Oxidative Stress, HSP70/HSP90 and eNOS/iNOS Serum Levels in Professional Divers during Hyperbaric Exposition

Heat shock proteins (HSPs) have protective effects against oxidative stress and decompression sickness. Nitric oxide may reduce bubble formation during decompression and its activity is regulated by HSPs. A simulated dive can cause the HSP response. The aim of this study was to describe the effect of simulated dives on the antioxidant system, HSPs, and nitric oxide synthase response and demonste the relationship between the concentration of HSPs and the intensification of oxidative stress. A total of 20 healthy professional divers took part in training, consisting of simulated dry dives in a hyperbaric chamber and split into experiment I (30 m exposure, 400 kPa) and experiment II (60 m exposure, 700 kPa) over 24 h. The activities of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) and the concentrations of malondialdehyde (MDA), heat shock protein 70 (HSP70), heat shock protein 90 (HSP90), endothelial (eNOS) and inducible (iNOS) nitric oxide synthase were measured. Increases in the activity of SOD and MDA concentration were demonstrated. The activity of GPx depended on the dive profile. The HSP70 serum level in both experiments was significantly lower after the dives. The mean HSP90 level was significantly higher after the simulated dive at 60 m. A significant relationship between HSP concentration and SOD/GPx activity was demonstrated. eNOS concentration increased after 60 m exposure. No change in iNOS concentration was observed. In conclusions, the simulated dive significantly affected the antioxidant system, heat shock protein expression and nitric oxide synthase; however, the changes depend on the diving conditions. There is a relationship between the expression of HSPs and the intensity of oxidative stress.