Sureda Antoni, Batle Juan M, Capó Xavier, Martorell Miquel, Córdova Alfredo, Tur Josep A, Pons Antoni
Laboratori de Ciències de la Activitat Física, Research Group on Community Nutrition and Oxidative Stress, Departament de Biologia Fonamental i Ciències de la Salut, University of Balearic Islands, Palma de Mallorca, Spain, and CIBER: CB12/03/30038 Fisiopatología de la Obesidad y la Nutrición, CIBERobn, Instituto de Salud Carlos III (ISCIII), Spain; and.
Department of Biochemistry and Physiology, School of Physical Therapy, University of Valladolid, Soria, Spain.
Physiol Genomics. 2014 Sep 1;46(17):647-54. doi: 10.1152/physiolgenomics.00028.2014. Epub 2014 Jul 8.
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.
水肺潜水的特点是高氧和高压，可增加活性氧的产生，活性氧作为信号分子诱导机体适应氧化应激。本研究旨在探讨水肺潜水对中性粒细胞炎症反应、氧化损伤诱导及一氧化氮合成的影响。
9名男性潜水员在50米深度进行潜水，总时长35分钟。在潜水前休息时、潜水后及潜水结束后3小时采集血样。
测定中性粒细胞中氧化和亚硝化损伤标志物、亚硝酸盐以及与一氧化氮和脂质介质合成、细胞因子合成及炎症相关基因的表达。
与中性粒细胞炎症和免疫反应相关的基因（除肿瘤坏死因子-α、髓过氧化物酶和Toll样受体（TLR）2外）的mRNA水平在恢复期后相对于潜水前和潜水后水平显著升高。核因子-κB、白细胞介素-6和TLR4基因表达在潜水后相对于潜水前值有显著差异。蛋白质硝基酪氨酸水平在潜水后显著升高，并在恢复过程中保持高位，而丙二醛未见显著差异。作为诱导型一氧化氮合酶（iNOS）活性指标的中性粒细胞亚硝酸盐水平在潜水和恢复后逐渐升高。iNOS蛋白水平在所有情况下均维持基础值。
结合高氧、高压和急性运动的水肺潜水会诱导亚硝化损伤，导致硝基酪氨酸水平升高，并引起中性粒细胞炎症反应。
