdehyde (MDA), hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>), and nitrate/nitrite (NOx). Quality of life was assessed using the SF-12 form and exercise time to exhaustion was recorded. Resting blood samples were analyzed for complete blood count (CBC), metabolic panel, and lipid panel before and after each 3 week supplementation period. Dietary intake during the week before each exercise test was recorded.</p> <p>Results</p> <p>No condition effects were noted for SF-12 data, for GXT time to exhaustion, or for any variable within the CBC, metabolic panel, or lipid panel (p > 0.05). Treatment with Ambrotose AO<sup>® </sup>resulted in an increase in resting levels of TEAC (p = 0.02) and ORAC (p < 0.0001). No significant change was noted in resting levels of MDA, H<sub>2</sub>O<sub>2</sub>, or NOx (p > 0.05). Exercise resulted in an acute increase in TEAC, MDA, and H<sub>2</sub>O<sub>2 </sub>(p < 0.05), all which were higher at 0 minutes post exercise compared to pre exercise (p < 0.05). No condition effects were noted for exercise related data (p > 0.05), with the exception of ORAC (p = 0.0005) which was greater at 30 minutes post exercise for Ambrotose AO<sup>® </sup>compared to placebo.</p> <p>Conclusion</p> <p>Ambrotose AO<sup>® </sup>at a daily dosage of 4 capsules per day increases resting blood antioxidant capacity and may enhance post exercise antioxidant capacity. However, no statistically detected difference is observed in resting or exercise-induced oxidative stress biomarkers, in quality of life, or in GXT time to exhaustion.</p
The longitudinal association between multiple job holding and long-term sickness absence among Danish employees: an explorative study using register-based data
Effect of vitamin E (Tri E®) on antioxidant enzymes and DNA damage in rats following eight weeks exercise
<p>Abstract</p> <p>Background</p> <p>Exercise is beneficial to health, but during exercise the body generates reactive oxygen species (ROS) which are known to result in oxidative stress. The present study analysed the effects of vitamin E (Tri E<sup>®</sup>) on antioxidant enzymes; superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (Cat) activity and DNA damage in rats undergoing eight weeks exercise.</p> <p>Methods</p> <p>Twenty four <it>Sprague-Dawley </it>rats (weighing 320-370 gm) were divided into four groups; a control group of sedentary rats which were given a normal diet, second group of sedentary rats with oral supplementation of 30 mg/kg/d of Tri E<sup>®</sup>, third group comprised of exercised rats on a normal diet, and the fourth group of exercised rats with oral supplementation of 30 mg/kg/d of Tri E<sup>®</sup>. The exercising rats were trained on a treadmill for 30 minutes per day for 8 weeks. Blood samples were taken before and after 8 weeks of the study to determine SOD, GPx, Cat activities and DNA damage.</p> <p>Results</p> <p>SOD activity decreased significantly in all the groups compared to baseline, however both exercised groups showed significant reduction in SOD activity as compared to the sedentary groups. Sedentary control groups showed significantly higher GPx and Cat activity compared to baseline and exercised groups. The supplemented groups, both exercised and non exercised groups, showed significant decrease in Cat activity as compared to their control groups with normal diet. DNA damage was significantly higher in exercising rats as compared to sedentary control. However in exercising groups, the DNA damage in supplemented group is significantly lower as compared to the non-supplemented group.</p> <p>Conclusions</p> <p>In conclusion, antioxidant enzymes activity were generally reduced in rats supplemented with Tri E<sup>® </sup>probably due to its synergistic anti-oxidative defence, as evidenced by the decrease in DNA damage in Tri E<sup>® </sup>supplemented exercise group.</p
Activation of cGMP-Dependent Protein Kinase Stimulates Cardiac ATP-Sensitive Potassium Channels via a ROS/Calmodulin/CaMKII Signaling Cascade
) channels, an ion channel critical for stress adaptation in the heart; however, the underlying mechanism remains largely unknown. The present study was designed to address this issue. channels was confirmed in intact ventricular cardiomyocytes, which was ROS- and CaMKII-dependent. Kinetically, PKG appeared to stimulate these channels by destabilizing the longest closed state while stabilizing the long open state and facilitating opening transitions. channels and contribute to cardiac protection against ischemia-reperfusion injury
Investigating interactions between phentermine, dexfenfluramine, and 5-HT2C agonists, on food intake in the rat
Sleep disturbances in highly stress reactive mice: Modeling endophenotypes of major depression
