Indexed on: 10 Jul '14Published on: 10 Jul '14Published in: Physiological genomics
Scuba diving, characterized by hyperoxia and hyperbaria, could increase reactive oxygen species production which acts as signaling molecules to induce adaptation against oxidative stress. The aim was to study the effects of scuba diving immersion on neutrophil inflammatory response, the induction of oxidative damage, and the NO synthesis.Nine male divers performed a dive at 50 m depth for a total time of 35 min. Blood samples were obtained at rest before the dive, after the dive, and 3 h after the diving session.Markers of oxidative and nitrosative damage, nitrite, and the gene expression of genes related with the synthesis of nitric oxide and lipid mediators, cytokine synthesis, and inflammation were determined in neutrophils.The mRNA levels of genes related with the inflammatory and immune response of neutrophils, except TNF-α, myeloperoxidase, and toll-like receptor (TLR) 2, significantly increased after the recovery period respect to predive and postdive levels. NF-κB, IL-6, and TLR4 gene expression reported significant differences immediately after diving respect to the predive values. Protein nitrotyrosine levels significantly rose after diving and remained high during recovery, whereas no significant differences were reported in malondialdehyde. Neutrophil nitrite levels as indicative of inducible nitric oxide synthase (iNOS) activity progressively increased after diving and recovery. The iNOS protein levels maintained the basal values in all situations.Scuba diving which combines hyperoxia, hyperbaria, and acute exercise induces nitrosative damage with increased nitrotyrosine levels and an inflammatory response in neutrophils.