PDF(Pubmed)
Abstract：
Introduction: Diving decompression theory hypothesizes inflammatory processes as a source of micronuclei which could increase related risks. Therefore, we tested 10 healthy, male divers. They performed 6-8 dives with a maximum of two dives per day at depths ranging from 21 to 122 msw with CCR mixed gas diving. Methods: Post-dive VGE were counted by echocardiography. Saliva and urine samples were taken before and after each dive to evaluate inflammation: ROS production, lipid peroxidation (8-iso-PGF2), DNA damage (8-OH-dG), cytokines (TNF-α, IL-6, and neopterin). Results: VGE exhibits a progressive reduction followed by an increase (p < 0.0001) which parallels inflammation responses. Indeed, ROS, 8-iso-PGF2, IL-6 and neopterin increases from 0.19 ± 0.02 to 1.13 ± 0.09 μmol.min-1 (p < 0.001); 199.8 ± 55.9 to 632.7 ± 73.3 ng.mg-1 creatinine (p < 0.0001); 2.35 ± 0.54 to 19.5 ± 2.96 pg.mL-1 (p < 0.001); and 93.7 ± 11.2 to 299 ± 25.9 μmol·mol-1 creatinine (p = 0.005), respectively. The variation after each dive was held constant around 158.3% ± 6.9% (p = 0.021); 151.4% ± 5.7% (p < 0.0001); 176.3% ± 11.9% (p < 0.0001); and 160.1% ± 5.6% (p < 0.001), respectively. Discussion: When oxy-inflammation reaches a certain level, it exceeds hormetic coping mechanisms allowing second-generation micronuclei substantiated by an increase of VGE after an initial continuous decrease consistent with a depletion of \"first generation\" pre-existing micronuclei.
摘要：
简介：潜水减压理论假设炎症过程是微核的来源，这可能会增加相关的风险。因此,我们测试了10个健康的，男性潜水员.他们进行了6-8次潜水，每天最多2次潜水，深度为21至122msw，使用CCR混合气体潜水。方法:采用超声心动图对潜水后VGE进行计数。在每次潜水之前和之后采集唾液和尿液样本以评估炎症：ROS产生，脂质过氧化（8-iso-PGF2），DNA损伤（8-OH-dG），细胞因子(TNF-α，IL-6和新蝶呤）。结果:VGE表现出逐渐减少,随后增加(p<0.0001),这与炎症反应平行。的确,ROS,8-异-PGF2，IL-6和新蝶呤从0.19±0.02增加到1.13±0.09μmol。min-1（p<0.001）；199.8±55.9至632.7±73.3ng。肌酸酐mg-1(p<0.0001);2.35±0.54至19.5±2.96pg。mL-1（p<0.001）；肌酐93.7±11.2至299±25.9μmol·mol-1（p=0.005），分别。每次潜水后的变化保持恒定，约为158.3％±6.9％（p=0.021）;151.4％±5.7％（p<0.0001）;176.3％±11.9％（p<0.0001）;和160.1％±5.6％（p<0.001），分别。讨论：当炎症达到一定水平时，它超过了允许第二代微核的治疗机制，在最初的连续下降与“第一代”先前存在的微核的耗尽一致后，VGE的增加证实了第二代微核。
