Biomedical subjects

José Magalhães

Publications and source records attributed to José Magalhães.

14 recordsLinked to original sources

PubMed2006

Effect of off-road competitive motocross race on plasma oxidative stress and damage markers.

AIM: To analyse the effect of an off-road motocross heat on plasma levels of oxidative stress and damage, blood leucocyte counts and urine catecholamine concentration. METHODS: Plasma contents of total, reduced and oxidised (GSSG) glutathione, %GSSG, malondialdehyde (MDA), protein carbonyl and sulphydryl groups, total antioxidant status (TAS), uric acid, and blood neutrophil and lymphocyte counts were evaluated in 10 male top-level riders before, immediately after (0 h) and 1 h after a simulated competitive motocross race. 24-h urine adrenaline, noradrenaline and dopamine concentrations were also measured. RESULTS: The motocross heat resulted in an increase in plasma oxidative stress and damage (p<0.05). This was shown by a significant increase in %GSSG, TAS, MDA and carbonyls, and by a decrease in sulphydryl groups after the race. There was a significant increase in both plasma uric acid and urine catecholamine concentration after the race (p<0.05). Blood neutrophil counts increased at 0 and 1 h after exercise (p<0.05). Lymphocyte count increased from baseline to 0 h, although it decreased from baseline and 0 to 1 h after exercise (p<0.05). CONCLUSION: The data reinforce the marked metabolic and hormonal demands imposed by motocross, resulting in a condition of enhanced plasma oxidative stress and damage.

Adult↗

PubMed2006

Exercise-induced cardioprotection--biochemical, morphological and functional evidence in whole tissue and isolated mitochondria.

Myocardial injury is a major contributor to the morbidity and mortality associated with coronary artery disease. Regular exercise has been confirmed as a pragmatic countermeasure to protect against cardiac injury. Specifically, endurance exercise has been proven to provide cardioprotection against cardiac insults in both young and old animals. Proposed mechanisms to explain the cardioprotective effects of exercise are mediated, at least partially, by redox changes and include the induction of myocardial heat shock proteins, improved cardiac antioxidant capacity, and/or elevation of other cardioprotective molecules. Understanding the molecular basis for exercise-induced cardioprotection is important in developing exercise strategies to protect the heart during and after insults. Data suggest that these positive modulator effects occur at different levels of cellular organization, being mitochondria fundamental organelles that are sensitive to disturbances imposed by exercise on basal homeostasis. At present, which of these protective mechanisms is essential for exercise-induced cardioprotection remains unclear. This review analyzes the biochemical, morphological and functional outcomes of acute and chronic exercise on the overall cardiac muscle tissue and in isolated mitochondria. Some redox-based mechanisms behind the cross-tolerance effects particularly induced by endurance training, against certain stressors responsible for the impairments in cardiac homeostasis caused by aging, diabetes, drug administration or ischemia-reperfusion are also outlined. Further work should be addressed in order to clarify the precise regulatory mechanisms by which physical exercise augments heart tolerance against many cardiotoxic agents.

Animals↗

PubMed2006

Skeletal muscle atrophy increases cell proliferation in mice gastrocnemius during the first week of hindlimb suspension.

The comprehension of the cellular mechanisms underlying skeletal muscle atrophy has been the aim of several experimental studies. However, the majority of them focused on alterations of the myocytes induced by different experimental conditions yet disregarding the contribution of other cells such as endothelial cells and fibroblasts. In this sense, 70 Charles River CD1 male mice were randomly assigned to seven groups (n=10 per group): control and 6, 12, 24, 48, 72 h and 1 week with respect to the period of hindlimb suspension. Forty-eight hours before sacrifice, the animals were injected with bromodeoxyuridine (BrdU) in order to identify proliferating cells. Immunohistochemistry and south-western blotting techniques were used to evaluate across the whole gastrocnemius muscle BrdU incorporation into the different proliferating cells. The contribution of the apoptotic response was also measured in order to ascertain whether the balance between cell survival and death was preserved. The results observed during 1 week of unloading-induced atrophy evidenced an intense peak of proliferating activity only after 6 h, mainly due to the duplication of satellite cells. Consequently to this unexpected activation of satellite cells, the addition of nuclei to the fibre syncytium was recognized at 12 h of unloading. After 48 h of weightlessness, the proliferating activity observed was largely due to an interstitial fibrosis. According to the apoptotic index profile observed during the analysed unloading period, this general proliferative activity was balanced by apoptosis, which strongly suggests the existence of a regulatory feedback response between anabolic and catabolic events in unloading-induced skeletal muscle atrophy.

