Photobiomodulation therapy before futsal matches improves the staying time of athletes in the court and accelerates post-exercise recovery.

This study aimed to analyze PBMT effects on futsal player's performance and recovery in a non-controlled field environment. It is a randomized, triple-blinded, placebo-controlled, crossover clinical trial. The research included six professional athletes and in each match phototherapy treatments were performed before matches (40 minutes), blood samples were collected before treatments, and samples immediately after the end of the matches and 48 h after. Furthermore, videos were analyzed to quantify the time athletes spent on the pitch and the distance they covered. PBMT was performed at 17 sites of each lower limb (40 mins before matches), employing a cluster with 12 diodes (4 laser diodes of 905 nm, 4 LEDs of 875 nm, and 4 LEDs of 640 nm, 30 J per site). The performance of the athlete could be quantified considering the time on the pitch and the distance covered; the biochemical markers evaluated were creatine kinase, lactate dehydrogenase, blood lactate, and oxidative damage to lipids and proteins. PBMT significantly increased the time of staying in the pitch and a significant improvement in all the biochemical markers evaluated. No statistically significant difference was found for the distance covered. Pre-exercise PBMT can enhance performance and accelerate recovery of high-level futsal players.

Antioxidants inhibit the inflammatory and apoptotic processes in an intermittent hypoxia model of sleep apnea.

BACKGROUND: Sleep apnea causes intermittent hypoxia (IH). We aimed to investigate the proteins related to oxidative stress, inflammation and apoptosis in liver tissue subjected to IH as a simulation of sleep apnea in conjunction with the administration of either melatonin (MEL, 200 µL/kg) or N-acetylcysteine (NAC, 10 mg/kg). METHODS: Seventy-two adult male Balb-C mice were divided: simulation of IH (SIH), SIH + MEL, SIH + NAC, IH, IH + MEL and IH + NAC. The animals were subjected to simulations of sleep apnea for 8 h a day for 35 days. The data were analyzed with ANOVA and Tukey tests with the significance set at p < 0.05. RESULTS: In IH, there was a significant increase in oxidative stress and expression of HIF-1a. In addition, we observed increase in the activation levels of NF-kB. This increase may be responsible for the increased expression of TNF-alpha and iNOS as well as the significant increase of VEGF signaling and expression of caspase-3 and caspase-6, which suggests an increase in apoptosis. In the groups treated with antioxidants, the analysis showed that the enzyme activity and protein levels were similar to those of the non-simulated group. CONCLUSIONS: Thus, we show that IH causes liver inflammation and apoptosis, which may be protected with either MEL or NAC.

N-acetylcysteine administration confers lung protection in different phases of lung ischaemia-reperfusion injury.

OBJECTIVES: To verify the effects of N-acetylcysteine (NAC) administered before and after ischaemia in an animal model of lung ischaemia-reperfusion (IR) injury. METHODS: Twenty-four Wistar rats were subjected to an experimental model of selective left pulmonary hilar clamping for 45 min followed by 2 h of reperfusion. The animals were divided into four groups: control group (SHAM), ischaemia-reperfusion, N-acetylcysteine-preischaemia (NAC-Pre) and NAC-postischaemia (NAC-Post). We recorded the haemodynamic parameters, blood gas analysis and histology. We measured the thiobarbituric acid reactive substances concentration; the expression of superoxide dismutase (SOD), inducible nitric oxide synthase (iNOS), nitrotyrosine, cleaved caspase 3, nuclear factor κB (NF-κB), NF-kappa-B inhibitor alpha (IκB-α), tumour necrosis factor alpha (TNF-α) and interleukin-1 beta (IL-1ß); myeloperoxidase activity (MPO). RESULTS: No significant differences were observed in the haemodynamic parameters, blood gas analysis and SOD activity among the groups. Lipid peroxidation was significantly higher in the IR and NAC-Pre groups (P < 0.01). The expression of nitrotyrosine, cleaved caspase 3, NF-κB, IκB-α, TNF-α and IL-1ß were significantly higher in the IR group when compared with the SHAM and NAC groups (P < 0.01). The NAC-Pre group showed a significantly higher expression of these proteins when compared with the SHAM and NAC-Post groups (P < 0.05). After reperfusion, the expression of iNOS increased almost uniformly in all groups when compared with the SHAM group (P < 0.01). The histological analysis showed fewer inflammatory cells in the NAC groups. CONCLUSIONS: The intravenous administration of NAC demonstrated protective properties against lung IR injury. The use of NAC immediately after reperfusion potentiates its protective effects.

Downregulation of uncoupling protein-1 mRNA expression and hypoadiponectinemia in a mouse model of sleep apnea.

