Effects of a 10 km race on physiological and immunological responses

Introduction: The number of 10 km running races has been increasing in Brazil and the number of finishers almost triplicated in the last decade. However, there is limited amount of data showing the relationship between this event and the immune system response. Aim: Investigate the effects of a 10 km running race on physiological and immunological response in healthy well trained male volunteers. Methods: Fourteen male participants (32,21 ± 10,24 years old, 78,80 ± 9,30 kg) took part in this study. Ratings of perceived exertion (RPE), visual analog scale (VAS), heart rate (HR) and blood samples were taken before, immediately and 24 hours after the race. Lactate, glucose, creatine kinase (CK) and C-reactive protein (CRP), as well as leukocyte number and subpopulation of T cell (CD4+ and CD8+) were analyzed. Results: Participants completed this race in 49,85 ± 7,04 min. There was a significant increase post-race compared to pre-race for HR (67 ± 9 to 159 ± 21 bpm), RPE (6 ± 0 to 15 ± 2) and lactate (3.6 to 6.6 mmol/dL). Glucose levels did not present any significant changes. CK level did not change immediately after the race, but was higher (131,21 ± 62,50 to 286,85 ± 234,35 U/L ) at the 24 h post-race time point. CRP was lower at 24 h (8,37 ± 2,23 to 4,50 ± 2,28 mg/dL). VAS values changed from 0 (before) to 5,64 ± 2,20 (immediately after) to 2,21 ± 2,86 (24 hours). The number of circulating leukocyte (5,83 ± 0,89 to 9,15 ± 1,77 103/µL), neutrophil (2,96 ± 0,49 to 4,34 ± 0,73 103/µL), lymphocyte (2,21 ± 0,57 to 3,92 ± 1,27 103/µL), monocyte (0,46 ± 0,10 to 0,64 ± 0,23 103/µL) and basophil (0,05 ± 0,02 to 0,09 ± 0,03 103/µL) increased significantly immediately after the race, returning to the basal level in 24 h. There was no difference in circulating eosinophils number. The absolute number of CD4+ (828,5 ± 215,8 to 1063,2 ± 235,3 cell/µL) and CD8+ (766,92 ± 347,79 to 1470,30 ± 782,90 cell/µL) also increased immediately after the race returning to basal in 24 h. Significant reduction of the CD4+/CD8+ lymphocyte subpopulation ratio (1,21 ± 0,45 to 0,85 ± 0,33 cell/µL) was observed post-race returning to basal level at 24 h post-race. Results are presented as mean ± SD. (p\u3c0,0001). Conclusion: These results suggest that a 10 km running race is an intense physical activity and induces physiological changes. In addition, intense running provokes a significantly, although transient, modulation of the immune system, specifically of leukocyte sub-population

The association between physical exercise and Reactive Oxygen Species (ROS) production.

The importance of exercise has been widely accepted by the public, professional organizations and the medical community, and the number of people around the world who practice day-to-day regular physical activity has recently increased. Physical activity is a primary requirement for the maintenance and promotion of health. However, intense exercise induces an increase in substrate utilization by the working muscles, resulting in an increased use of oxygen. This rise in oxygen consumption combined with the activation of specific metabolic pathways during or after exercise results in the generation of Reactive Oxygen Species (ROS). These substances are produced naturally by oxidative metabolic processes and are highly reactive. ROS can be useful in some situations; for example, macrophages use hydrogen peroxide to destroy bacteria. ROS increases during high-intensity exercise and its production is related to a large number of diseases, such as emphysema, inflammatory diseases, atherosclerosis, cancer and aging. During evolution, living organs developed an endogenous mechanism to minimize the damage caused by ROS, termed the antioxidant defense system. The imbalance between the production of ROS and the removal of these compounds by the antioxidant defense system causes a condition known as oxidative stress. This interesting paradox is exemplified by the hypothesis that physical exercises known to promote appropriate standards of health are also related to increased ROS production, which in turn closely correlate with various diseases. Recent publications have shown that ROS produced by exercise in adequate amounts may be linked to exercise benefits, both for health and for athletic performance. Thus, the aim of this article is to examine the close association between physical exercise and the production of ROS through an extensive literature review

Organotins in Neuronal Damage, Brain Function, and Behavior: A Short Review

The consequences of exposure to environmental contaminants have shown significant effects on brain function and behavior in different experimental models. The endocrine-disrupting chemicals (EDC) present various classes of pollutants with potential neurotoxic actions, such as organotins (OTs). OTs have received special attention due to their toxic effects on the central nervous system, leading to abnormal mammalian neuroendocrine axis function. OTs are organometallic pollutants with a tin atom bound to one or more carbon atoms. OT exposure may occur through the food chain and/or contaminated water, since they have multiple applications in industry and agriculture. In addition, OTs have been used with few legal restrictions in the last decades, despite being highly toxic. In addition to their action as EDC, OTs can also cross the blood–brain barrier and show relevant neurotoxic effects, as observed in several animal model studies specifically involving the development of neurodegenerative processes, neuroinflammation, and oxidative stress. Thus, the aim of this short review is to summarize the toxic effects of the most common OT compounds, such as trimethyltin, tributyltin, triethyltin, and triphenyltin, on the brain with a focus on neuronal damage as a result of oxidative stress and neuroinflammation. We also aim to present evidence for the disruption of behavioral functions, neurotransmitters, and neuroendocrine pathways caused by OTs

