Effect of Prolonged Simulated Microgravity on Metabolic Proteins in Rat Hippocampus: Steps toward Safe Space Travel

Mitochondria
are not only the main source of energy in cells but
also produce reactive oxygen species (ROS), which result in oxidative
stress when in space. This oxidative stress is responsible for energy
imbalances and cellular damage. In this study, a rat tail suspension
model was used in individual experiments for 7 and 21 days to explore
the effect of simulated microgravity (SM) on metabolic proteins in
the hippocampus, a vital brain region involved in learning, memory,
and navigation. A comparative 18O-labeled quantitative
proteomic strategy was used to observe the differential expression
of metabolic proteins. Forty-two and sixty-seven mitochondrial metabolic
proteins were differentially expressed after 21 and 7 days of SM,
respectively. Mitochondrial Complex I, III, and IV, isocitrate dehydrogenase
and malate dehydrogenase were down-regulated. Moreover, DJ-1 and peroxiredoxin
6, which defend against oxidative damage, were up-regulated in the
hippocampus. Western blot analysis of proteins DJ-1 and COX 5A confirmed
the mass spectrometry results. Despite these changes in mitochondrial
protein expression, no obvious cell apoptosis was observed after 21
days of SM. The results of this study indicate that the oxidative
stress induced by SM has profound effects on metabolic proteins.