Combined Effects of Simulated Microgravity and Isolation Drive Oxidative Stress Response

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Simulated Microgravity and Isolation

Spaceflight is known to disrupt the immune system in astronauts. Previous research has also shown immune dysregulation in humans subjected to isolation on Earth.

In a newly published paper, researchers subjected transgenic (MCAT) mice to isolation and simulated microgravity to study their combined effects and the underlying mechanisms that drive immune dysregulation in the Central Nervous System (CNS). Findings from the study reveal isolation and long-term simulated microgravity altered cytokine expression levels in both the hippocampus and plasma.

These effects in the brain were mitigated in the MCAT mice, implicating an important role for mitochondrial ROS in aspects of the neuroimmune response to microgravity and isolation. These findings, along with other previous studies, provide a rationale for the use of antioxidant-based approaches to address anticipated CNS changes during spaceflight and in situations of isolation and reduced mobility on Earth.

Previous findings have shown that isolation can modify immune responses to simulated spaceflight and that the combination of these two spaceflight stressors can lead to discrete immune deficits. MCAT mice have been developed to overexpress human catalase localized to the mitochondria and were used in this study to test the role of oxidative stress response to simulated spaceflight conditions.

Catalase is a very important enzyme in protecting the cell from oxidative damage by reactive oxygen species. There have been few studies exploring oxidative damage as a mechanism by which space environmental factors, singly or in combination, mediate aspects of CNS immune responses.

Overexpression of catalase in mitochondria mitigates changes in hippocampal cytokine expression following simulated microgravity and isolation

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