Hyperbaric oxygen (HBO) therapy, i.e. breathing pure oxygen
under increased environmental pressures serves as a treatment
for diverse medical conditions. However, elevated oxygen
concentration can be detrimental to central nervous system or
lungs. Our study aimed to evaluate the effects of repeated
exposure to HBO on mitochondrial respiration assessed by highresolution respirometry (HRR), cell viability estimated by
PrestoBlue® reaction, morphology analyzed by routine phase
contrast and fluorescent microscopy, and superoxide dismutase
(SOD) and citrate synthase (CS) activities using human lung
fibroblasts. The cells were exposed to HBO for 2 h per day for
5 consecutive days. One day after the last exposure, HBO cells
displayed significantly smaller area and perimeter, compromised
viability and elevated SOD activity. No changes were detected in
CS activity or quality of mitochondrial network. HRR revealed
impaired mitochondrial oxygen consumption manifested by
increased leak respiration, decreased activity of complex II and
compromised ATP-related oxygen consumption when fatty acids
were oxidized. Our findings document that in conditions
mimicking chronic intermittent exposure to HBO, lung fibroblasts
suffer from compromised mitochondrial respiration linked to
complex II and impaired cellular growth in spite of increased
antioxidant defense. Underlying mechanism of this HBO-induced
mitochondrial dysfunction should be further explored.