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Brain adaptation to hypoxia and hyperoxia in mice
Laura Terraneo1, Rita Paroni1, Paola Bianciardi1
1Department of Health Science, University of Milan, 20142 Milan, Italy.
Redox Biology
|November 12, 2016
Summary
Both mild hypoxia and hyperoxia cause brain damage by disrupting the balance between reactive oxygen species (ROS) generation and antioxidant defenses. This study reveals similar, yet distinct, cellular responses to altered oxygen levels.
Area of Science:
- Neuroscience
- Physiology
- Biochemistry
Background:
- Hyperoxic and hypoxic breathing can disrupt cerebral redox balance and signaling pathways.
- Oxidative stress is a concern in both oxygen excess and deficiency, impacting brain function.
Purpose of the Study:
- To investigate the cerebral tissue responses to varying oxygen fractions.
- To assess redox imbalance and hypoxia signaling pathways under different oxygen conditions.
Main Methods:
- Mice were exposed to mild hypoxia (10% O2), normoxia (21% O2), or mild hyperoxia (30% O2) for 28 days.
- Brain tissue was analyzed for reactive oxygen species (ROS) sources, antioxidant regulators, apoptosis, and hypoxia-inducible factors (HIFs).
Main Results:
- Neither mild hypoxia nor mild hyperoxia linearly affected all measured variables.
- NADPH oxidase subunit 4 increased in hypoxia, but not hyperoxia; HIF-2α expression was elevated in both conditions compared to normoxia.
- Neuron apoptosis and cerebral hydroperoxides increased in both hypoxia and hyperoxia groups, indicating oxidative stress.
Conclusions:
- Prolonged mild hyperoxia causes persistent cerebral damage, similar to prolonged mild hypoxia.
- The underlying mechanism involves a similar imbalance between ROS generation and antioxidant defense, though at different magnitudes.
