Breathing air with too much oxygen can disrupt how cells make proteins. A study from researchers at a major university was published in a leading science journal to share fresh insights into this phenomenon.
Earlier work mainly looked at what happens when oxygen is scarce, especially how it affects gene activity. In the new study, mice were exposed to air with three distinct oxygen levels: 8% representing deficiency, 21% as normal air, and 60% as excess oxygen. This setup allowed scientists to observe how different oxygen environments influence protein dynamics in lung tissue, the heart, and the brain.
In the experiments, the animals consumed a diet containing nitrogen markers. Nitrogen is essential for building proteins. By tracking nitrogen-tagged proteins, researchers could measure how quickly proteins formed and how rapidly they were broken down in the lungs, heart, and brain under each oxygen condition.
The findings showed that oxygen levels had the strongest impact on lung proteins, with comparatively smaller effects on heart and brain functions. A protein called MYBBP1A drew particular attention. When oxygen is excessive, MYBBP1A tends to accumulate and directly regulate many genes. It also participates in ribosome production, the cellular machines responsible for assembling proteins. Therefore, accumulating MYBBP1A due to high oxygen can disrupt protein production at the cellular level. The study identifies MYBBP1A as a potential target for drugs aimed at reducing the negative consequences of breathing air with too much oxygen.
The researchers underscored the real-world relevance of these findings. More than a million people in the United States rely on supplemental oxygen daily for medical reasons, and in some cases the therapy may worsen the underlying condition. The new work provides a clearer picture of how the body responds to elevated oxygen and what cellular pathways mediate these responses. It also lays a foundation for Canadian and American clinicians to fine-tune oxygen therapy, aiming for maximum therapeutic benefit with minimal adverse effects.
As a broader context, prior studies have explored how external factors such as light exposure can influence gene activity related to aging. For instance, emerging research suggests that blue light from digital devices can alter gene regulation linked to aging processes. These broader lines of inquiry help explain how environmental inputs shape cellular function across organs and over time.