One of the most important functions of lungs is to maintain an adequate oxygenation in the organism. This organ can be affected by hypoxia facing both physiological and pathological situations. Exposure to this condition favors the increase of reactive oxygen species from mitochondria, as from NADPH oxidase, xanthine oxidase/reductase, and nitric oxide synthase enzymes, as well as establishing an inflammatory process. In lungs, hypoxia also modifies the levels of antioxidant substances causing pulmonary oxidative damage. Imbalance of redox state in lungs induced by hypoxia has been suggested as a participant in the changes observed in lung function in the hypoxic context, such as hypoxic vasoconstriction and pulmonary edema, in addition to vascular remodeling and chronic pulmonary hypertension. In this work, experimental evidence that shows the implied mechanisms in pulmonary redox state by hypoxia is reviewed. Herein, studies of cultures of different lung cells and complete isolated lung and tests conductedin vivoin the different forms of hypoxia, conducted in both animal models and humans, are described.

Okadaic acid-group (OA-group) is a set of lipophilic toxins produced only in seawater by species of the Dinophysis and Prorocentrum genera, and characterized globally by being associated with harmful algal blooms (HABs). The diarrhetic shellfish poisoning toxins okadaic acid (OA) and dinophysistoxin-1 (DTX-1) are the most prevalent toxic analogues making up the OA-group, which jeopardize environmental safety and human health through consumption of hydrobiological organisms contaminated with these toxins that produce diarrhetic shellfish poisoning (DSP) syndrome in humans. Consequently, a regulatory limit of 160 μg of OA-group/kg was established for marine resources (bivalves). The aim of this study was to investigate effects varying concentrations of 1–15 μg/ml OA or DTX-1 on toxicity, development, and oxidative damage in zebrafish larvae (Danio rerio). After determining the lethal concentration 50 (LC₅₀) in zebrafish larvae of 10 and 7 μg/ml (24 h) and effective concentration 50 (EC₅₀) of 8 and 6 μg/ml (24 h), different concentrations (5, 6.5, or 8 μg/ml of OA and 4, 4.5, or 6 μg/ml of DTX-1) were used to examine the effects of these toxins on oxidative damage to larvae at different time points between 24 and 120 hpf. Macroscopic evaluation during the exposure period showed alterations in zebrafish including pericardial edema, cyclopia, shortening in the anteroposterior axis, and developmental delay. The activity levels of biochemical biomarkers superoxide dismutase (SOD) and catalase (CAT) demonstrated a concentration-dependent decrease while glutathione peroxidase (GPx) and glutathione reductase (GR) were markedly elevated. In addition, increased levels of oxidative damage (malondialdehyde and carbonyl content) were detected following toxin exposure. Data demonstrate that high concentrations of OA and DTX-1produced pathological damage in the early stages of development <48 h post-fertilization (hpf) associated with oxidative damage.

The mechanisms involved in the generation of oxidative damage and lung inflammation induced by physical exercise are described. Changes in lung function induced by exercise involve cooling of the airways, fluid evaporation of the epithelial surface, increased contact with polluting substances, and activation of the local and systemic inflammatory response. The present work includes evidence obtained from the different types of exercise in terms of duration and intensity, the effect of both acute performance and chronic performance, and the influence of special conditions such as cold weather, high altitude, and polluted environments. Levels of prooxidants, antioxidants, oxidative damage to biomolecules, and cellularity, as well as levels of soluble mediators of the inflammatory response and its effects on tissues, are described in samples of lung origin. These samples include tissue homogenates, induced sputum, bronchoalveolar lavage fluid, biopsies, and exhaled breath condensate obtained in experimental protocols conducted on animal and human models. Finally, the need to simultaneously explore the oxidative/inflammatory parameters to establish the interrelation between them is highlighted.