Animals↗

PubMed2006

Motor imagery in blind subjects: the influence of the previous visual experience.

Mental simulation of movements has been widely used to infer about representational aspects of action. On a daily basis, motor planning and execution depends crucially both upon vision and kinesthesia. What if the former is lost? In this study we investigate the physiological changes induced during a mental simulation task in subjects with early and late onset blindness, analyzing simultaneously stabilometric (body sway), electromyographic (EMG, lateral gastrocnemius) and eletrocardiographic (ECG) signals. Subjects were asked to stand up on a force platform and instructed either to: rest during 20s; count mentally from 1 to 15; imagine themselves executing a bilateral plantar flexion 15 times and execute the same movement 15 times. Discriminant analysis was employed to have access to the differences in the groups with respect to heart rate variability (HRV), EMG and body sway measurements for each condition. We found an overall correct classification of 100 and 90.9%, respectively, for the stabilometric parameters and HRV. This result was found only for the mental simulation task (p<0.05), being absent for resting, counting and executing. Previous studies have shown that motor simulation in a kinesthetic mode strongly associates with somatic and autonomic changes. In late blind subjects, however, movement simulation would tend to unfold with the use of both visual and kinesthetic representations. Thus, our results suggest that early and late blind subjects make use of distinct body representations during motor imagery.

Adolescent↗

PubMed2005

Endurance training limits the functional alterations of rat heart mitochondria submitted to in vitro anoxia-reoxygenation.

BACKGROUND: Studies analysing the effect of endurance training on heart mitochondrial function submitted to in vitro anoxia-reoxygenation (A-R) are missing. The present study aimed to investigate the effect of moderate endurance treadmill training (14 weeks) against rat heart mitochondrial dysfunction induced by in vitro A-R. METHODS: Respiratory parameters (state 3, state 4, ADP/O and respiratory control ratio-RCR) and oxidative damage markers (carbonyl groups and malondialdehyde) were determined in isolated mitochondria before and after 1 min anoxia followed by 4 min reoxygenation. Levels of heat shock protein 60 kDa (HSP60) and 70 kDa (HSP70) were measured before A-R in mitochondria and whole muscle homogenate, respectively. RESULTS: A-R significantly impaired the rate of state 3 and state 4 respiration, as well as the RCR and ADP/O in the sedentary group. However, mitochondrial state 3 respiration was significantly higher in trained than in the sedentary group both before and after A-R. The impairments in RCR, ADP/O ratio and state 4 induced by A-R in sedentary group were significantly attenuated in endurance-trained group. The inhibition of state 4 induced by GDP was significantly higher in trained than in sedentary group. Oxidative modifications of mitochondrial proteins and phospholipids were found in sedentary group after A-R, although limited in trained group. Increased levels of mitochondrial HSP60 and tissue HSP70 accompanied the lower decrease in the respiratory function after A-R observed in trained group. CONCLUSION: We therefore concluded that endurance training limited the impairments on rat heart mitochondria caused by the oxidant insult inflicted by in vitro A-R.

Animals↗

PubMed2005

Acute and severe hypobaric hypoxia increases oxidative stress and impairs mitochondrial function in mouse skeletal muscle.

Severe high-altitude hypoxia exposure is considered a triggering stimulus for redox disturbances at distinct levels of cellular organization. The effect of an in vivo acute and severe hypobaric hypoxic insult (48 h at a pressure equivalent to 8,500 m) on oxidative damage and respiratory function was analyzed in skeletal muscle mitochondria isolated from vitamin E-supplemented (60 mg/kg ip, 3 times/wk for 3 wk) and nonsupplemented mice. Forty male mice were randomly divided into four groups: control + placebo, hypoxia + placebo (H + P), control + vitamin E, and hypoxia + vitamin E. Significant increases in mitochondrial heat shock protein 60 expression and protein carbonyls group levels and decreases in aconitase activity and sulfhydryl group content were found in the H + P group when compared with the control + placebo group. Mitochondrial respiration was significantly impaired in animals from the H + P group, as demonstrated by decreased state 3 respiratory control ratio and ADP-to-oxygen ratio and by increased state 4 with both complex I- and II-linked substrates. Using malate + pyruvate as substrates, hypoxia decreased the respiratory rate in the presence of carbonyl cyanide m-chlorophenylhydrazone and also stimulated oligomycin-inhibited respiration. However, vitamin E treatment attenuated the effect of hypoxia on the mitochondrial levels of heat shock protein 60 and markers of oxidative stress. Vitamin E was also able to prevent most mitochondrial alterations induced by hypobaric hypoxia. In conclusion, hypobaric hypoxia increases mitochondrial oxidative stress while decreasing mitochondrial capacity for oxidative phosphorylation. Vitamin E was an effective preventive agent, which further supports the oxidative character of mitochondrial dysfunction induced by hypoxia.