PURPOSE: The knowledge on the effect of intermittent hypoxia on adipose tissue-mediated processes is incipient. The aim of the present study was to assess the effect of a sleep apnea model on a limited set of specific molecular, biochemical, histological, and behavioral parameters of adipose tissue function. METHODS: Mice were exposed to either intermittent hypoxia or sham hypoxia during 8 h a day for 37 days. Uncoupling protein-1 expression in brown adipose tissue was measured by real-time PCR and immunohistochemistry. Digital quantification of adipose cells and immunohistochemistry of uncoupling protein-1 were performed to determine cell dimensions, positive area, and staining intensity. Serum levels of leptin, adiponectin, and cortisol were measured by ELISA. RESULTS: In comparison with the control group, animals in the hypoxia group had significantly lower chow ingestion, weight gain, and smaller white and brown adipocytes on histological examination. Adiponectin levels were also lower in the hypoxia group. Uncoupling protein-1 mRNA was abolished in the mice exposed to hypoxia; accordingly, fewer cells positive for uncoupling protein-1 and lighter staining intensity were observed in brown adipocytes. CONCLUSIONS: An experimental model of sleep apnea produced changes in uncoupling protein-1 expression and adiponectin levels. These results confirm previous findings on the response of brown adipose tissue to intermittent hypoxia and indicate a yet-unknown interference of intermittent hypoxia on energy control, which may participate in the propensity to weight gain observed in patients with sleep apnea. Brown adipose tissue activity in this patient population needs to be further investigated.

Chromosome instability and oxidative stress markers in patients with ataxia telangiectasia and their parents.

Ataxia telangiectasia (AT) is a rare neurodegenerative disorder, inherited in an autosomal recessive manner. Total blood samples were collected from 20 patients with AT, 13 parents of patients, and 17 healthy volunteers. This study aimed at evaluating the frequency of chromosomal breaks in spontaneous cultures, induced by bleomycin and ionizing radiation, and further evaluated the rates of oxidative stress in AT patients and in their parents, compared to a control group. Three cell cultures were performed to each individual: the first culture did not receive induction to chromosomal instability, the second was exposed to bleomycin, and the last culture was exposed to ionizing radiation. To evaluate the rates of oxidative stress, the markers superoxide dismutase (SOD), catalase (CAT), and thiobarbituric acid (TBARS) were utilized. Significant differences were observed between the three kinds of culture treatments (spontaneous, bleomycin, and radiation induced) and the breaks and chromosomal aberrations in the different groups. The oxidative stress showed no significant differences between the markers. This study showed that techniques of chromosomal instability after the induction of ionizing radiation and bleomycin are efficient in the identification of syndrome patients, with the ionizing radiation being the most effective.

Endobronchial perfluorocarbon administration decreases lung injury in an experimental model of ischemia and reperfusion.

OBJECTIVE: To verify the effects of liquid endobronchial perfluorocarbon (PFC) administered before reperfusion in an animal model of lung ischemia-reperfusion injury. METHODS: Eighteen Wistar rats were subjected to an experimental model of selective left pulmonary artery clamping for 45 min followed by reperfusion for 2 h. The animals were divided into three groups: the ischemia-reperfusion (IR) group, the sham group, and the PFC group. We recorded the hemodynamic parameters, blood gas analysis, and histology. A Western blot assay was used to measure the inducible nitric oxide synthase, caspase 3, and nuclear factor қB (subunit p65) activities. Lipid peroxidation was assessed by the thiobarbituric acid reactive substances assay and the activity of the antioxidant enzyme superoxide dismutase. RESULTS: No significant differences were observed in lipid peroxidation among the groups. The superoxide dismutase activity was increased (P < 0.05) in the PFC-treated group. The expressions of nuclear factor қB, inducible nitric oxide synthase, and caspase 3 were significantly lower in the PFC group than in the IR group (P < 0.05). The histologic analysis showed a reduction in lung injuries in the PFC group compared with the sham and IR groups. CONCLUSION: The use of endobronchial PFC reduces the inflammatory response, preserves the alveolar structure, and protects the lungs against the hazardous effects of ischemia-reperfusion injuries.

Endobronchial perfluorocarbon reduces inflammatory activity before and after lung transplantation in an animal experimental model.