<p>Abstract</p> <p>Background</p> <p>Neuronal mechanisms underlying affective disorders such as major depression (MD) are still poorly understood. By selectively breeding mice for high (HR), intermediate (IR), or low (LR) reactivity of the hypothalamic-pituitary-adrenocortical (HPA) axis, we recently established a new genetic animal model of extremes in stress reactivity (SR). Studies characterizing this SR mouse model on the behavioral, endocrine, and neurobiological levels revealed several similarities with key endophenotypes observed in MD patients. HR mice were shown to have changes in rhythmicity and sleep measures such as rapid eye movement sleep (REMS) and non-REM sleep (NREMS) as well as in slow wave activity, indicative of reduced sleep efficacy and increased REMS. In the present study we were interested in how far a detailed spectral analysis of several electroencephalogram (EEG) parameters, including relevant frequency bands, could reveal further alterations of sleep architecture in this animal model. Eight adult males of each of the three breeding lines were equipped with epidural EEG and intramuscular electromyogram (EMG) electrodes. After recovery, EEG and EMG recordings were performed for two days.</p> <p>Results</p> <p>Differences in the amount of REMS and wakefulness and in the number of transitions between vigilance states were found in HR mice, when compared with IR and LR animals. Increased frequencies of transitions from NREMS to REMS and from REMS to wakefulness in HR animals were robust across the light-dark cycle. Detailed statistical analyses of spectral EEG parameters showed that especially during NREMS the power of the theta (6-9 Hz), alpha (10-15 Hz) and eta (16-22.75 Hz) bands was significantly different between the three breeding lines. Well defined distributions of significant power differences could be assigned to different times during the light and the dark phase. Especially during NREMS, group differences were robust and could be continuously monitored across the light-dark cycle.</p> <p>Conclusions</p> <p>The HR mice, i.e. those animals that have a genetic predisposition to hyper-activating their HPA axis in response to stressors, showed disturbed patterns in sleep architecture, similar to what is known from depressed patients. Significant alterations in several frequency bands of the EEG, which also seem to at least partly mimic clinical observations, suggest the SR mouse lines as a promising animal model for basic research of mechanisms underlying sleep impairments in MD.</p
Obesity-Related Oxidative Stress: the Impact of Physical Activity and Diet Manipulation
Obesity-related oxidative stress, the imbalance between pro-oxidants and antioxidants (e.g., nitric oxide), has been linked to metabolic and cardiovascular disease, including endothelial dysfunction and atherosclerosis. Reactive oxygen species (ROS) are essential for physiological functions including gene expression, cellular growth, infection defense, and modulating endothelial function. However, elevated ROS and/or diminished antioxidant capacity leading to oxidative stress can lead to dysfunction. Physical activity also results in an acute state of oxidative stress. However, it is likely that chronic physical activity provides a stimulus for favorable oxidative adaptations and enhanced physiological performance and physical health, although distinct responses between aerobic and anaerobic activities warrant further investigation. Studies support the benefits of dietary modification as well as exercise interventions in alleviating oxidative stress susceptibility. Since obese individuals tend to demonstrate elevated markers of oxidative stress, the implications for this population are significant. Therefore, in this review our aim is to discuss (i) the role of oxidative stress and inflammation as associated with obesity-related diseases, (ii) the potential concerns and benefits of exercise-mediated oxidative stress, and (iii) the advantageous role of dietary modification, including acute or chronic caloric restriction and vitamin D supplementation
Effects of Long Acting Methylphenidate on Ghrelin Levels in Male Children with Attention Deficit Hyperactivity Disorder: An Open Label Trial
The Sobolev orthogonality and spectral analysis of the Laguerre polynomials L_{n, -k} gor positive intergers k
AbstractFor k∈N, we consider the analysis of the classical Laguerre differential expressionℓ−k[y](x)=1x−ke−x(−(x−k+1e−xy′(x))′+rx−ke−xy(x))(x∈(0,∞)),where r⩾0 is fixed, in several nonisomorphic Hilbert and Hilbert–Sobolev spaces.In one of these spaces, specifically the Hilbert space L2((0,∞);x−ke−x), it is well known that the Glazman–Krein–Naimark theory produces a self-adjoint operator A−k, generated by ℓ−k[·], that is bounded below by rI, where I is the identity operator on L2((0,∞);x−ke−x). Consequently, as a result of a general theory developed by Littlejohn and Wellman, there is a continuum of left-definite Hilbert spaces {Hs,−k=(Vs,−k,(·,·)s,−k)}s>0 and left-definite self-adjoint operators {Bs,−k}s>0 associated with the pair (L2((0,∞);x−ke−x),A−k). For A−k and each of the operators Bs,−k, it is the case that the tail-end sequence {Ln−k}n=k∞ of Laguerre polynomials form a complete set of eigenfunctions in the corresponding Hilbert spaces.In 1995, Kwon and Littlejohn introduced a Hilbert–Sobolev space Wk[0,∞) in which the entire sequence of Laguerre polynomials is orthonormal. In this paper, we construct a self-adjoint operator in this space, generated by the second-order Laguerre differential expression ℓ−k[·], having {Ln−k}n=0∞ as a complete set of eigenfunctions. The key to this construction is in identifying a certain closed subspace of Wk[0,∞) with the kth left-definite vector space Vk,−k
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