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A Doença de Alzheimer (DA), é um tipo de demência progressiva, que se agrava ao longo do tempo, apresentando perda das funções cognitivas, reduzindo assim a capacidade do indivíduo no trabalho e nas relações sociais de forma gradativa. O acompanhamento de um idoso com DA produz desgaste psicológico, físico e financeiro para o cuidador, pois o tratamento é dispendioso e o paciente irá evoluir para um quadro de total dependência. Nos casos em que o cuidador também é membro familiar questões emocionais e psicológicas mais complexas e fortes são somadas. Entender essa realidade é o ponto de partida para melhorar as condições do cuidador familiar. Percebeu-se a importância de enfatizar a necessidade de uma assistência ao membro familiar e cuidador do indivíduo com DA.

A Doença de Parkinson (DP) é uma desordem neurodegenerativa que compro­mete os neurônios dopaminérgicos da substância nigra da pars compacta, a qual leva a uma debilitante disfunção motora. O estresse oxidativo tem sido constantemente associado com o desenvolvimento da DP devido às elevadas condições oxidativas que predomina nos neurônios dopaminérgicos. Acredita-se que o exercí­cio fí­sico regular exerça um efeito neuroprotetor sobre a resposta neuroquí­mica e comportamental. Pretende-se com este estu­do verificar na literatura os benefí­cios do exercí­cio fí­sico (EF) no envolvimento da disfunção mitocondrial e do estresse oxidativo, os quais exercem um papel importante na patogênese desta enfermidade. Com este estudo, pôde-se observar que existem poucos trabalhos na literatura enfocando esta temática, mas parece haver uma tendência em acreditar que o exercí­cio fí­sico regular é benéfico, pois pode proporcionar valor terapêutico para o tratamento da doença de Parkinson, uma ferramenta que auxilia a terapia medicamentosa.Palavras-chave: exercí­cio fí­sico, estresse oxidativo, espécies reativas de oxigênio, doença de Parkinson.Â

AIM To identify anthropometric indicators that could predict pelvic floor muscle distress (PFMD) in young women. METHOD A cross-sectional study was conducted, whose sample consisted of 54 women aged between 18 and 35 years. The Pelvic Floor Distress Inventory was used to assess the PFMD. The anthropometric indicators evaluated were body mass index (BMI) being measured the weight and height, body fat percentage (skinfolds), waist circumference (WC), waist-to-hip ratio (WHR), and relative fat mass (RFM), which is calculated from height and WC. Descriptive and inferential statistics (Spearman correlation, simple linear regression, and receiver operating characteristic curve) were used, with a significance level of 5%. RESULTS The PFMD and the anthropometric indicators BMI (r = .43), body fat percentage (r = .42), WC (r = .46), WHR (r = .49), and RFM (r = .48) showed a positive and moderate correlation (P

Obesity is associated with low-grade chronic inflammation and oxidative stress, affecting the brain's reward system by decreasing dopaminergic neurotransmission. It is known that dopaminergic neurotransmission is also reduced in Parkinson's disease (PD), and high adiposity is considered a risk factor for the development of several neurodegenerative diseases, including PD. This study aimed to assess the effects of obesity on neuroinflammatory and neurochemical parameters in an animal model of reserpine-induced PD. The obese group showed increased inflammation and oxidative damage as well as inhibition of mitochondrial respiratory chain complexes I and II and DNA damage in the evaluated structures. The PD group did not show inflammation or mitochondrial dysfunction but exhibited oxidative damage in the hippocampus. The combination group (obesity + PD) showed reduced inflammation and oxidative stress and increased activity of complexes I and II of the mitochondrial respiratory chain in most of the analyzed structures. On the other hand, obesity + PD caused oxidative damage to proteins in the liver, prefrontal cortex, striatum, and cerebral cortex and oxidative stress in the hypothalamus, resulting in reduced catalase activity. Furthermore, the combination group showed DNA damage in blood, liver, and cerebral cortex. In conclusion, it was observed that the association of obesity and PD did not increase inflammation, oxidative stress, or mitochondrial dysfunction in most of the evaluated structures but increased oxidative damage and induced mechanisms that led to DNA damage in peripheral tissues and brain structures.

Orientações são essenciais para prevenir complicações durante e após a internação hospitalar. Este trabalho teve como objetivo relatar a experiência da implantação de dois projetos no Sul de Santa Catarina, com o intuito de utilizar a orientação como estratégia de educação, prevenção e tratamento em indivíduos hospitalizados. As atividades foram implantadas na enfermaria do Hospital Regional de Araranguá, no período de março a dezembro de 2019, possibilitando o acompanhamento de 243 pacientes. O acompanhamento foi feito mediante uma triagem, avaliação e intervenção através de orientações que incluíam informação com relação ao cuidado, fornecimento de material impresso e realização de atividades para promoção da movimentação corporal. Espera-se que as ações destes projetos tenham contribuído com a formação acadêmica dos alunos e com a prestação de serviços para a comunidade, incluindo a redução de complicações relacionadas à restrição ao leito durante e após a internação hospitalar.