One of the etiopathogenic factors frequently associated with generalized organ damage after spinal cord injury corresponds to the imbalance of the redox state and inflammation, particularly of the respiratory, autonomic and musculoskeletal systems. Our goal in this review was to gain a better understanding of this phenomenon by reviewing both animal and human studies. At the respiratory level, the presence of tissue damage is notable in situations that require increased ventilation due to lower thoracic distensibility and alveolar inflammation caused by higher levels of leptin as a result of increased fatty tissue. Increased airway reactivity, due to loss of sympathetic innervation, and levels of nitric oxide in exhaled air that are similar to those seen in asthmatic patients have also been reported. In addition, the loss of autonomic control efficiency leads to an uncontrolled release of catecholamines and glucocorticoids that induce immunosuppression, as well as a predisposition to autoimmune reactions. Simultaneously, blood pressure regulation is altered with vascular damage and atherogenesis associated with oxidative damage. At the muscular level, chronically elevated levels of prooxidants and lipoperoxidation associated with myofibrillar atrophy are described, with no reduction or reversibility of this process through antioxidant supplementation.

The aim of the present study was to determine the effects of three weeks of hyperbaric oxygen (HBO₂) training on oxidative stress markers and endurance performance in young soccer players. Participants (18.6±1.6 years) were randomized into hyperbaric-hyperoxic (HH) training (n=6) and normobaric normoxic (NN) training (n=6) groups. Immediately before and after the 5th, 10th, and 15th training sessions, plasma oxidative stress markers (lipid hydroperoxides and uric acid), plasma antioxidant capacity (6-hydroxy-2,5,7,8-tetramethylchroman-2-carboxylic acid [TROLOX]), arterial blood gases, acid-base balance, bases excess (BE), and blood lactate analyses were performed. Before and after intervention, maximal oxygen uptake (VO₂max) and peak power output (PPO) were determined. Neither HH nor NN experienced significant changes on oxidative stress markers or antioxidant capacity during intervention. VO₂max and PPO were improved (moderate effect size) after HH training. The results suggest that HBO₂ endurance training does not increase oxidative stress markers and improves endurance performance in young soccer players. Our findings warrant future investigation to corroborate that HBO₂ endurance training could be a potential training approach for highly competitive young soccer players.

This study aimed to evaluate if the changes in oxygen saturation levels at intercostal muscles (SmO₂-m.intercostales) assessed by near-infrared spectroscopy (NIRS) using a wearable device could determine the respiratory compensation point (RCP) during exercise. Fifteen healthy competitive triathletes (eight males; 29 ± 6 years; height 167.6 ± 25.6 cm; weight 69.2 ± 9.4 kg; $\dot{\mathrm{V}}$O₂-máx 58.4 ± 8.1 mL·kg⁻¹·min⁻¹) were evaluated in a cycle ergometer during the maximal oxygen-uptake test ($\dot{\mathrm{V}}$O₂-máx), while lung ventilation ($\dot{\mathrm{V}}$E), power output (watts, W) and SmO₂-m.intercostales were measured. RCP was determined by visual method (RCP_visual: changes at ventilatory equivalents ($\dot{\mathrm{V}}$E·$\dot{\mathrm{V}}$CO₂⁻¹, $\dot{\mathrm{V}}$E·$\dot{\mathrm{V}}$O₂⁻¹) and end-tidal respiratory pressure (PetO₂, PetCO₂) and NIRS method (RCP_NIRS: breakpoint of fall in SmO₂-m.intercostales). During exercise, SmO₂-m.intercostales decreased continuously showing a higher decrease when $\dot{\mathrm{V}}$E increased abruptly. A good agreement between methods used to determine RCP was found (visual vs NIRS) at %$\dot{\mathrm{V}}$O₂-máx, $\dot{\mathrm{V}}$O₂, $\dot{\mathrm{V}}$E, and W (Bland-Altman test). Correlations were found to each parameters analyzed (r = 0.854; r = 0.865; r = 0.981; and r = 0,968; respectively. p < 0.001 in all variables, Pearson test), with no differences (p < 0.001 in all variables, Student’s t-test) between methods used (RCP_visual and RCP_NIRS). We concluded that changes at SmO₂-m.intercostales measured by NIRS could adequately determine RCP in triathletes.