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<p>The pathophysiology of decompression sickness (DCS) is not fully understood. Apart from bubble formation, endothelial dysfunction and reactive oxygen species (ROS) production, participate in DCS. We aimed to evaluate the redox profile (redox potential, adenosine deaminase activity (ADA), and xanthine oxidase activity (XO) and the effects of GYY4137, an H<sub>2</sub>S donor with antiradical properties, on the mortality of mice exposed to experimental DCS. Sixty Mice were injected intraperitoneally with either GYY4137 or saline, then subjected to high pressure in a hyperbaric chamber, followed by a quick decompression. GYY4137 increased survival with a median lethal dose (LD<sub>50</sub>) of 120&#xa0;m compared with those injected with saline (&lt; 100&#xa0;m; <i>p</i> = 0.038) but did not affect significantly ADA or XO activities. The redox potential (RP: mV) was lower in the GYY4137 group (median-range, 116[78–189]) than that in the saline group: 150[88–226], <i>p</i> = 0.04. Experimental DCS itself was associated with an increase in RP. We concluded that GYY4137 protects mice while reducing RP and ROS production. Our results seem to indicate that the reduction of the redox potential induced by the administration of H<sub>2</sub>S donor could reduce mortality during DCS.</p>

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Therapeutic Potential of GYY4137 in Reducing Oxidative Stress and Mortality in Experimental Decompression Sickness

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年3月5日

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  • Lucile Daubresse,
  • Marion Marlinge,
  • Hélène Lavner,
  • Julia-Sophie Dodivers,
  • Alexandrine Bertaud,
  • Simon Lledo,
  • Samantha Conte,
  • Julien Fromonot,
  • Marguerite Gastaldi,
  • Jean Jacques Risso,
  • Jean Claude Rostain,
  • Jean Eric Blatteau,
  • Nicolas Vallee,
  • Régis Guieu,
  • Regis Guieu

摘要

The pathophysiology of decompression sickness (DCS) is not fully understood. Apart from bubble formation, endothelial dysfunction and reactive oxygen species (ROS) production, participate in DCS. We aimed to evaluate the redox profile (redox potential, adenosine deaminase activity (ADA), and xanthine oxidase activity (XO) and the effects of GYY4137, an H2S donor with antiradical properties, on the mortality of mice exposed to experimental DCS. Sixty Mice were injected intraperitoneally with either GYY4137 or saline, then subjected to high pressure in a hyperbaric chamber, followed by a quick decompression. GYY4137 increased survival with a median lethal dose (LD50) of 120 m compared with those injected with saline (< 100 m; p = 0.038) but did not affect significantly ADA or XO activities. The redox potential (RP: mV) was lower in the GYY4137 group (median-range, 116[78–189]) than that in the saline group: 150[88–226], p = 0.04. Experimental DCS itself was associated with an increase in RP. We concluded that GYY4137 protects mice while reducing RP and ROS production. Our results seem to indicate that the reduction of the redox potential induced by the administration of H2S donor could reduce mortality during DCS.