Major depressive disorder (MDD) is one of the most prevalent forms of mental illness also affecting older adults. Recent evidence suggests a relationship between MDD and neurodegenerative diseases, including Parkinson's disease (PD). Individuals with PD have a predisposition to developing MDD, and both neurobiological conditions are associated with oxidative stress. Thus, we conducted this study to investigate depressive-like behavior and oxidative stress parameters using both animal models of PD and stress. Adult Wistar rats were subjected to chronic mild stress (CMS) protocol by 40 days and then it was used 6-hydroxydopamine (6−OHDA) as a model of PD, into the striatum. The experimental groups were: Control + Sham, Stress + Sham, Control+6−OHDA, and Stress+6−OHDA. Depressive like-behavior was evaluated by the forced swimming test (FST) and spontaneous locomotor activity by open-field test. Oxidative stress parameters were measured in the striatum, hippocampus, and prefrontal cortex (PFC). The results showed effects to increase immobility and decrease climbing times in the FST in Stress + Sham, Control+6−OHDA, and Stress+6−OHDA groups. The number of crossings and rearings were decreased in the Stress+6−OHDA group. The lipid peroxidation was increased in the PFC of Stress + Sham, and the hippocampus and striatum of Stress + Sham and Control+6−OHDA groups. Carbonyl protein levels increased in the PFC of Stress + Sham and striatum in Control+6−OHDA. Nitrite/Nitrate concentration was elevated in the PFC of Stress + Sham, in the hippocampus of Control+6−OHDA, the striatum of Stress + Sham, and Control+6−OHDA groups. Myeloperoxidase (MPO) activity was increased in the PFC and hippocampus of Stress + Sham and Control+6−OHDA groups. The activity of catalase decreased in the PFC of the Stress + Sham group. The activity of the superoxide dismutase (SOD) was decreased in the PFC of the Stress + Sham group, in the hippocampus of Stress + Sham and Control+6−OHDA groups, and the striatum of Control+6−OHDA group. These findings suggest that both stress and 6−OHDA induce depressive-like behavior and oxidative stress in the brain. The joining models have little evidence of the effects. Thus these findings suggest that other pathways are involved in the common point of the pathophysiology of PD and MDD.

OBJECTIVE Test the association between the practice of physical activity (PA) according to the gestational trimesters and the occurrence of cesarean delivery, prematurity, and low birth weight in puerperal women assisted in the Unified Health System of Santa Catarina, Brazil. METHODS A cross-sectional study was conducted with a probabilistic sample of puerperal women who gave birth in public maternity hospitals in Santa Catarina from January to August 2019. The cesarean delivery outcome was self-reported, and information on premature birth (< 37 gestational weeks) and low birth weight (< 2,500 grams) were obtained from medical records. The practice of PA during pregnancy and according to each trimester was self-reported. Multivariate Logistic Regression analyses and interviews with 3,580 puerperal women were carried out. RESULTS PA practice during any period of pregnancy was reported by 20.6% of the sample, with a gradual reduction in prevalence according to the gestational trimester (16.2%, 15.4%, and 12.8%). The highest prevalences of outcomes concerning the total sample were observed in puerperal women who did not practice PA in the third trimester, with 43.9% for cesarean delivery, 7.7% for low birth weight, and 5.5% for premature birth. The odds of cesarean delivery (OR = 1.40; 95%CI 1.10–1.76) and low birth weight (OR = 1.99; 95%CI 1.04–3.79) were, respectively, 40% and 99% higher among puerperal women who did not practice PA in the third trimester of pregnancy when compared to those who practiced PA. There was no association between PA practice and prematurity. CONCLUSION Puerperal women who did not practice PA in the third trimester of pregnancy were more likely to have cesarean delivery and low birth weight newborns.

Blood brain barrier (BBB) permeability and oxidative stress have been reported to be important mechanisms for brain damage following ischemic stroke and stanniocalcin-1 (STC-1), a neuroprotective protein, has anti-inflammatory and anti-oxidative stress properties. Herein, we report the effect of STC-1 on BBB permeability and brain oxidative stress after stroke in an animal model. Male Wistar received an intracerebroventricularly injection of human recombinant STC-1 (100 ng/kg) or saline and were subjected to sham procedure or global cerebral ischemia/reperfusion (I/R) model. Six and 24 h after I/R, neurological evaluation was performed; at 24 h brain water content was evaluated in the total brain, and BBB permeability, nitrite/nitrate (N/N) concentration, lipid peroxidation, protein carbonyls formation, superoxide dismutase (SOD) and catalase (CAT) activity were determined in the hippocampus, cortex, prefrontal cortex, striatum and cerebellum. Rats exhibited neurological deficit at 6 and 24 h after I/R and STC-1 reduction at 24 h. After I/R there were an increase of brain water content, BBB permeability in the hippocampus, cortex and pre-frontal cortex and N/N in the hippocampus, and STC-1 decreased this level only in the hippocampus. STC-1 decreased lipid peroxidation in the hippocampus, cortex and prefrontal cortex and protein oxidative damage in the hippocampus and cortex. SOD activity decreased in the hippocampus, cortex and prefrontal cortex after I/R and STC-1 reestablished these levels in the hippocampus and cortex. CAT activity decreased only in the hippocampus and cortex and STC-1 increased the CAT activity in the hippocampus. Our data provide the first experimental demonstration that STC-1 reduced brain dysfunction associated with cerebral I/R in rats, by decreasing BBB permeability and oxidative stress parameters.

The aim of the study described here was to investigate the effects of pulsed ultrasound and gold nanoparticles (AuNPs) on behavioral, inflammatory and oxidative stress parameters in an experimental model of overuse. Wistar rats performed 21 d of exercise on a treadmill at different intensities and were exposed to ultrasound in the presence or absence of AuNPs. The overuse model promoted behavioral changes and increased creatine kinase, superoxide dismutase and glutathione peroxidase activity, as well as the levels of superoxide, nitrotyrosine, nitric oxide, thiobarbituric acid reactive substance, carbonyl, tumor necrosis factor α and interleukin-6. These values were significantly decreased by AuNPs and by AuNPs plus ultrasound. Catalase activity remained unchanged and the glutathione level increased significantly after exposure to AuNPs plus ultrasound. These results suggest a susceptibility to anxiety as well as elevated levels of oxidative stress. However, therapeutic interventions with AuNPs plus ultrasound reduced the production of oxidants and oxidative damage and improved the anti-oxidant defense system.