The Pollutant Organotins Leads to Respiratory Disease by Inflammation: A Mini-Review

Organotins (OTs) are organometallic pollutants. The OTs are organometallic pollutants that are used in many industrial, agricultural, and domestic products, and it works as powerful biocidal compound against large types of microorganisms such as fungi and bacteria. In addition, OTs are well known to be endocrine-disrupting chemicals, leading abnormalities an “imposex” phenomenon in the female mollusks. There are some studies showing that OTs’ exposure is responsible for neural, endocrine, and reproductive dysfunctions in vitro and in vivo models. However, OTs’ effects over the mammalian immune system are poorly understood, particularly in respiratory diseases. The immune system, as well as their cellular components, performs a pivotal role in the control of the several physiologic functions, and in the maintenance and recovery of homeostasis. Thus, it is becoming important to better understand the association between environmental contaminants, as OTs, and the physiological function of immune system. There are no many scientific works studying the relationship between OTs and respiratory disease, especially about immune system activation. Herein, we reported studies in animal, humans, and in vitro models. We searched studies in PUBMED, LILACS, and Scielo platforms. Studies have reported that OTs exposure was able to suppress T helper 1 (Th1) and exacerbate T helper 2 (Th2) response in the immune system. In addition, OTs’ contact could elevate in the airway inflammatory response, throughout a mechanism associated with the apoptosis of T-regulatory cells and increased oxidative stress response. In addition, OTs induce macrophage recruitment to the tissue, leading to the increased necrosis, which stimulates an inflammatory cytokines secretion exacerbating the local inflammation and tissue function loss. Thus, the main intention of this mini-review is to up to date the main findings involving the inflammatory profile (especially Th1 and Th2 response) in the respiratory tract as a result of OTs’ exposure

PPAR-α Deletion Attenuates Cisplatin Nephrotoxicity by Modulating Renal Organic Transporters MATE-1 and OCT-2

Cisplatin is a chemotherapy drug widely used in the treatment of solid tumors. However, nephrotoxicity has been reported in about one-third of patients undergoing cisplatin therapy. Proximal tubules are the main target of cisplatin toxicity and cellular uptake; elimination of this drug can modulate renal damage. Organic transporters play an important role in the transport of cisplatin into the kidney and organic cations transporter 2 (OCT-2) has been shown to be one of the most important transporters to play this role. On the other hand, multidrug and toxin extrusion 1 (MATE-1) transporter is the main protein that mediates the extrusion of cisplatin into the urine. Cisplatin nephrotoxicity has been shown to be enhanced by increased OCT-2 and/or reduced MATE-1 activity. Peroxisome proliferator-activated receptor alpha (PPAR-α) is the transcription factor which controls lipid metabolism and glucose homeostasis; it is highly expressed in the kidneys and interacts with both MATE-1 and OCT-2. Considering the above, we treated wild-type and PPAR-α knockout mice with cisplatin in order to evaluate the severity of nephrotoxicity. Cisplatin induced renal dysfunction, renal inflammation, apoptosis and tubular injury in wild-type mice, whereas PPAR-α deletion protected against these alterations. Moreover, we observed that cisplatin induced down-regulation of organic transporters MATE-1 and OCT-2 and that PPAR-α deletion restored the expression of these transporters. In addition, PPAR-α knockout mice at basal state showed increased MATE-1 expression and reduced OCT-2 levels. Here, we show for the first time that PPAR-α deletion protects against cisplatin nephrotoxicity and that this protection is via modulation of the organic transporters MATE-1 and OCT-2

Chronic Kidney Disease Induced by Cisplatin, Folic Acid and Renal Ischemia Reperfusion Induces Anemia and Promotes GATA-2 Activation in Mice