BACKGROUND: The aim of this study was to evaluate the use of liquid perfluorocarbon (PFC) as an adjuvant substance for lung preservation and assess its role in pulmonary protection after transplantation. METHODS: Seventy-two rat lungs were flushed with low-potassium dextran (LPD) solution and randomized into three main groups: control with LPD alone and experimental with 3 (PFC3) and 7 mL/kg (PFC7) of endobronchial PFC instilled just after harvest. Each group was divided into four subgroups according to preservation time (3, 6, 12, and 24 hours). Afterwards, we performed lung transplantation using rat lungs preserved for 12 hours with LPD alone or with 7 mL/kg of endobronchial PFC. RESULTS: There was a significant increase in oxidative stress in the control group at 6 h of cold ischemic time compared with the PFC3 and PFC7 groups. The apoptotic activity and NF-κB expression were significantly higher in the control group compared with the PFC groups at 3, 12, and 24 h of cold preservation. After transplantation, the NF-κB, iNOS, and nitrotyrosine expression as well as caspase 3 activity were significantly lower in the PFC groups. CONCLUSION: The use of endobronchial PFC as an adjuvant to the current preservation strategy improved graft viability.

Simulating sleep apnea by exposure to intermittent hypoxia induces inflammation in the lung and liver.

Sleep apnea is a breathing disorder that results from momentary and cyclic collapse of the upper airway, leading to intermittent hypoxia (IH). IH can lead to the formation of free radicals that increase oxidative stress, and this mechanism may explain the association between central sleep apnea and nonalcoholic steatohepatitis. We assessed the level of inflammation in the lung and liver tissue from animals subjected to intermittent hypoxia and simulated sleep apnea. A total of 12 C57BL/6 mice were divided into two groups and then exposed to IH (n = 6) or a simulated IH (SIH) (n = 6) for 35 days. We observed an increase in oxidative damage and other changes to endogenous antioxidant enzymes in mice exposed to IH. Specifically, the expression of multiple transcription factors, including hypoxia inducible factor (HIF-1α), nuclear factor kappa B (NF-κB), and tumor necrosis factor (TNF-α), inducible NO synthase (iNOS), vascular endothelial growth factor (VEGF), and cleaved caspase 3 were shown to be increased in the IH group. Overall, we found that exposure to intermittent hypoxia for 35 days by simulating sleep apnea leads to oxidative stress, inflammation, and increased activity of caspase 3 in the liver and lung.

The effect of taurine on hepatic steatosis induced by thioacetamide in zebrafish (Danio rerio).

BACKGROUND: Nonalcoholic fatty liver disease is one of the most prevalent forms of chronic liver disease in the Western world. Taurine is a conditionally essential amino acid in humans that may be a promising therapy for treating this disease. AIM: To evaluate the effect of taurine on hepatic steatosis induced by thioacetamide in Danio rerio. METHODS: Animals were divided into four groups: control (20 µl of saline solution), taurine (1,000 mg/kg), thioacetamide (300 mg/kg), and the taurine-thioacetamide group (1,000 + 300 mg/kg). Thioacetamide was injected intraperitoneally three times a week for 2 weeks. The mRNA expression, lipoperoxidation, antioxidant enzymatic activity, and histological analyses were evaluated in the liver and the triglyceride content was assessed in the serum. RESULTS: Thioacetamide injection induced steatosis, as indicated by histological analyses. The lipoperoxidation showed significant lipid damage in the thioacetamide group compared to the taurine-thioacetamide group (p < 0.001). Superoxide dismutase (SOD) activity in the taurine-thioacetamide group (5.95 ± 0.40) was significantly increased compared to the thioacetamide group (4.14 ± 0.18 U SOD/mg of protein) (p < 0.001). The mRNA expression of SIRT1 (0.5-fold) and Adiponectin receptor 2 (0.39-fold) were lower in the thioacetamide group than the control (p < 0.05). TNF-α mRNA expression was 6.4-fold higher in the thioacetamide group than the control (p < 0.05). SIRT1 mRNA expression was 2.6-fold higher in the taurine-thioacetamide group than in the thioacetamide group. CONCLUSIONS: Taurine seems to improve hepatic steatosis by reducing oxidative stress and increasing SIRT1 expression.

Oxidative stress and pulmonary changes in experimental liver cirrhosis.

The use of carbon tetrachloride (CCl(4)) in rats is an experimental model of hepatic tissue damage; which leads to fibrosis, and at the long term, cirrhosis. Cirrhosis is the consequence of progressive continued liver damage, it may be reversible when the damaging noxae have been withdrawn. The aim of this study is to evaluate the changes caused by cirrhosis in lung and liver, through the experimental model of intraperitoneal CCI(4) administration. We used 18 male Wistar rats divided into three groups: control (CO) and two groups divided by the time of cirrhosis induction by CCI(4): G1 (11 weeks), G2 (16 weeks). We found significant increase of transaminase levels and lipid peroxidation (TBARS) in liver and lung tissue and also increased antioxidant enzymes SOD and CAT, as well as the expression of TNF-α and IL-1ß in the lung of cirrhotic animals. We observed changes in gas exchange in both cirrhotic groups. We can conclude that our model reproduces a model of liver cirrhosis, which causes alterations in the pulmonary system that leads to changes in gas exchange and size of pulmonary vessels.