Original Research ARTICLE
Reduction in the level of plasma mitochondrial DNA in human diving, followed by an increase in the event of an accident.
- 1Hôpital d'Instruction des Armées Sainte-Anne, France
- 2ERRSO, Institut de Recherche Biomédicale des Armées (IRBA), France
- 3Biotech Services, Université de Toulon, France
Circulating mitochondrial DNA (mtDNA) is receiving increasing attention as a danger-associated molecular pattern in conditions such as autoimmunity or trauma. In the context of decompression sickness (DCS), the course of which is sometimes erratic, we hypothesize that mtDNA plays a not insignificant role particularly in neurological type accidents. This study is based on the comparison of circulating mitochondrial DNA (mtDNA) levels in humans presenting with various types of diving accidents, and punctured upon their admission at the hyperbaric facility. 114 volunteers took part in the study. According to the clinical criteria there were 12 Cerebro DCS, 57 Medullary DCS, 15 Vestibular DCS, 8 Ctrl + (accident-free divers) and 22 Ctrl - (non-divers). This work demonstrates that accident-free divers have less mtDNA than non-divers, which leads to the assumption that hyperbaric exposure degrades the mtDNA. mtDNA levels are on average greater in divers with DCS compared with accident-free divers. On another hand, the amount of double strand DNA (dsDNA) is neither significantly different between controls, nor between the different DCS types. Initially the increase in circulating oligonucleotides was attributed to the destruction of cells by bubble abrasion following necrotic phenomena. If there really is a significant difference between the Medullary DCS and the Ctrl-, this difference is not significant between these same DCS and the Ctrl +. This refutes the idea of massive degassing and suggests the need for new research in order to verify that oxidative stress could be a key element without necessarily being sufficient for the occurrence of a neurological type of accident.
Keywords: dive, Ischemia, systemic inflammation, Pressure, Stroke, Inert gas, PAMPS, TLR, Neutrophil
Received: 12 Sep 2018;
Accepted: 09 Nov 2018.
Edited by:Costantino Balestra, Haute École Bruxelles-Brabant (HE2B), Belgium
Reviewed by:François Guerrero, Université de Bretagne Occidentale, France
Jacek Kot, Gdańsk Medical University, Poland
Virginie Papadopoulou, University of North Carolina at Chapel Hill, United States
Copyright: © 2018 Blatteau, Gaillard, de Maistre, Richard, Louges, Gempp, Druelles, Lehot, Morin, Castagna, Abraini, Risso and Vallée. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Dr. Nicolas Vallée, Institut de Recherche Biomédicale des Armées (IRBA), ERRSO, Bretigny sur Orge, 91220, France, email@example.com