Repeated exposure to hyperbaric hyperoxia affects mitochondrial functions of the lung fibroblasts
The result's identifiers
Result code in IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11140%2F18%3A10384992" target="_blank" >RIV/00216208:11140/18:10384992 - isvavai.cz</a>
Result on the web
<a href="http://www.biomed.cas.cz/physiolres/pdf/2018/67_S633.pdf" target="_blank" >http://www.biomed.cas.cz/physiolres/pdf/2018/67_S633.pdf</a>
DOI - Digital Object Identifier
—
Alternative languages
Result language
angličtina
Original language name
Repeated exposure to hyperbaric hyperoxia affects mitochondrial functions of the lung fibroblasts
Original language description
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(R) 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.
Czech name
—
Czech description
—
Classification
Type
J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database
CEP classification
—
OECD FORD branch
10610 - Biophysics
Result continuities
Project
<a href="/en/project/LO1503" target="_blank" >LO1503: BIOMEDIC</a><br>
Continuities
P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)<br>S - Specificky vyzkum na vysokych skolach<br>I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace
Others
Publication year
2018
Confidentiality
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Data specific for result type
Name of the periodical
Physiological Research
ISSN
0862-8408
e-ISSN
—
Volume of the periodical
67
Issue of the periodical within the volume
Suppl. 4
Country of publishing house
CZ - CZECH REPUBLIC
Number of pages
11
Pages from-to
"S633"-"S643"
UT code for WoS article
000454598300008
EID of the result in the Scopus database
2-s2.0-85059494258