Antioxidants, endothelial dysfunction, and DCS: in vitro and in vivo study

Area of Science:

• Physiology
• Biochemistry
• Marine Medicine

Background:

• Undersea diving is known to increase reactive oxygen species (ROS) production.
• Endothelial dysfunction and decompression sickness (DCS) are potential consequences of diving.
• The precise relationship between ROS, endothelial function, and DCS requires further elucidation.

Purpose of the Study:

• To investigate the role of ROS in endothelial dysfunction and DCS.
• To assess the efficacy of antioxidants, N-acetylcysteine (NAC) and vitamin C, in mitigating diving-induced oxidative stress and DCS.

Main Methods:

• In vitro diving simulation analyzing N-acetylcysteine (NAC) effects on superoxide, peroxynitrite, nitric oxide (NO) generation, and cell viability.
• In vivo diving simulation assessing vitamin C and NAC effects on plasma glutathione thiol, thiobarbituric acid reactive substances (TBARS), angiotensin-converting enzyme (ACE) activity, angiotensin-II levels, and DCS morbidity.
• Measurement of oxidative stress markers and endothelial function indicators.

Main Results:

• In vitro: NAC reversed diving-induced superoxide and peroxynitrite overproduction, NO attenuation, and cell death in vascular endothelial cells.
• In vivo: Plasma glutathione thiol decreased post-dive, partially attenuated by NAC. TBARS levels increased, but NAC and vitamin C did not prevent DCS.
• Plasma ACE activity and angiotensin-II levels remained unaffected by diving or antioxidant treatment.

Conclusions:

• Endothelial oxidative stress, mediated by superoxide and peroxynitrite, contributes to NO attenuation and cell death during simulated diving.
• The study failed to confirm a direct link between diving-induced oxidative stress and DCS occurrence in vivo.
• Diving-related ROS and bubble formation may cause embolic or biochemical stress leading to DCS, indicating oxidative stress is not the sole causative factor.