Despite decades of research, the fundamental neurochemical and molecular mechanisms underlying the major depressive disorder (MDD) are still poorly understood, and current antidepressant treatments have limited clinical efficacy. In clinical conditions, the rapprochement between the disease and the corrective actions of drugs in laboratory animals is essential for developing effective therapies. Thus, the aim of this study was to evaluate the antidepressant effects of ketamine (N-metil- d -asparte (NMDA) receptor antagonist), minocycline (tetracycline antibiotic), and amitriptyline (classical antidepressant), on behavior and oxidative stress parameters in animals submitted to the chronic mild stress (CMS) and maternal deprivation protocols. For this aim, male Wistar rats were submitted to maternal deprivation or CMS. To induce maternal deprivation, Wistar rats were deprived of maternal care during the first 10 days of life. To induce CMS, Wistar rats were submitted to the CMS for 40 days. To reverse the effects of stress, treatment was done intraperitoneally with a single dose of ketamine (15 mg/kg), and minocycline (25 mg/kg) and amitriptyline (10 mg/kg) by 20 days. After treatment, the animals were submitted to the forced swimming test and then analyzed oxidative stress parameters in the prefrontal cortex (PFC), hippocampus, amygdala and nucleus accumbens (NAc). Treatment with ketamine, minocycline and amitriptyline were able to exert antidepressant effects in the forced swimming test. However, these antidepressant effects were dependent on the stress model by which the animals were exposed. In certain brain regions some treatment strategies had a pro-oxidant effect. Though, most of the strategies used in this study had antioxidant effects, as reported by a decrease on protein and lipid damage, nitrite/nitrate concentration and myeloperoxidase activity. In addition, an increase in the antioxidant superoxide dismutase (SOD) and catalase (CAT) enzymes activities were also evident after treatments. In conclusion, the antidepressant effects of ketamine and minocycline, in the present study, may be associated, at least in part, with its antioxidant and neuroprotective effects in animals subjected to maternal deprivation or CMS.

Exercise increases both the consumption of oxygen and the production of reactive species in biological tissues, and this is counterbalanced by antioxidant adaptations to regular physical training. When the intensity of exercise fluctuates between mild and moderate, it improves the status of reduction-oxidation balance in the brain and induces neuroplasticity. However, intense exercise can oxidize the brain and impair neurological function. The effect of the frequency of exercise, which is an important factor in physical training, is still unknown. The effect of periodic exercise on biomarkers of oxidative stress in the hippocampus of mice was evaluated in this study. Mice were made to run on a treadmill for 8 weeks, two, three, or five times per week, and their hippocampi and quadriceps femoris muscles were then dissected. Biomarkers of oxidative damage were negatively correlated with the frequency of exercise and mitochondrial muscular activity, while the sulfhydryl contents were positively correlated with exercise frequency. A logistic analysis revealed a dose-dependent effect of exercise on these biomarkers. In summary, these results suggested that manipulating the frequency of physical exercise could induce antioxidant-related adaptations in the hippocampi of adult mice.

The purpose of the present study was to investigate the effects of taurine supplementation on muscle performance, oxidative stress, and inflammation response after eccentric exercise (EE) in males. Twenty-one participants (mean age, 21 ± 6 years; weight, 78.2 ± 5 kg; height, 176 ± 7 cm) were selected and randomly divided into two groups: placebo (n = 10) and taurine (n = 11). Fourteen days after starting supplementation, subjects performed EE (3 sets until exhaustion, with EE of the elbow flexors on the Scott bench, 80% 1 repetition maximum (RM)). Blood samples were collected and muscle performance was measured on days 1, 14, 16, 18, and 21 after starting the supplements. Then, performance, muscle damage, oxidative stress, and inflammatory markers were analyzed. The taurine supplementation resulted in increased strength levels and thiol total content and decreased muscle soreness, lactate dehydrogenase level, creatine kinase activity, and oxidative damage (xylenol and protein carbonyl). Antioxidant enzymes (superoxide dismutase, catalase, and gluthatione peroxidase) and inflammatory markers (tumor necrosis factor, interleukin-1β (IL-1β), and interleukin-10 (IL-10)) were not altered during the recovery period compared with the placebo group. The results suggest that taurine supplementation represents an important factor in improving performance and decreasing muscle damage and oxidative stress but does not decrease the inflammatory response after EE.

Com aumento da expectativa de vida os indivíduos vem alcançando idade mais avançada e desenvolvendo doenças neurodegenerativas como a doença de Alzheimer. Uma doença que leva danos cognitivos, proprioceptivas e a demência. Se apresenta em três estágios: Estagio 1: No inicio da doença com problemas moderados de memória como esquecimento; Estagio 2: o indivíduos necessita de cuidados ocorre perda da funcionalidade, temporalidade e esquecimentos, perda de memória recentes, a interpretação dos estímulos é prejudicada. Não consegue mais realizar suas atividades diárias sozinho. Estagio 3: perda quase completa da capacidades cognitiva, completa dependência de um cuidador. Métodos Foram realizadas buscas sistematizadas em bases de dados eletrônicas (Scielo, Pubmed, Google Acadêmico). Resultados e conclusão: Os estudos analisados sugerem a eficácia da Fisioterapia, na melhora da função motora, para manter o equilíbrio, a força e a cognição em pacientes com DA. Além disso, exercício está associado com menor prevalência e incidência de demência (32%), bem como de declínio cognitivo. a Biomedicina é muito importante para auxiliar nas áreas que envolvam avaliações da qualidade de vida deste paciente, criar estratégias educativas, de prevenção, promoção e intervenção na busca de uma velhice bem-sucedida junto aos familiares e cuidadores.

The objective of the present study was to investigate the effects of eccentric training on the activity of mitochondrial respiratory chain enzymes, oxidative stress, muscle damage, and inflammation of skeletal muscle. Eighteen male mice (CF1) weighing 30-35 g were randomly divided into 3 groups (N = 6): untrained, trained eccentric running (16°; TER), and trained running (0°) (TR), and were submitted to an 8-week training program. TER increased muscle oxidative capacity (succinate dehydrogenase and complexes I and II) in a manner similar to TR, and TER did not decrease oxidative damage (xylenol and creatine phosphate) but increased antioxidant enzyme activity (superoxide dismutase and catalase) similar to TR. Muscle damage (creatine kinase) and inflammation (myeloperoxidase) were not reduced by TER. In conclusion, we suggest that TER improves mitochondrial function but does not reduce oxidative stress, muscle damage, or inflammation induced by eccentric contractions.