Acute Disease↗

PubMed2005

Endurance training attenuates doxorubicin-induced cardiac oxidative damage in mice.

BACKGROUND: There is a lack of studies reporting the influence of DOX treatment on chronically exercised animals. This study intended to determine the effect of endurance swimming training on cardiac muscle tolerance to in vivo DOX-induced damage, analyzing the levels of oxidative stress markers, the response of antioxidant system and the expression of 60 and 70 kDa heat shock proteins (HSP). METHODS: Forty-four Charles River CD1 male mice were randomly assigned to either non-trained placebo (NT+P) and non-trained DOX (NT+DOX) or trained placebo (T+P) and trained DOX (T+DOX). Twenty-four hours after completion of a 14-week training, cardiac ventricles were extracted for biochemical assays of oxidative stress and damage markers, antioxidant enzymes and HSPs. RESULTS: DOX treatment per se (single 20 mg kg(-1) dose), administrated 24 h after the last exercise bout, elevated (p<0.05) plasma cardiac troponin I (cTnI), HSP60, % oxidized glutathione, thiobarbituric acid reactive substances and carbonyl groups and reduced -SH groups. However, training induced a significant increase (p<0.05) on total and reduced glutathione (GSH), HSP60 expression, and decreased the rise of plasma cTnI as well as cardiac carbonyl groups contents in DOX hearts, when compared to NT+DOX mice. Although catalase activity of T+DOX was significantly higher than T+P, no changes were observed in the activities of superoxide dismutase, glutathione peroxidase and glutathione reductase. Neither DOX nor training induced significant variations in HSP70. CONCLUSION: Training improved myocardial tolerance to DOX-induced damage. It is likely that the improvement in responses to DOX was related to training-induced increases in GSH and HSP60.

Animals↗

PubMed2005

Moderate endurance training prevents doxorubicin-induced in vivo mitochondriopathy and reduces the development of cardiac apoptosis.

The objective of this work was to test the hypothesis that endurance training may be protective against in vivo doxorubicin (DOX)-induced cardiomyopathy through mitochondria-mediated mechanisms. Forty adult (6-8 wk old) male Wistar rats were randomly divided into four groups (n = 10/group): nontrained, nontrained + DOX treatment (20 mg/kg), trained (14 wk of endurance treadmill running, 60-90 min/day), and trained + DOX treatment. Mitochondrial respiration, calcium tolerance, oxidative damage, heat shock proteins (HSPs), antioxidant enzyme activity, and apoptosis markers were evaluated. DOX induces mitochondrial respiratory dysfunction, oxidative damage, and histopathological lesions and triggers apoptosis (P < 0.05, n = 10). However, training limited the decrease in state 3 respiration, respiratory control ratio (RCR), uncoupled respiration, aconitase activity, and protein sulfhydryl content caused by DOX treatment and prevented the increased sensitivity to calcium in nontrained + DOX-treated rats (P < 0.05, n = 10). Moreover, training inhibited the DOX-induced increase in mitochondrial protein carbonyl groups, malondialdehyde, Bax, Bax-to-Bcl-2 ratio, and tissue caspase-3 activity (P < 0.05, n = 10). Training also increased by approximately 2-fold the expression of mitochondrial HSP-60 and tissue HSP-70 (P < 0.05, n = 10) and by approximately 1.5-fold the activity of mitochondrial and cytosolic forms of SOD (P < 0.05, n = 10). We conclude that endurance training protects heart mitochondrial respiratory function from the toxic effects of DOX, probably by improving mitochondrial and cell defense systems and reducing cell oxidative stress. In addition, endurance training limited the DOX-triggered apoptosis.

Animals↗

PubMed2005

Strenuous exercise aggravates MDMA-induced skeletal muscle damage in mice.

