Hydrogen Protects Lung Cells from Oxygen Damage in Premature Rats
- Authors
- Lan Yao, Feng Xu, Chong Luo, Pan Yu, Xinxin Dong, Xuejun Sun, Chengjun Liu
- Journal
- Journal of Southern Medical University
- Year
- 2013
- Study Type
- Cell Culture
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Bronchopulmonary Dysplasia
- Body System
- Respiratory
TL;DR
Hydrogen treatment helps protect baby rat lung cells from damage caused by too much oxygen.
Key Finding
Hydrogen treatment significantly reduced oxidative stress damage in lung cells exposed to high oxygen by increasing antioxidant enzyme activity, decreasing damage markers, and preserving mitochondrial function.
Summary
Researchers tested whether hydrogen could protect lung cells from damage caused by high oxygen exposure. They grew premature rat lung cells in normal air, high oxygen, or high oxygen plus hydrogen. Cells exposed to high oxygen showed reduced growth and increased damage markers, but adding hydrogen reversed these harmful effects by boosting the cells' natural antioxidant defenses and protecting their internal structures.
Practical Takeaway
This laboratory study in rat cells suggests hydrogen may help protect lung tissue from high-oxygen damage, which is relevant to premature infants who require supplemental oxygen. However, this is early-stage cell research and does not demonstrate effects in living organisms or humans, so much more research is needed before any clinical applications can be considered.
Abstract
To investigate the protective effect of hydrogen against hyperoxia-induced oxidative stress injury in premature rat type II alveolar epithelial cells (AECs). The type II AECs isolated from premature rats were randomly divided into air (21% oxygen) control group, hyperoxia (95% oxygen) control group, air + hydrogen group, and hyperoxia+ hydrogen group. The cells with hydrogen treatment were cultured in the presence of rich hydrogen. After the corresponding exposure for 24 h, the cell morphology was observed microscopically. MTT assay was used to evaluated the cell proliferation ability, and JC-1 fluorescence probe was used to detect the mitochondrial membrane potential (δφ) changes of the type II AECs. The concentration of maleic dialdehyde (MDA) and superoxide dismutase (SOD) activity in the cell supernatant were detected using colorimetric method. No significant differences were found in cell growth or measurements between air control and air + hydrogen groups. Compared with air control group, the cells exposed to hyperoxia showed significantly suppressed proliferation, reduced mitochondrial membrane potential, increased MDA content, and decreased SOD activity. Intervention with hydrogen resulted in significantly increased cell proliferation and SOD activity and lowered MDA content, and restored the mitochondrial membrane potential in the cells with hyperoxia exposure (P<0.05). Hydrogen can significantly reduce hyperoxia-induced oxidative stress injury in premature rat type II AECs, improve the cellular antioxidant capacity, stabilize the mitochondrial membrane potential, and reduce the inhibitory effect of hyperoxia on cell proliferation.