Inflammation plays a crucial role in the development of many complex diseases and disorders including autoimmune diseases, metabolic syndrome, neurodegenerative diseases, and cardiovascular pathologies. Prostaglandins play a regulatory role in inflammation. Cyclooxygenases are the main mediators of inflammation by catalyzing the initial step of arachidonic acid metabolism and prostaglandin synthesis. The differential expression of the constitutive isoform COX-1 and the inducible isoform COX-2, and the finding that COX-1 is the major form expressed in the gastrointestinal tract, lead to the search for COX-2-selective inhibitors as anti-inflammatory agents that might diminish the gastrointestinal side effects of traditional non-steroidal anti-inflammatory drugs (NSAIDs). COX-2 isoform is expressed predominantly in inflammatory cells and decidedly upregulated in chronic and acute inflammations, becoming a critical target for many pharmacological inhibitors. COX-2 selective inhibitors happen to show equivalent efficacy with that of conventional NSAIDs, but they have reduced gastrointestinal side effects. This review would elucidate the most recent findings on selective COX-2 inhibition and their relevance to human pathology, concretely in inflammatory pathologies characterized by a prolonged pro-inflammatory status, including autoimmune diseases, metabolic syndrome, obesity, atherosclerosis, neurodegenerative diseases, chronic obstructive pulmonary disease, arthritis, chronic inflammatory bowel disease and cardiovascular pathologies.

Humans can reduce inorganic nitrate (NO(3)(-)) to nitrite (NO(2)(-)), nitric oxide (NO), and other bioactive nitrogen oxides. The purpose of this study was to test the hypothesis that a single dose of inorganic nitrate before exercise might enhance the tolerance of endurance athletes to high intensity exercise. Eleven cyclists (age = 34.3 ± 4.8 yr, VO(2peak) = 65.1 ± 6.2 mL·kg(-1)·min(-1)) participated in this randomized, double-blind, crossover study. Subjects received dietary supplementation with nitrate (NaNO(3) 10 mg·kg(-1) of body mass) or a placebo (NaCl) 3 h before exercise. They then performed a cycle ergometer test that consisted of four 6-min submaximal workloads, corresponding to 2.0, 2.5, 3.0, and 3.5 W·kg(-1) of body mass, interspersed with 3 min of passive recovery. After a 5-min recovery period, subjects performed one incremental exercise test until exhaustion. Plasma nitrate and nitrite were significantly higher (P < 0.05) 3 h after supplementation (nitrate = 250 ± 80 μM, nitrite = 2313 ± 157 nM) than after the placebo (nitrate = 29 ± 8 μM, nitrite = 1998 ± 206 nM) at resting conditions. Nitrate supplementation significantly reduced VO(2peak)(nitrate = 4.64 ± 0.35 L·min(-1), placebo = 4.82 ± 0.33 L·min(-1), P = 0.010) and the ratio between VO(2) and power at maximal intensity (nitrate = 11.2 ± 1.1 mL·min(-1)·W(-1), placebo = 11.8 ± 1.1 mL·min(-1)·W(-1), P = 0.031). This reduction of VO(2) occurred without changes in the time to exhaustion (nitrate = 416 ± 32 s, placebo = 409 ± 27 s) or in the maximal power (nitrate = 416 ± 29 W, placebo = 410 ± 28 W). A single oral dose of inorganic nitrate acutely reduces VO(2peak)without compromising the maximal exercise performance.

The aims of this study were to assess the effects of a swimming session on the peripheral blood neutrophil and lymphocyte pro- and antioxidant system, identify any differences between the sexes and the regulatory mechanisms that might induce the immune cell adaptive response to exercise. Twenty-four swimmers (15 males, 9 females) participated in a one-hour swimming session at 75-80% of their maximal capacity. The session induced neutrophilia and decreased antioxidant enzyme activities and ascorbate levels in neutrophils. Malondialdehyde rose in neutrophils in males and females, whereas the carbonyl index only increased in males. Lymphocyte glutathione peroxidase activity was higher in males at baseline and rose as a consequence of exercise. The exercise decreased uncoupling protein-3 and Bcl-2 gene expression. The expression of PPARgamma coactivator-1 alpha (PGC-1alpha) correlated positively with that of sirtuin 3 (SIRT3) and catalase. In summary, a swimming session of one hour at 75-80% of maximal capacity produced oxidative damage in neutrophils and induced the antioxidant defences in lymphocytes. PGC-1alpha and SIRT3 appear to be key effectors of this adaptive response in lymphocytes. Both the neutrophil and lymphocyte response to exercise were slightly weaker in females than males.

Chronic and non-healing wounds, especially diabetic foot ulcers and radiation injuries, imply remarkable morbidity with a significant effect on the quality of life and a high sanitary cost. The management of these wounds requires complex actions such as surgical debris, antibiotic treatment, dressings and even revascularization. These wounds are characterized by poor oxygen supply resulting in inadequate oxygenation of the affected tissue. The adjuvant treatment with hyperbaric oxygen therapy (HBOT) may increase tissue oxygenation favoring the healing of wounds which do not respond to the usual clinical care. The increase in the partial pressure of oxygen contributes to cover the energy demands necessary for the healing process and reduces the incidence of infections. Moreover, the increase in oxygen leads to the production of reactive species with hormetic activity, acting on signaling pathways that modulate the synthesis of inflammation mediators, antioxidants and growth factors which can contribute to the healing process. Studies performed with cell cultures and in animal models seem to demonstrate the beneficial effects of HBOT. However, clinical trials do not show such conclusive results; thus, additional randomized placebo-controlled studies are necessary to determine the real efficacy of HBOT and the mechanism of action for various types of wounds.

The aim was to study the effects of a scuba diving session on the lymphocyte antioxidant system, NO synthesis, the capability to produce reactive oxygen species and the antioxidant response in neutrophils. For that purpose seven male divers performed an immersion at a depth of 40 m for 25 min. The same parameters were measured after an hyperbaric oxygen (HBO) treatment at resting conditions in a hyperbaric chamber. Lymphocyte H2O2 production rose after diving and after HBO treatment. Glutathione peroxidase (GPx) and catalase activities increased after diving in lymphocytes, while after HBO exposure only increased GPx activity. Lymphocyte HO-1 mRNA expression increased after diving and after HBO exposure, while iNOS levels and nitrite levels significantly increased after diving. The hyperoxia associated to scuba diving leads to a condition of oxidative stress with increased lymphocyte H2O2 production, HO-1 expression, NO synthesis and antioxidant enzyme adaptations in order to avoid oxidative damage.