Major depressive disorder (MDD) is one of the most prevalent and life-threatening forms of mental illnesses affecting elderly people and has been associated with poor cognitive function. Recent evidence suggests a strong relationship between MDD and neurodegenerative diseases, including Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease (HD), Amyotrophic Lateral Sclerosis (ALS), as well as natural processes of aging. Changes in the neuroplasticity, morphology, and neurotransmission in the brain are seem to be associated to both, MDD and neurodegenerative diseases. In addition, there is evidence that psychological stress and MDD are associated with molecular and cellular signs of accelerated aging. This review will highlight the relationship between MDD, the aging process, and neurodegenerative diseases, emphasizing the neurochemical processes involved.

Major depressive disorder (MDD) affects approximately 121 million individuals globally and poses a significant burden to the healthcare system. Around 50-60% of patients with MDD respond adequately to existing treatments that are primarily based on a monoaminergic system. However, the neurobiology of MDD has not been fully elucidated; therefore, it is possible that other biochemical alterations are involved. The glutamatergic system and its associated receptors have been implicated in the pathophysiology of MDD. In fact, the N-methyl-d-aspartate (NMDA) receptor, a glutamate receptor, is a binding or modulation site for both classical antidepressants and new fast-acting antidepressants. Thus, this review aims to present evidence describing the effect of antidepressants that modulate NMDA receptors and the mechanisms that contribute to the antidepressant response.

Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS) caused by demyelination, immune cell infiltration, and axonal damage. Herein, we sought to investigate the influence of physical exercise on mice experimental autoimmune encephalomyelitis (EAE), a reported MS model. Data show that both strength and endurance training protocols consistently prevented clinical signs of EAE and decreased oxidative stress, an effect which was likely due to improving genomic antioxidant defense-nuclear factor erythroid 2-related factor (Nrf2)/antioxidant response elements (ARE) pathway-in the CNS. In addition, physical exercise inhibited the production of pro-inflammatory cytokines interferon (IFN)-γ, interleukin (IL)-17, and IL-1β in the spinal cord of mice with EAE. Of note, spleen cells obtained from strength training group incubated with MOG35-55 showed a significant upregulation of CD25 and IL-10 levels, with a decrease of IL-6, MCP-1, and tumor necrosis factor (TNF)-α production, mainly, during acute and chronic phase of EAE. Moreover, these immunomodulatory effects of exercise were associated with reduced expression of adhesion molecules, especially of platelet and endothelial cell adhesion molecule 1 (PECAM-1). Finally, physical exercise also restored the expression of tight junctions in spinal cord. Together, these results demonstrate that mild/moderate physical exercise, when performed regularly in mice, consistently attenuates the progression and pathological hallmarks of EAE, thereby representing an important non-pharmacological intervention for the improvement of immune-mediated diseases such as MS. Graphical Abstract Schematic diagram illustrating the beneficial effects of physical exercise during experimental model of MS. Physical exercise, especially strength (ST) and endurance (ET) training protocols, inhibits the development and progression of disease, measured by the mean maximal clinical score (1.5 and 1.0, respectively), with inhibition of 30 % and 50 %, respectively, based on the AUC, compared with EAEuntreated group. In addition, ST and ET decreased oxidative stress, possibly, through genomic antioxidant defense, Nrf2-Keap1 signaling pathway, in the CNS. Physical exercise inhibited the production of inflammatory cytokines, such as IFN-γ, IL-17 and IL-1β in the spinal cord after EAE induction, as well as spleen cells obtained from ST group showed a significant upregulation of regulatory T cell markers, such as CD25 and IL-10 levels, and blocked IL-6, MCP-1 and TNF-α production, mainly, during acute and chronic phase of EAE. Finally, these immunomodulatory effects of exercise were associated with inhibition of adhesion molecules and reestablishment of tight junctions expression in spinal cord tissue, thereby limiting BBB permeability and transmigration of autoreactive T cells to the CNS. NO, nitric oxide; GPx, glutathione peroxidase, GSH, glutathione; Nrf2, nuclear factor (erythroid-derived 2)-like 2; CNS, central nervous system; BBB, blood-brain barrier; IFN-g, interferon-gamma; IL-17, interleukin 17; IL-1b, interleukin-1beta.

Major depressive disorder (MDD) affects approximately 121 million individuals globally and poses a significant burden to the healthcare system. Around 50-60% of patients with MDD respond adequately to existing treatments that are primarily based on a monoaminergic system. However, the neurobiology of MDD has not been fully elucidated; therefore, it is possible that other biochemical alterations are involved. The glutamatergic system and its associated receptors have been implicated in the pathophysiology of MDD. In fact, the N-methyl-d-aspartate (NMDA) receptor, a glutamate receptor, is a binding or modulation site for both classical antidepressants and new fast-acting antidepressants. Thus, this review aims to present evidence describing the effect of antidepressants that modulate NMDA receptors and the mechanisms that contribute to the antidepressant response.

It is well known that high-fat diets (HFDs) induce obesity and result in an increase in oxidative stress in adipose tissue, which leads to an impairment of fat mobilization by a downregulation of the lipases, such as hormone-sensitive lipase (HSL) and adipose triglyceride lipase (ATGL). On the other hand, exercise training leads to a reduction in adipose tissue and an improvement of antioxidant status and the lipolytic pathway. Our aim was to examine the influence of exercise and moderate intensity training on oxidative stress parameters and the relationship between the proteins involved in the lipolysis of animals subjected to a high-fat fed diet. Twenty-four mice were used and divided into 4 groups (n=6): standard diet (SD); standard diet plus exercise (SD+Ex); high-fat diet (HFD); and high-fat diet plus exercise (HFD+Ex). The animals received HFD for 90 days and submitted to a daily training protocol in swinging. The animals were euthanized 48 h after the last session of exercise. White adipose tissue epididymal fat was excised for the measurement of oxidative stress parameters and protein levels of lipolytic enzymes by Western blotting. The results show an increase in body weight after 90 days of HFD, and exercise training prevented great gain. In adipose tissue, lipid peroxidation and protein carbonylation increased after HFD and decreased significantly after exercise training. The protein level of CGI-58 was reduced, and FAS was increased in the HFD than in SD, whereas ATGL exhibited an increase (p0.05) in HFD than in SD. The exercise plays a significant role in reducing oxidative damage, along with the regulation of proteins that are involved in the lipolysis of animals exposed to HFD.

