Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Effects of gold sodium thiomalate (GSTM) on membrane potential and tetanus tension were examined to elucidate whether the gold compound improves mechanical and electrical muscle dysfunction produced by continuous repeated stimulation of frog skeletal muscles. Continuous stimulation (50 Hz for 2 min, 0.05 ms pulse duration) to the sartorius muscle depolarized the membrane, decreased action potential amplitude, and prolonged action potential duration. GSTM (0.1 mM), unlike thiomalic acid (0.1 mM), markedly decreased impairment of these electrical parameters produced during the stimulation period. In the presence of 500 units/mL of catalase, fatigue stimulation still lengthened by 1.5-fold the half-duration of the action potential after a 5-min rest. The prolongation was, however, smaller than that in controls (no catalase). Application of both catalase and GSTM led to no further changes in action potential compared with the application of catalase alone. GSTM did not affect resting tension of single toe muscle fibers though it suppressed the maximum tension after continuous stimulation. These findings suggest that GSTM can inhibit excitable dysfunction of skeletal muscles subjected to continuous stimulation and that such protective effects of GSTM may be partially mediated by H2O2.
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PMID:Gold sodium thiomalate improves membrane potential impaired by high-frequency stimulation. 1518 64

Low-density lipoproteins (LDL) are very sensitive to oxidative processes initiated by oxygen free radicals, known to be produced in large quantities during intense physical exercise. Oxidatively modified lipoprotein particles (oxLDL) are strongly atherogenic and immunogenic, as a consequence specific autoantibodies (oLAB) against oxLDL are produced by the immune system. This study was designed to evaluate the oLAB titres in professional soccer players and to find out whether the immune response to oxidative modification of LDL correlates with the antioxidant status of individual players. Eleven players volunteered to participate in an incremental treadmill running exercise to volitional fatigue twice (in October and January) during the competitive season. Venous blood samples were withdrawn before and 3 min after the cessation of the test. Serum levels of oLAB were measured by ELISA (Biomedica). Blood samples were analyzed for glutathione peroxidase, reduced glutathione, superoxide dismutase, catalase and glutathione reductase. The activity of creatine kinase (CK) and concentrations of malondialdehyde (MDA), vitamin E and retinol were determined in plasma. From 11 subjects only in 4 players, in both graded running tests, the oLAB titres were low (< 200 mU.ml(-1)). The remaining athletes presented elevated oLAB (800-1400 mU.ml(-1)). Significantly lower activities of catalase and glutathione reductase and lower concentration of alpha-tocopherol were recorded in the 2nd trial. When the data were arranged according to the oLAB titres no significant between-group differences were found in either pre- and post-test activities of antioxidant enzymes or in concentrations of antioxidants. However, significantly higher CK activities and a tendency towards more elevated plasma MDA concentrations were observed in subjects with higher oLAB levels. It seems justified to presume that high titres of antibodies against oxLDL, as evidenced in most of the players, could be accounted for by their higher in vivo susceptibility of LDL to structural modification under conditions of intensive training-induced oxidative stress, despite their apparently normal antioxidant status.
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PMID:Evaluation of autoantibodies against oxidized LDL (oLAB) and blood antioxidant status in professional soccer players. 1564 38

Muscular exercise results in an increased production of free radicals and other forms of reactive oxygen species (ROS). Further, developing evidence implicates cytotoxins as an underlying etiology of exercise-induced stimuli in muscle redox status, which could result in muscle fatigue and/or injury. Two major classes of endogenous protective mechanisms (enzymatic and nonenzymatic antioxidants) work together to reduce the harmful effects of oxidants in the cell. This study examined the effects of acute physical exercise on the enzymatic antioxidant systems of different athletes and comparison was made to the mechanism of action of three main antioxidant enzymes in the blood. Handball players (n = 6), water-polo players (n = 20), hockey players (n = 22), basketball players (n = 24), and a sedentary control group (n = 10 female and n = 9 male) served as the subjects of this study. The athletes were divided into two groups according to the observed changes of activity of superoxide dismutase enzyme. The antioxidant enzyme systems were characterized by catalase (CAT), glutathione-peroxidase (GPX), and superoxide-dismutase (SOD) and measured by spectrophotometry. An important finding in the present investigation is that when the activities of SOD increased, the activities of GPX and CAT increased also and this finding related to the physical status of interval-trained athletes. Positive correlation between SOD and GPX activities was observed (r = 0.38 females, r = 0.56 males; p < 0.05). We have observed that the changes in the primary antioxidant enzyme systems of athletes are sport specific, and different from control subjects. Presumably, with interval-trained athletes, hydrogen-peroxide is significantly eliminated by glutathione-peroxidase. From these results it can be concluded that the blood redox status should be taken into consideration when establishing a fitness level for individual athletes.
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PMID:Antioxidant status of interval-trained athletes in various sports. 1647 56