Anemia is a common feature of chronic kidney disease (CKD). It is a process related to erythropoietin deficiency, shortened erythrocyte survival, uremic erythropoiesis inhibitors, and disordered iron homeostasis. Animal models of CKD-induced anemia are missing and would be desirable in order to study anemia mechanisms and facilitate the development of novel therapeutic tools. We induced three different models of CKD in mice and evaluated the development of anemia characteristics. Mice were subjected to unilateral ischemia-reperfusion or received repeated low doses of cisplatin or folic acid to induce nephropathy. Renal function, kidney injury and fibrotic markers were measured to confirm CKD. Moreover, serum hemoglobin, ferritin and erythropoietin were analyzed. Renal mRNA levels of HIF-2α, erythropoietin, hepcidin, GATA-2, and GATA-2 target genes were also determined. All three CKD models presented increased levels of creatinine, urea, and proteinuria. Renal up-regulation of NGAL, KIM-1, and TNF-α mRNA levels was observed. Moreover, the three CKD models developed fibrosis and presented increased fibrotic markers and α-SMA protein levels. CKD induced decreased hemoglobin and ferritin levels and increased erythropoietin levels in the serum. Renal tissue showed decreased erythropoietin and HIF-2α mRNA levels, while an increase in the iron metabolism regulator hepcidin was observed. GATA-2 transcription factor (erythropoietin repressor) mRNA levels were increased in all CKD models, as well as its target genes. We established three models of CKD-induced anemia, regardless of the mechanism and severity of kidney injury

The Pollutant Organotins Leads to Respiratory Disease by Inflammation: A Mini-Review

Organotins (OTs) are organometallic pollutants. The OTs are organometallic pollutants that are used in many industrial, agricultural, and domestic products, and it works as powerful biocidal compound against large types of microorganisms such as fungi and bacteria. In addition, OTs are well known to be endocrine-disrupting chemicals, leading abnormalities an ?imposex? phenomenon in the female mollusks. There are some studies showing that OTs? exposure is responsible for neural, endocrine, and reproductive dysfunctions in vitro and in vivo models. However, OTs? effects over the mammalian immune system are poorly understood, particularly in respiratory diseases. The immune system, as well as their cellular components, performs a pivotal role in the control of the several physiologic functions, and in the maintenance and recovery of homeostasis. Thus, it is becoming important to better understand the association between environmental contaminants, as OTs, and the physiological function of immune system. There are no many scientific works studying the relationship between OTs and respiratory disease, especially about immune system activation. Herein, we reported studies in animal, humans, and in vitro models. We searched studies in PUBMED, LILACS, and Scielo platforms. Studies have reported that OTs exposure was able to suppress T helper 1 (Th1) and exacerbate T helper 2 (Th2) response in the immune system. In addition, OTs? contact could elevate in the airway inflammatory response, throughout a mechanism associated with the apoptosis of T-regulatory cells and increased oxidative stress response. In addition, OTs induce macrophage recruitment to the tissue, leading to the increased necrosis, which stimulates an inflammatory cytokines secretion exacerbating the local inflammation and tissue function loss. Thus, the main intention of this mini-review is to up to date the main findings involving the inflammatory profile (especially Th1 and Th2 response) in the respiratory tract as a result of OTs? exposure

Organotin Exposure and Vertebrate Reproduction: A Review

Organotin (OTs) compounds are organometallic compounds that are widely used in industry, such as in the manufacture of plastics, pesticides, paints, and others. OTs are released into the environment by anthropogenic actions, leading to contact with aquatic and terrestrial organisms that occur in animal feeding. Although OTs are degraded environmentally, reports have shown the effects of this contamination over the years because it can affect organisms of different trophic levels. OTs act as endocrine-disrupting chemicals (EDCs), which can lead to several abnormalities in organisms. In male animals, OTs decrease the weights of the testis and epididymis and reduce the spermatid count, among other dysfunctions. In female animals, OTs alter the weights of the ovaries and uteri and induce damage to the ovaries. In addition, OTs prevent fetal implantation and reduce mammalian pregnancy rates. OTs cross the placental barrier and accumulate in the placental and fetal tissues. Exposure to OTs in utero leads to the accumulation of lipid droplets in the Sertoli cells and gonocytes of male offspring in addition to inducing early puberty in females. In both genders, this damage is associated with the imbalance of sex hormones and the modulation of the hypothalamic–pituitary–gonadal axis. Here, we report that OTs act as reproductive disruptors in vertebrate studies; among the compounds are tetrabutyltin, tributyltin chloride, tributyltin acetate, triphenyltin chloride, triphenyltin hydroxide, dibutyltin chloride, dibutyltin dichloride, diphenyltin dichloride, monobutyltin, and azocyclotin

Adipokines, diabetes and atherosclerosis: an inflammatory association

Cardiovascular diseases can be considered the most important cause of death in diabetic population and diabetes can in turn increase the risk of cardiovascular events. Inflammation process is currently recognized as responsible for the development and maintenance of diverse chronic diseases, including diabetes and atherosclerosis. Considering that adipose tissue is an important source of adipokines, which may present anti and proinflammatory effects, the aim of this review is to explore the role of the main adipokines in the pathophysiology of diabetes and atherosclerosis, highlighting the therapeutic options that could arise from the manipulation of these signaling pathways both in humans and in translational models