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ROS production from endothelial cells during in vitro simulated dives: effects of hydrostatic and gas pressures
Author(s) -
Theron michael,
Wang Qiong,
Lambrechts Kate,
Mazur Alexandra,
Buzzacott Peter,
Guerrero François
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.678.11
Subject(s) - peroxynitrite , reactive oxygen species , mitochondrion , microbiology and biotechnology , chemistry , calcium , superoxide , hydrostatic pressure , mitochondrial ros , oxygen , programmed cell death , biochemistry , biology , apoptosis , enzyme , physics , organic chemistry , thermodynamics
ROS are known to be involved in post‐dive endothelial dysfunction which is itself thought to be associated with decompression sickness. The aims of this study were to assess the impact of air diving on ROS production from endothelial cells (EC) during diving, and to differentiate the effects of physical parameters of the dive (hydrostatic ‐HP‐ and gas pressures). This work particularly focused on the mitochondria, one the pathways of ROS production. During in vitro diving simulation (45 min at 8 ATA, compression 1ATA/min), superoxide (O 2 °‐ ) production, mitochondrial membrane potential (MMP) and cell death were analyzed on EC when HP, oxygen and nitrogen pressures were increased together (air dive) or independently. Then, O 2 °‐ , peroxynitrite, NO° productions and mitochondrial calcium concentration were examined during air dive. Air diving increased O 2 °‐ , decreased MMP and promoted endothelial cell death. O 2 °‐ production was mainly due to oxygen partial pressure but also to HP. HP, oxygen and nitrogen pressures modified mitochondrial membrane potential and cell death. During air diving, endothelial cells showed excessive O 2 °‐ and peroxynitrite production, attenuation of NO production and up‐regulation of mitochondrial calcium storage. This study clearly demonstrates the overproduction of ROS and RNS (O 2 °‐ and peroxinitrite) during a dive; it furthermore shows that MMP and mitochondrial calcium are modified. It is proposed that, during diving, mitochondrial calcium may promote peroxynitrite formation and O 2 °‐ overproduction through the activation of mitochondrial NO° generation. These phenomena could explain the observed decreased viability of endothelial cells.