Free radicals are reactive compounds that are naturally produced in the human body. They can exert positive effects (e.g. on the immune system) or negative effects (e.g. lipids, proteins or DNA oxidation). To limit these harmful effects, an organism requires complex protection - the antioxidant system. This system consists of antioxidant enzymes (catalase, glutathione peroxidase, superoxide dismutase) and non-enzymatic antioxidants (e.g. vitamin E [tocopherol], vitamin A [retinol], vitamin C [ascorbic acid], glutathione and uric acid). An imbalance between free radical production and antioxidant defence leads to an oxidative stress state, which may be involved in aging processes and even in some pathology (e.g. cancer and Parkinson's disease). Physical exercise also increases oxidative stress and causes disruptions of the homeostasis. Training can have positive or negative effects on oxidative stress depending on training load, training specificity and the basal level of training. Moreover, oxidative stress seems to be involved in muscular fatigue and may lead to overtraining.
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PMID:Oxidative stress : relationship with exercise and training. 1657 58

Oxidative stress is associated with muscle fatigue and weakness in skeletal muscle of ischemic heart disease patients. Recently, it was found that endurance training elevates protective heat shock proteins (HSPs) and antioxidant enzymes in skeletal muscle in healthy subjects and antioxidant enzymes in heart failure patients. However, it is unknown whether coronary ischemia and mild infarct without heart failure contributes to impairment of stress proteins and whether exercise training reverses those effects. We tested the hypothesis that exercise training would reverse alterations in muscle TNF-alpha, oxidative stress, HSP70, SOD (Mn-SOD, Cu,Zn-SOD), glutathione peroxidase (GPX), and catalase (CAT) due to chronic coronary occlusion of the left circumflex (CCO). Yucatan swine were divided into three groups (n = 6 each): sedentary with CCO (SCO); 12 wk of treadmill exercise training following CCO (ECO); and sham surgery controls (sham). Forelimb muscle mass-to-body mass ratio decreased by 27% with SCO but recovered with ECO. Exercise training reduced muscle TNF-alpha and oxidative stress (4-hydroxynonenal adducts) caused by CCO. HSP70 levels decreased with CCO (-45%), but were higher with exercise training (+348%). Mn-SOD activity, Mn-SOD protein expression, and Cu,Zn-SOD activity levels were higher in ECO than SCO by 72, 82, and 112%, respectively. GPX activity was 177% greater in ECO than in SCO. CAT trended higher (P = 0.059) in ECO compared with SCO. These data indicate that exercise training following onset of coronary artery occlusion results in recovery of critical stress proteins and reduces oxidative stress.
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PMID:Exercise training reverses downregulation of HSP70 and antioxidant enzymes in porcine skeletal muscle after chronic coronary artery occlusion. 1687 55

Overreaching (OVR) is defined as the initial phase of overtraining syndrome and is known as a metabolic imbalance leading to short-term fatigue. Exercise increases reactive oxygen species production, which can oxidize intracellular structures impairing cell function and thus leads to OVR process. The aim of this work is to study the behavior of oxidative stress markers in subjects submitted to an OVR protocol. Thirty rats were divided in exercise and control group, and submitted to an 8-week-endurance training (ET) and a 3-week-OVR protocol. Thiobarbituric acid reactive substances (TBARs), reactive carbonylated derivatives (RCD), glutathione reductase (GR), catalase (CAT) and citrate synthase (CS) activities and stress protein HSP72 were measured in soleus (SO), extensor digital longus (EDL) and semitendinuous (ST) muscles. ET induced significant enhancement (P<0.05) in CS, GR, CAT, TBARs, RCD and HSP72 in SO, EDL and ST. OVR induced higher levels (P<0.05) of TBARs, RCD and HSP72 compared with ET only in SO, while in EDL and ST all measured parameters ranged at same levels reached during ET. We concluded that stress-induced OVR protocol is fiber type dependent, the SO muscle fiber type I being the most affected by this treatment.
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PMID:Overreaching-induced oxidative stress, enhanced HSP72 expression, antioxidant and oxidative enzymes downregulation. 1734 86

