Szyller Jakub, Kozakiewicz Mariusz, Siermontowski Piotr, Kaczerska Dorota
Division of Clinical Chemistry and Laboratory Hematology, Department of Medical Laboratory Diagnostics, Faculty of Pharmacy, Wroclaw Medical University, Borowska 211A Str., 50-556 Wroclaw, Poland.
Division of Biochemistry and Biogerontology, Department of Geriatrics, Faculty of Health Sciences, L. Rydygier Collegium Medicum, Dębowa 3 Str., 85-626 Bydgoszcz, Poland.
Antioxidants (Basel). 2022 May 20;11(5):1008. doi: 10.3390/antiox11051008.
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.
热休克蛋白（HSPs）对氧化应激和减压病具有保护作用。一氧化氮可减少减压过程中的气泡形成，其活性受HSPs调节。模拟潜水可引发HSP反应。本研究旨在描述模拟潜水对抗氧化系统、HSPs和一氧化氮合酶反应的影响，并证明HSPs浓度与氧化应激增强之间的关系。共有20名健康的专业潜水员参加训练，训练包括在高压舱内进行模拟干式潜水，并在24小时内分为实验I（30米暴露，400千帕）和实验II（60米暴露，700千帕）。测量了超氧化物歧化酶（SOD）、过氧化氢酶（CAT）和谷胱甘肽过氧化物酶（GPx）的活性以及丙二醛（MDA）、热休克蛋白70（HSP70）、热休克蛋白90（HSP90）、内皮型（eNOS）和诱导型（iNOS）一氧化氮合酶的浓度。结果显示SOD活性和MDA浓度增加。GPx的活性取决于潜水剖面。两个实验中潜水后血清HSP70水平均显著降低。模拟60米潜水后HSP90的平均水平显著升高。证明了HSP浓度与SOD/GPx活性之间存在显著关系。60米暴露后eNOS浓度增加。未观察到iNOS浓度变化。总之，模拟潜水显著影响抗氧化系统、热休克蛋白表达和一氧化氮合酶；然而，这些变化取决于潜水条件。HSPs的表达与氧化应激强度之间存在关系。
