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A mitohormetic response to pro-oxidant exposure in the house mouse
Yufeng Zhang1, Frances Humes1, Gregory Almond2
1Department of Biological Science, Auburn University , Auburn, Alabama.
Abstract:
Mitochondria are hypothesized to display a biphasic response to reactive oxygen species (ROS) exposure. In this study, we evaluated the time course changes in mitochondrial performance and oxidative stress in house mice following X-irradiation. Forty-eight mice were equally divided among six groups, including a nonirradiated control and five experimental groups that varied in time between X-ray exposure and euthanasia (1 h and 1, 4, 7, and 10 days after X-irradiation). We measured parameters associated with mitochondrial respiratory function and ROS emission from isolated liver and skeletal muscle mitochondria and levels of oxidative damage and antioxidants in liver, skeletal muscle, and heart tissues. Mitochondrial function dropped initially after X-irradiation but recovered quickly and was elevated 10 days after the exposure. Hydrogen peroxide production, lipid peroxidation, and protein carbonylation showed inverse U-shaped curves, with levels returning to control or lower than control, 10 days after X-irradiation. Enzymatic antioxidants and markers for mitochondrial biogenesis exhibited a tissue-specific response after irradiation. These data provide the first chronological description of the mitohormetic response after a mild dose of irradiation and highlight the protective response that cells display to ROS exposure. This study also provides valuable information and application for future mitochondrial and oxidative stress studies in numerous physiological settings.
Insights
Mitochondria show a biphasic response to X-irradiation, with initial decreased function followed by enhanced mitochondrial performance and reduced oxidative stress. This study details the mitohormetic response to irradiation.
Area of Science:
- Mitochondrial biology
- Oxidative stress research
- Radiation biology
Background:
- Mitochondria's role in cellular signaling and energy production.
- Reactive oxygen species (ROS) are implicated in cellular damage and aging.
- The hypothesized biphasic, or mitohormetic, response of mitochondria to ROS exposure.
Purpose of the Study:
- To chronologically evaluate mitochondrial function and oxidative stress markers in mice after X-irradiation.
- To investigate the time-dependent changes in mitochondrial performance and ROS emission.
- To analyze tissue-specific responses of antioxidants and mitochondrial biogenesis markers.
Main Methods:
- Mice were exposed to X-irradiation and euthanized at various time points (1 hour to 10 days).
- Mitochondrial respiratory function and ROS emission were measured in liver and skeletal muscle.
- Oxidative damage markers (lipid peroxidation, protein carbonylation) and antioxidant levels were assessed in multiple tissues.
Main Results:
- Mitochondrial function initially declined post-irradiation but recovered and increased by day 10.
- ROS production (hydrogen peroxide) and oxidative damage markers followed an inverse U-shaped curve.
- Antioxidant levels and mitochondrial biogenesis markers showed tissue-specific responses.
Conclusions:
- Mitochondria exhibit a mitohormetic response to X-irradiation, characterized by initial dysfunction followed by enhanced function.
- Cells display protective mechanisms against ROS-induced damage, with a notable recovery and potentiation of mitochondrial activity.
- This study provides a chronological framework for understanding mitochondrial adaptation to oxidative stress, relevant for various physiological settings.