Catalase is a major antioxidant enzyme. Increasing catalase expression represents a promising avenue to improve muscle function in certain physiological conditions and in some muscle diseases. We hypothesized that catalase overexpression should not impair normal muscle contraction. We delivered a hemagglutinin (HA)-tagged human catalase gene to normal mouse muscle by an adeno-associated viral vector (AAV). Western blot and immunostaining revealed efficient expression of HA-tagged catalase. Enzymatic assay demonstrated an approximately threefold increase in catalase activity in AAV-infected muscles. Catalase overexpression impaired neither twitch nor tetanic tension in the extensor digitorum longus (EDL) muscle. Furthermore, EDL fatigue response was not altered. Taken together, we have developed a novel AAV vector to enhance catalase expression. Lack of apparent toxicity in normal muscle strongly supports further exploration of this vector to reduce oxidative stress-induced muscle damage.
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PMID:Catalase overexpression does not impair extensor digitorum longus muscle function in normal mice. 1769 55

This study examined the effects of Y-27632, a selective Rho-kinase inhibitor, on organophosphate-induced acute toxicity in rats. Rats were randomly divided into four groups as control (corn oil), dichlorvos (30 mg kg(-1) i.p.), 1 and 10 mg kg(-1) Y-27632 + dichlorvos groups. Cholinergic signs (fatigue, tremor, cyanosis, hyper-secretion, fasciculations) were observed in all the rats in the dichlorvos group and the mortality rate was 50%. No cholinergic findings and deaths were observed in the control and Y-27632 groups. Plasma cholinesterase activities were suppressed with dichlorvos and these reductions were attenuated with Y-27632 pretreatment. There was a marked increase in plasma malondialdehyde level in the dichlorvos group, but Y-27632 pretreatment abolished this elevation. Dichlorvos markedly depressed cardiac paraoxonase activity, but these changes were not markedly modified with Y-27632. Total antioxidant capacities, total oxidant status, oxidative stress index, total free sulfhydryl groups and catalase activities in plasma and cardiac tissues were not markedly different between the groups. No significant changes were observed with cardiac myeloperoxidase activities or plasma arylesterase and ceruloplasmin activities. In conclusion, our results suggest that Rho-kinase pathway is involved in organophosphate intoxication, and a decrease in cardiac paraoxonase activities may play a role in the pathogenesis of acute organophosphate poisoning in rats.
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PMID:Effects of a selective Rho-kinase inhibitor Y-27632 on oxidative stress parameters in acute dichlorvos poisoning in rats. 1863 19

We proposed to assess antioxidant status and nitric oxide in fibromyalgia (FM) patients in comparison to healthy controls. Additionally, the association between the serum antioxidant levels and clinical findings in FM patients was also investigated. Thirty-seven FM patients and 37 healthy controls were enrolled in this study. Severity of fatigue and pain were determined by Visual Analogue Scale. Functional capacity in daily living activities was evaluated by fibromyalgia impact questionnaire. Serum NO, catalase and glutathione were measured. Serum glutathione and catalase levels were significantly lower in FM patients than controls. However, no significant difference was seen in serum NO levels between the two groups. A significant correlation was evident between serum NO level and pain. Additionally, the correlation between glutathione level and morning stiffness was found to be significant. These findings support other studies, we assume that these two antioxidants might have impact on the pathogenesis of FM disease.
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PMID:Serum antioxidants and nitric oxide levels in fibromyalgia: a controlled study. 1885 66

The present study was conducted with the aim of elucidating the possible role of nitric oxide (NO) in the neuroprotective effects of trazodone used to treat chronic fatigue syndrome (CFS) in mice. Male albino mice were forced to swim for a six minute session each day for 7 days and the immobility period was recorded every other day. Trazodone (5 mg/kg and 10 mg/kg) was administered each day 30 min before the forced swim test. In addition, L-arginine (100 mg/kg) and L-NAME (5 mg/kg) were administered 15 min before administration of trazodone (5 mg/kg). Various behavioral tests, including locomotor (actophotometer) and anxiety (mirror chamber and plus maze) tests, as well as biochemical parameters (lipid peroxidation, reduced glutathione, catalase, and nitrites) were evaluated on the 8th day. Forced swimming for 7 days caused a chronic fatigue-like condition, anxiety-like behavior, impairments in locomotor activity, and oxidative damage (increased lipid peroxidation and nitrite levels, and depletions in the reduced forms of glutathione and catalase activity) in animals. Pretreatment with L-NAME (5 mg/kg) potentiated the antioxidant effect of trazodone (5 mg/kg). However, L-arginine (100 mg/kg) pretreatment reversed the protective effect of trazodone (5 mg/kg) (p<0.05). The present study suggests the possible involvement of NO signaling in the protective effect of trazodone.
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PMID:Nitric oxide modulation mediates the protective effect of trazodone in a mouse model of chronic fatigue syndrome. 1906 12


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