The objective of the present study was to investigate the effects of exercise training on behavior and neurochemical parameters in mice exposed to cigarette smoke. To this aim, mice (C57 BL6) male (30-35 g) were exposed to cigarette smoke 60 consecutive days three times a day and they were subjected to treadmill training 8 weeks for 5 days/week. For behavior assessment, mice were tested in the open-field and forced to a swim test. The superoxide anion, thiobarbituric acid reactive substances and protein carbonyl formation were measured as markers of oxidative stress in hippocampus of mice. In addition, the brain-derived neurotrophic factor (BDNF) levels were measured in the hippocampus samples. Cigarette smoke group and cigarette smoke plus exercise group, increased immobility time in forced swimming test in rats compared to the control group, without affecting spontaneous locomotor activity. There was an increase in the levels of superoxide, TBARS and of protein carbonyl and a decreased in BDNF levels in the hippocampus of rats exposed to cigarette smoke and cigarette smoke plus exercise. Exercise alone did not change any of the parameters evaluated in this study. In conclusion, we observed that physical training improves the oxidative stress parameters, but does not alter depressive-like behavior neither prevent the decreases in BDNF levels in hippocampus induced by cigarette smoke.

INTRODUÇÃO: O uso terapêutico do laser de baixa potência na fisioterapia tem aumentado significativamente. OBJETIVO: Avaliar os efeitos da laserterapia de baixa potência nos parâmetros oxidativos na cicatrização de feridas em ratos. MÉTODOS: Dezoito ratos Wistar foram divididos randomicamente em 3 grupos (controle 5 dias, n=6; 5 dias/2 J/cm², n=6; 5 dias/4 J/cm², n=6). Uma única ferida circular medindo 8 X 8 mm foi cirurgicamente realizada no dorso do rato. Trinta minutos após a última irradiação, os ratos foram submetidos à eutanásia, e o tecido irradiado foi removido cirurgicamente e armazenado a -70ºC. Foi determinada a atividade das enzimas da cadeia respiratória: DCIP oxirredutase (complexo II) e succinato desidrogenase solúvel (SDH), atividade do citocromo c oxidase (complexo IV), produção de ânion superóxido, atividade da superóxido dismutase (SOD) e catalase (CAT). A lipoperoxidação foi avaliada pela técnica de TBARS. RESULTADOS: Os resultados mostram uma diminuição na atividade do complexo II nos grupos irradiados por 5 dias com 2 e 4 J/cm², enquanto a produção de ânion superóxido mostrou uma diminuição significativa no grupo irradiado por 5 dias com 4 J/cm² em relação ao grupo controle. Além disso, um aumento significativo na atividade da catalase foi observado no grupo irradiado por 5 dias com 2 J/cm², como também uma diminuição da peroxidação lipídica nos dois grupos irradiados. CONCLUSÕES: Os resultados do presente estudo indicam que o laser estimula a atividade antioxidante e protege a célula contra danos oxidativos durante o processo de cicatrização de feridas cutâneas em ratos. BACKGROUND: Therapeutic use of low-level laser in physical therapy has increased significantly. OBJECTIVE: To assess the effects of low-level laser therapy on the oxidative parameters of wound healing in rats. METHODS: Eighteen Wistar rats were randomly divided into three groups (control, 5 days, n=6; 2 J/cm², 5 days, n=6; 4 J/cm², 5 days, n=6). A single circular wound measuring 8 x 8 mm was surgically created on the rats' backs. Thirty minutes after the last irradiation, the rats were euthanized and the irradiated tissue was surgically removed and stored at -70°C. We determined the activity of the respiratory chain enzymes DCIP oxidoreductase (complex II) and soluble succinate dehydrogenase (SDH); the activity of cytochrome c oxidase (complex IV); the production of superoxide anion; and the activity of superoxide dismutase (SOD) and catalase (CAT). Lipid peroxidation was assessed by means of the TBARS assay. RESULTS: There was a decrease in the complex II activity in the groups irradiated for 5 days with 2 and 4 J/cm², while superoxide anion production decreased significantly in the group irradiated for 5 days with 4 J/cm² when compared with the control group. There was also a significant increase in CAT activity in the group irradiated for 5 days with 2 J/cm² as well as a decrease in lipid peroxidation activity in the two irradiated groups. CONCLUSIONS: The results of the present study indicate that laser stimulates antioxidant activity and protects cells against oxidative damage during the wound healing process in rats.

The objective of the study was to verify the effect of N-acetylcysteine (NAC) supplementation on parameters of oxidative damage and inflammatory response after high-intensity eccentric exercise (EE). 29 participants with a mean age of 21.3 ± 4 yr, weight of 74.5 ± 7.7 kg, and height of 177.2 ± 6.9 cm were selected and divided randomly into 3 groups: placebo (21 days; n = 8), NAC (21 days; n = 9), and NAC plus placebo (14 days; n = 8). Four participants withdrew from the study for personal reasons. 14 days after starting supplementation, the participants performed EE: 3 sets until exhaustion (elbow flexion and extension on the Scott bench, 80% 1RM). Blood samples were collected before and on the 2nd, 4th, and 7th day after EE. Muscle soreness (MS), lipoperoxidation, protein carbonylation, tumor-necrosis factor-cc(TNF-(), and interleukin 10 (IL-10) were determined. Results showed a significant increase in MS in all the groups on the 2nd day after EE and a decrease in the following days. A significant increase was observed in malondialdehyde and carbonyl levels on the 4th and 7th days after EE in all groups. TNF-EEincreased significantly on the 2nd day after eccentric exercise and decreased in the following days irrespective of NAC supplementation; concentration of IL-10 increased significantly on the 4th day in all groups. Only the supplemented groups maintained high levels of IL-10 on the 7th day after EE. The results suggest that treatment with NAC represents an important factor in the defense against muscle soreness and has different effects on oxidative damage and pro- and anti-inflammatory cytokines.