The aim of this study was to investigate the influence of ecstasy (MDMA) administration on body temperature and soleus muscle histology in exercised and non-exercised mice. Charles-River mice were distributed into four groups: Control (C), exercise (EX), MDMA treated (M), and M + EX. The treated animals received an i.p. injection (10 mg/kg) of MDMA (saline for C and EX), and the exercise consisted of a 90 min level run at a velocity of 900 m/h, immediately after the MDMA or saline administration. Body temperature was recorded every 30 min via subcutaneous implanted transponder. Animals were sacrificed 1.5, 25.5, and 49.5 h after i.p. injection and the soleus muscles were removed and processed for light and electron microscopy. The MDMA-treated animals showed a significant increase in body temperature (similar in M and M + EX groups), reaching the peak 90 min after i.p. administration; their temperature remained higher than control for more than 5 h. The EX group evidenced a similar and parallel, yet lower temperature increase during exercise and recovery. Morphological signs of damage were rarely encountered in the EX group; they were more pronounced in M group and even aggravated in M + EX group. In conclusion, MDMA and exercise per se increased body temperature but in conjunction did not have a cumulated effect. However, ecstasy and concomitant physical activity might severely accumulate with regard to skeletal muscle toxicity and may lead to rhabdomyolysis.

Animals↗

PubMed2004

Effect of a high-altitude expedition to a Himalayan peak (Pumori, 7,161 m) on plasma and erythrocyte antioxidant profile.

The effects of a high-altitude exposure were studied in six mountaineers who spent 3 weeks at an altitude range between 5,250 and 7,161 m after 1 week in an acclimatization trek (2,800-5,250 m). Blood drawn from the antecubital vein was collected at sea level 1 day before and 1 day after the expedition to analyse some haematological variables [haemoglobin (Hb), haematocrit (Htc) and red blood cell (RBC) count], erythrocyte antioxidant enzyme activity [superoxide dismutase (SOD), glutathione peroxidase (GPx) and glutathione reductase (Gr)] and membrane fatty acid profile [mono-unsaturated fatty acids (MUFA), polyunsaturated fatty acids (PUFA), saturated fatty acids (SFA), trans fatty acids (TRANS)]. Moreover, total antioxidant status (TAS), thiobarbituric acid reactive substances (TBARS), thiol protein groups (SH), SOD, GPx and Gr were measured in plasma. High-altitude exposure induced polycythaemia, with significant increases in RBC count (5.26%), Hb concentration (4.83%) and Htc (6.26%). Furthermore, a significant increase in plasma TBARS, SOD and Gr was observed after the expedition, whereas SH, TAS and GPx decreased. Erythrocyte glutathione-cycle-related antioxidant enzyme activity was upregulated, whereas SOD activity was maintained after the expedition. In addition, despite the unchanged (MUFA+PUFA)/SFA ratio, the membrane erythrocyte fatty acid content showed a significant increase in PUFAs and a decrease in TRANS, suggesting enhanced membrane fluidity. In conclusion, it seems that high-altitude exposure, besides quantitative variations in RBC expression, induced plasma oxidative stress and damage, and significant changes in erythrocyte components, namely in antioxidant enzyme activity and membrane fatty acid profile that might modify RBC functionality.

Adaptation, Physiological↗

PubMed2004

[Mental stimulation strategy affects postural control].

Recent studies have proposed that the mental rotation of body parts can be accomplished by calling upon visual and somatomotor resources which, at a functional level, would correspond to different routes toward a single solution [1]. In this study, we investigated the effect of somato-motor and visual strategies upon the mental simulation of a task that involved postural adjustments. Subjects were asked to stand up on a vertical force platform and instructed either to 1) rest during 20 s (ST), 2) count mentally from 1 to 15 (CO), 3) imagine themselves executing a bilateral plantar flexion 15 times (IM), and 4) execute the same movement 15 times (EX). They were further classified as visual or somato-motor dominant, according to the strategy reported as adopted to perform IM. Mental chronometry showed that mean time spent in IM matched that of EX, differing from CO for both groups. Index of stabilometric modulation during IM was computed by reference to CO. Higher index values for area and amplitude of displacement in the antero posterior (y) axis were found for the somato-motor as compared to the visual group. The stabilometric departure found for visual and somato-motor dominant subjects suggests that each imagery mode activates a distinct subset of cortical and subcortical brain networks.

Adult↗

PubMed2004

Oxidative stress in humans during and after 4 hours of hypoxia at a simulated altitude of 5500 m.

