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Difference between revisions of "Dejmek 2018 Physiol Res"

From Bioblast
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::: Human  fetal  lung  fibroblasts  (HFL1), ROUTINE respiration per cell: 31.6±8.5 pmol·s<sup>-1</sup>·x<sup>-1</sup>
::: Human  fetal  lung  fibroblasts  (HFL1), ROUTINE respiration per cell: 31.6±8.5 amol·s<sup>-1</sup>·x<sup>-1</sup>

Revision as of 10:01, 15 June 2021

Publications in the MiPMap
Dejmek J, Kohoutová M, Kripnerová M, Čedíková M, Tůma Z, Babuška V, Bolek L, Kuncová J (2018) Repeated exposure to hyperbaric hyperoxia affects mitochondrial functions of the lung fibroblasts. Physiol Res 67(Suppl 4):S633-S643.

» PMID: 30607970 Open Access

Dejmek J, Kohoutova M, Kripnerova M, Cedíkova M, Tuma Z, Babuska V, Bolek L, Kuncova Jitka (2018) Physiol Res

Abstract: 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 high-resolution 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.

Bioblast editor: Gnaiger E O2k-Network Lab: CZ Pilsen Kuncova J


Labels: MiParea: Respiration 

Stress:Oxidative stress;RONS  Organism: Human  Tissue;cell: Lung;gill, Fibroblast  Preparation: Permeabilized cells, Intact cells  Enzyme: Marker enzyme 

Coupling state: LEAK, ROUTINE, OXPHOS, ET  Pathway: F, N, S, CIV, NS, ROX  HRR: Oxygraph-2k 


Human fetal lung fibroblasts (HFL1), ROUTINE respiration per cell: 31.6±8.5 amol·s-1·x-1