Twenty-four adult male CF1 mice were assigned to three groups: non-runners control, level running exercise (0 degrees incline) and downhill running exercise (16 degrees decline). Exercise groups were given running treadmill training for 5 days/week over 8 weeks. Blood lactate analysis was performed in the first and last exercise session. Mice were sacrificed 48 h after the last exercise session and their solei (citrate synthase activity) and brain cortices (BDNF levels and cytochrome c oxidase activity) were surgically removed and immediately stored at -80 degrees C for later analyses. Training significantly increased (P

There are conflicts between the effects of free radical over-production induced by exercise on neurotrophins and brain oxidative metabolism. The objective of this study was to investigate the effects of intense physical training on brain-derived neurotrophic factor (BDNF) levels, COX activity, and lipoperoxidation levels in mice brain cortex. Twenty-seven adult male CF1 mice were assigned to three groups: control untrained, intermittent treadmill exercise (3 × 15 min/day) and continuous treadmill exercise (45 min/day). Training significantly (P

This study aimed to evaluate the effects of two different protocols for physical exercise (strength and aerobic training) on mitochondrial and inflammatory parameters in the 6-OHDA experimental model of Parkinson’s disease. Six experimental groups were used (n=12per group): untrained + vehicle (Sham), strength training + vehicle (STR), treadmill training + vehicle (TTR), untrained + 6-OHDA (U + 6-OHDA), strength training + 6-OHDA (STR + 6-OHDA), and treadmill training + 6-OHDA (TTR + 6-OHDA). The mice were subjected to strength or treadmill training for 8 weeks. PD was inducedviastriatal injection of 6-OHDA 24 h after the last exercise session. Mice were euthanized by cervical dislocation and the striatum and hippocampus were homogenized to determine levels of tyrosine hydroxylase (TH), nuclear factor kappa B (NF-κB) p65, and sirtuin 1 (Sirt1) by western blot; tumor necrosis factor-α(TNF-α), interleukin-1β(IL-1β), IL-17, interferon-γ(IFN-γ), and transforming growth factorβ1 (TGF-β1) levels by ELISA; NO content; and complex I (CI) activity. STR + 6-OHDA mice had higher TH levels and CI activity and lower NF-κB p65 and IFN-γlevels in the striatum compared to U + 6-OHDA mice, while TTR + 6-OHDA mice had higher Sirt1 levels and CI activity in both the striatum and the hippocampus, compared to U + 6-OHDA mice. Strength training increased CI activity and TH and Sirt1 levels and reduced NO, NF-κB p65, TNF-α, IFN-γ, IL-1β, and TGF-β1 levels in 6-OHDA mice, while treadmill exercise increased CI activity and NO, TH, and Sirt1 levels and reduced NF-κB p65, TNF-α, IFN-γ, and IL-1βlevels. Our results demonstrated that both treadmill training and strength training promote neuroprotection, possibly by stimulating Sirt1 activity, which may in turn regulate both mitochondrial function and neuroinflammationviadeacetylation of NF-κB p65. Changes in nitric oxide levels may also be a mechanism by which 6-OHDA-induced inflammation is controlled.

Estudos têm apontado o exercício físico regular de baixa a moderada intensidade como um importante agente no combate ao estresse oxidativo. O objetivo deste estudo foi investigar o efeito do exercício físico regular na resposta oxidativa pulmonar após a inalação de pó de carvão mineral. Vinte e quatro ratos Wistar machos (200-250g) foram divididos aleatoriamente em dois grupos com respectivos controles (treinado, n = 6 e não-treinado, n = 6). Os animais receberam, por instilação traqueal, pó de carvão mineral (3mg/0,5ml salina, três dias/semana, durante três semanas) ou 0,5ml de solução salina 0,9%. Quarenta e oito horas após a última instilação, o grupo treinado foi submetido a um programa de exercício progressivo em esteira durante 12 semanas (até 17m.min-1, 50min.dia-1, 10% de inclinação). Quarenta e oito horas após a última sessão de treinamento, todos os animais foram mortos por decapitação e os pulmões e sóleo foram cirurgicamente removidos para posterior análise bioquímica. A atividade da citrato-sintase foi determinada no músculo sóleo e os danos em lipídios e proteínas foram avaliados nos pulmões pela concentração de TBARS e pela determinação de grupos carbonil, respectivamente. Os resultados mostram que a prática regular de exercício físico reduz significativamente os níveis presentes de TBARS em ratos treinados e diminui os níveis de oxidação em proteínas em ambos os grupos quando comparados com os respectivos controles. Os resultados nos levam a sugerir que o exercício físico regular em esteira é um agente capaz de amenizar os danos oxidativos pulmonares induzidos pela inalação de partículas de carvão mineral.Los estudios han estado apuntando el ejercicio físico regular de intensidad baja a moderada como un agente importante en el combate a la tensión oxidativa. El objetivo de ese estudio era investigar el efecto del ejercicio físico para regular la respuesta oxidativa pulmonar después de la inhalación de polvo de carbón mineral. Veinticuatro ratones varones Wistar (200-250g) fueron aleatoriamente divididos en 2 grupos con los mandos respectivos (, n = 6 y Ningún -, n = 6). Los animales recibieron, por instilación traqueal polvo de carbón mineral (3mg/0,5ml salina, 3 dias/semana, durante 3 semanas) o 0,5ml de solución salina 0,9%. Cuarenta ocho horas después de la última instilación, el grupo especializado fue sometido a un programa de ejercicio progresivo en la cinta durante 12 semanas (a 17m.min-1, 50min.dia-1, 10% de inclinación). Cuarenta ocho horas después de la última sesión de entrenamiento, todos los animales fueron sacrificados por decapitación y los pulmones y el músculo sóleo fueron extirpados por cirugía para el análisis bioquímico subsecuente. La actividad de la citrato-sintetasa fue determinada en los músculos así como los daños y perjuicios en los lipidos y las proteínas se estimaron en los pulmones para la concentración de TBARS y para la determinación de carbonilo de estos grupos, respectivamente. Los resultados mostraron que el ejercicio físico regular reduce los niveles presentes de TBARS significativamente en los ratones especializados y reduce los niveles de la oxidación en las proteínas en ambos grupos cuando se compararon los grupos respectivos. Los resultados permitieron sugerir que el ejercicio físico regular en la cinta es un agente capaz minimizarlos daños y perjuicios oxidativos pulmonares inducidos por la inhalación de partículas de carbón mineral.Several studies have pointed the regular low to moderate intensity physical exercise an important agent to combat the oxidant stress. The purpose of this study was to investigate the effect of the physical exercise in the pulmonary oxidant response after inhaling mineral coal dust. Twenty-four male Wistar rats (200-250 g) were randomly divided in two groups with their respective controls (trained, n = 6; non-trained, n = 6). All animals received mineral coal dust via tracheal instillation (saline 3 mg/0.5 ml, 3 days/week for 3 weeks), or 0.5 ml of 0.9% saline solution. Forty-eight hours after the last instillation, the trained group was submitted to a progressive exercise program on treadmill for twelve weeks (up to 17 m.min-1, 50 min/day-1, 10% inclination). Forty-eight hours after the last training session, every animal was killed by decapitation, and their lungs and soleus were surgically removed for later biochemical analysis. The citrate synthase activity was determined in the soleus muscle, and the damages on the lipids and proteins were assessed into the lungs by means of the TBARS concentration and by determining the carbonyl groups, respectively. The results show that the regular practice of physical exercises reduces significantly the present TBARS levels in trained rats, decreasing the oxidation levels in proteins of both groups compared to their respective controls. The results lead us to suggest that the regular physical exercise on treadmill is an agent capable to soften the pulmonary oxidant damages caused by inhaling mineral coal particles.