BACKGROUND: High-altitude hypoxia may induce oxidative stress in humans. However, the effect of acute, severe, and non-acclimatized short-term hypobaric hypoxia exposure in humans has not been described. Additionally, little is known regarding the confounding role of reoxygenation in the extent of oxidative stress and damage markers in hypoxia. Our goals were to analyze the effect of of hypobaric hypoxia and reoxygenation on plasma oxidative stress and oxidative damage. METHODS: There were six male volunteers exposed to a simulated altitude of 5500 m (52.52 kPa) in the INEFC-UB hypobaric chamber over 4 h and returned to sea level (SL) in 30 min. Data were collected at baseline SL at 1 h and 4 h of hypoxia at 5500 m and immediately after return to sea level (RSL). RESULTS: Elevated scores of acute mountain sickness (13) and significant changes in arterial oxygen saturation (97.5 +/- 0.5; 53.3 +/- 1.9; 97.1 +/- 0.3%, p < 0.05 at SL, 4 h, and RSL, respectively) were observed. Significant reductions (p < 0.05) on total glutathione (TGSH) content were measured from SL and 1 h vs. 4 h and RSL. The percentage of oxidized glutathione (%GSSG) as an indicator of redox oxidative changes increased significantly (SL vs. 1 h; 1 h vs. 4 h, and RSL). Lipid peroxidation (TBARS), protein oxidation (SH protein groups), and total antioxidant status (TAS) followed the redox changes suggested by the glutathione system throughout the protocol. CONCLUSIONS: Hypobaric hypoxia increased the burden of plasma oxidative stress and damage markers all through the hypoxia period. However, no additional changes were observed with reoxygenation at the end of the reoxygenation period.

Acute Disease↗

PubMed2003

Acute and severe hypobaric hypoxia-induced muscle oxidative stress in mice: the role of glutathione against oxidative damage.

This study intended to analyze: (1) the effects of acute and severe hypoxia exposure on skeletal muscle oxidative stress and oxidative damage markers; (2) the protective role of the antioxidant glutathione against oxidative damage; and (3) the expression of heat shock protein 70 kDa (HSP70) induced by this hypoxic insult. Forty mice were divided into four groups: control + placebo (C+P), hypoxia + placebo (H+P), control + l-buthionine-[ S, R]-sulfoximine (BSO, a GSH-depleting compound) (C+BSO) and hypoxia + BSO (H+BSO). Hypoxia groups were continuously exposed for 24 h to a hypobaric hypoxic environment equivalent to an altitude of 7000 m and sacrificed immediately after. Control groups were maintained at sea level during the experimental protocol. Analyzed biochemical parameters were: reduced (GSH) and oxidized (GSSG) glutathione, thiobarbituric acid reactive substances (TBARS), sulfhydryl protein groups (SH), N-acetyl-beta- d-glucosaminidase (NAG) and HSP70 protein. Hypoxia (H+P) per se, compared to C+P, induced a significant increase in %GSSG (5.68 vs. 1.14%), TBARS (436.7 vs. 227.9 nM), NAG (4.49 vs. 3.35 U/mg) and HSP70 (178.7 vs. 100%). Compared with H+P, H+BSO showed a significant decrease in total glutathione (19.30 vs. 6.13 nmol/mg) and an additional increase in %GSSG (5.68 vs. 11.33%) and in HSP70 expression (178.7 vs. 202.2%). However, no further oxidative damage was observed in H+BSO. These data suggest that acute hypoxia per se might enhance oxidative stress; however, the glutathione system seems to have a modest role in skeletal muscle protection against hypoxia-induced oxidative stress. Moreover, hypoxia and BSO treatment is a sufficient stimulus to promote HSP70 overexpression.

Acute Disease↗

PubMed2003

Exercise and cardiac oxidative stress.

Cardiac muscle is frequently affected by many stimuli responsible for loss of cell homeostasis, including physical exercise. While exercise has been presented as a recommended activity for health reasons, it also provides favorable conditions for additional production of reactive oxygen species. These compounds are associated with fundamental mechanisms of cell metabolism but are also related to the etiology and pathophysiology of some cardiac diseases. Cardiac muscle tissue has a high oxidative metabolic rate and relatively low activity of the main antioxidant enzymes, which could enhance its susceptibility to oxidative injury after acute exercise. However, physical training could be considered an important stimulus for the different antioxidant systems like glutathione and those related to the activity of some important antioxidant enzymes in myocardial protection such as superoxide dismutase and glutathione peroxidase. Endurance training seems to induce up-regulation in some antioxidant defenses, protecting cardiac muscle in potentially harmful situations that induce additional oxidative stress. Nevertheless, the mechanisms related to this cross-tolerance effect of training are not yet well understood.

Animals↗