Repeated exposure to hyperbaric hyperoxia affects mitochondrial functions of the lung fibroblasts

Title:

Repeated exposure to hyperbaric hyperoxia affects mitochondrial functions of the lung fibroblasts

Creator:

Dejmek, J., Kohoutová, M., Kripnerová, M., Čedíková, M., Tůma, Z., Babuška, V., Bolek, L., and Kuncová , J.

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:459bc9e9-9268-42ec-b4dd-69b3e86729a8
uuid:459bc9e9-9268-42ec-b4dd-69b3e86729a8

Subject:

hyperbaric hyperoxia, high resolution respirometry, human fetal lung fibroblasts, mitochondria, and superoxide dismutase

Type:

model:article and TEXT

Format:

bez média and svazek

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 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.

Language:

English

Rights:

http://creativecommons.org/publicdomain/mark/1.0/
policy:public

Source:

Physiological research | 2018 Volume:67 | Number:Suppl 4

Harvested from:

CDK

Metadata only:

false