Los estudios han estado apuntando el ejercicio fisico regular de intensidad baja a moderada como un agente importante en el combate a la tension oxidativa. El objetivo de ese estudio era investigar el efecto del ejercicio fisico para regular la respuesta oxidativa pulmonar despues de la inhalacion de polvo de carbon mineral. Veinticuatro ratones varones Wistar (200-250g) fueron aleatoriamente divididos en 2 grupos con los mandos respectivos (, n = 6 y Ningun -, n = 6). Los animales recibieron, por instilacion traqueal polvo de carbon mineral (3mg/0,5ml salina, 3 dias/semana, durante 3 semanas) o 0,5ml de solucion salina 0,9%. Cuarenta ocho horas despues de la ultima instilacion, el grupo especializado fue sometido a un programa de ejercicio progresivo en la cinta durante 12 semanas (a 17m.min-1, 50min.dia-1, 10% de inclinacion). Cuarenta ocho horas despues de la ultima sesion de entrenamiento, todos los animales fueron sacrificados por decapitacion y los pulmones y el musculo soleo fueron extirpados por cirugia para el analisis bioquimico subsecuente. La actividad de la citrato-sintetasa fue determinada en los musculos asi como los danos y perjuicios en los lipidos y las proteinas se estimaron en los pulmones para la concentracion de TBARS y para la determinacion de carbonilo de estos grupos, respectivamente. Los resultados mostraron que el ejercicio fisico regular reduce los niveles presentes de TBARS significativamente en los ratones especializados y reduce los niveles de la oxidacion en las proteinas en ambos grupos cuando se compararon los grupos respectivos. Los resultados permitieron sugerir que el ejercicio fisico regular en la cinta es un agente capaz minimizarlos danos y perjuicios oxidativos pulmonares inducidos por la inhalacion de particulas de carbon mineral.

Depression is a neuropsychiatric disorder that is commonly found in patients with Parkinson's disease (PD). Many studies have suggested that physical exercise can have an antidepressant effect by increasing the levels of brain-derived neurotrophic factor (BDNF), and may also prevent neurodegenerative disease. However, different forms of training may promote different changes in the brain. The aim of this study was to investigate the effects of two types of physical training on depressive-like behavior, and on the levels of proBDNF, BDNF, and its receptor, TrkB, in a mouse model of PD. C57BL/6 mice were subjected to 60 days of exercise: either running on a treadmill or performing a strength exercise. PD was induced by striatal administration of 6-OHDA 24 h after the last physical exercise session. Seven days after 6-OHDA injection, depressive-like behavior and apomorphine-induced rotational behavior were evaluated. The levels of proBDNF, BDNF, and TRKB were measured in the striatum and the hippocampus of mice by immunoblotting assay. The 6-OHDA-treated animals showed a significant increase in immobility time and rotational behavior compared with the control group. In addition, significant decreases in the levels of proBDNF, BDNF, and its receptor, TrkB were observed in the 6-OHDA group. Both types of physical exercise prevented depressive-like behavior and restored the levels of proBDNF, BDNF, and TrkB in the striatum and hippocampus of mice administered 6-OHDA. Our results demonstrate that exercise training was effective for neuroprotection in the striatum and the hippocampus in an experimental model of PD.

The effect of physical training on the neurochemical and oxidative stress markers were evaluated in the striatum of rats with Parkinson's disease (PD). Untrained+sham-operated (USO), untrained+PD (UPD), trained+sham-operated (TSO), and trained+PD (TPD) were submitted to training on the treadmill. The PD was induced and 7 days after the lesion, the animals underwent a rotational test and euthanasia by decapitation. The striatum was homogenized for Western Blot with anti-tyrosine hydroxylase (TH), anti-brain-derived neurotrophic factor (BDNF), anti-α-synuclein, anti-sarcoplasmic reticulum Ca(2+)-ATPase (SERCA II), anti-superoxide dismutase (SOD), anti-catalase (CAT), anti-glutathione peroxidase (GPX), and specific buffer for oxidative damage (TBARS and carbonyl content). The UPD and TPD groups showed a clear rotational asymmetry, apart from a significant reduction in the level of TH, BDNF, α-synuclein, SOD, CAT, and GPX as well as an increase in the TBARS and carbonyl content, as observed in the UPD group. The TH level was not significantly altered but the TPD group increased the levels of BNDF, SERCA II, SOD, and CAT and decreased the oxidative damage in lipids and protein. The effects of exercise on PD indicate the possibility that exercise, to a certain extent, modulates neurochemical status in the striatum of rats, possibly by improving the oxidative stress parameters.

During the muscle contraction induced by exercises there is an increase in the reactive oxygen species production, causing oxidative stress in several organs, including liver and heart. The exercise may can increases antioxidant defenses and decrease oxidative stress in these organs. However, the number of the sessions a week necessary to improve the parameters of oxidative stress is not to well defined. The aim of the study was to investigate the frequency effects of exercise performed two and three times a week on changes in biomarkers of oxidative stress in the liver and heart. Were used 18 male mice (CF1), young (30 to 35g) and divided into groups (n=6/group): not trained (NT) trained twice a week (T2) and trained three times a week (T3). The animals were subjected to training for eight weeks. Forty-eight hours after the last session, the animals were killed. The liver and heart were removed and stored in - 70°C. Were analyzed the thiobarbituric acid reactive substances, protein carbonyls, content of total thiols, superoxide dismutase, catalase and glutathione peroxidase. Our findings showed that the group T3 reduced oxidative damage. There was increase in content of total thiols, superoxide dismutase and catalase in the T3 group when compared to NT. The glutathione peroxidase activity showed no significant difference between groups. This study demonstrated that only the frequency of training performed three times a week was able to reduces oxidative damage and increases the efficiency of antioxidant system of mice. Durante a contração muscular intensa induzida pelo exercício físico, há aumento na produção de espécies reativas de oxigênio, ocasionando estresse oxidativo em diversos órgãos, dentre eles o fígado e o coração. O treinamento físico pode aumentar as defesas antioxidantes e diminuir o estresse oxidativo. Contudo, ainda existem dúvidas sobre a frequência de treinamento necessária para melhorar parâmetros de estresse oxidativo. Este trabalho tem como objetivo verificar o efeito das frequências de duas e três vezes de exercício por semana sobre biomarcadores de estresse oxidativo no fígado e coração. Foram utilizados 18 camundongos machos (CF1), jovens (30 a 35g) divididos em grupos (n=6/grupo): não treinado (NT); treinado duas vezes por semana (T2) e treinado três vezes por semana (T3). Os animais foram submetidos ao treinamento durante oito semanas. Quarenta e oito horas após a última sessão os animais foram sacrificados. O fígado e o coração foram removidos e armazenados em freezer – 70ºC. Foram analisadas as substâncias reativas ao ácido tiobarbitúrico, carbonilação de proteínas, conteúdo total de tióis, atividades da superóxido dismutase , catalase e glutationa peroxidase. Os resultados demonstraram que apenas o grupo T3 reduziu dano oxidativo. Ademais, houve aumento no conteúdo total de tióis, atividades da superóxido dismutase e catalase no mesmo grupo em comparação com o não treinado. A atividade da glutationa peroxidase não apresentou diferença significativa entre os grupos. Este estudo demonstrou que somente a frequência de treinamento de três vezes por semana reduz dano oxidativo e aumenta a eficiência do sistema enzimático antioxidante de camundongos.

The purpose of this study was to investigate the effects of vitamin E supplementation on muscular and oxidative damage, as well as the inflammatory response induced by eccentric exercise (EE) in humans. Twenty-one participants with a mean age of 22.5 +/- 4 years, weight of 68.2 +/- 4.9 kg, and height of 173 +/- 4.3 cm were selected and divided randomly into two groups: supplemented (S) (n = 11) and placebo (P) (n = 10). Fourteen days after starting supplementation, subjects performed EE (three sets until exhaustion with elbow flexion and extension on the Scott bench, 80% 1 RM). Blood samples were collected on days 0, 2, 4, and 7 after EE. Muscle soreness (MS), lactate dehydrogenase (LDH) activity, lipid peroxidation, protein carbonylation, tumor necrosis factor-alpha (TNF-alpha), and interleukin 10 (IL-10) levels were determined. We measured a significant increase in MS, LDH, lipid peroxidation, and carbonylation in both groups on days 2, 4, and 7 after eccentric contractions (EC). Values of the supplement group were lower than those of the placebo group at 4 and 7 days after EC in all parameters. Both groups showed significantly increased TNF-alpha on the second day and IL-10 concentration on the fourth and seventh days after EE. The results suggest that vitamin E supplementation represents an important factor in the defense against oxidative stress and muscle damage but not against the inflammatory response in humans.

Considerable evidence has indicated a pro-oxidant status in the brain of people with Down's syndrome (DS), which may contribute to motor and cognitive impairments verified in this condition. On the other hand, previous studies addressing the role of physical exercise on oxidative stress and antioxidant status in DS have indicated conflicting results. Here, we investigated the effects of a supervised judo training of controlled intensity and monitored on the basis of lactate threshold on the blood oxidative stress status and motor coordination in 21 young adults with DS. The training extended over a period of 16 weeks and consisted of three sessions per week. The exercise improved the motor function and significantly decreased lactate production in the DS subjects. However, blood markers of oxidative damage to lipids (TBARS and lipid peroxides) and proteins (carbonyls) were increased by the judo training. Moreover, superoxide dismutase and catalase activity also increased, while glutathione peroxidase activity remained unaltered after exercise. These results reinforce the notion that physical exercise can improve motor disabilities in people with DS. More importantly, our findings demonstrate that the beneficial effects are accompanied by some degree of oxidative stress, suggesting that young adults with DS may be more susceptible to physical training-induced oxidative stress than adolescents with DS, which should be taken into account in physical training programs for this population.