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Spaceflight Stressors Impact on Mitochondrial Function and the Development of Ocular Pathology
Background The spaceflight environment imposes harmful stressors such as microgravity and ionizing radiation on the human body. The eye is especially susceptible to damage from these stressors due to their effects on mitochondrial function. These stressors result in mitochondrial DNA damage, oxidative stress, impaired oxidative metabolism, and overall decreased mitochondrial function. Mitochondrial DNA acquires mutations more readily than nuclear DNA and has weaker genetic repair mechanisms. The result of these insults is the development of spaceflight-associated ocular pathologies such as Light Flashes (LF), Cataracts, and Spaceflight Associated Neuro-Ocular Syndrome (SANS). Mitochondrial dysfunction is becoming more apparent as a causative factor of these conditions. Therefore, a greater understanding of the pathogenesis is necessary to develop effective countermeasures to preserve ocular health in astronauts as they embark on longer missions.
Methods A literature review was conducted using online databases such as PubMed and Science Direct. The reference articles were analyzed to develop a narrative.
Results Conditions that impact astronauts in spaceflight have associations with terrestrial conditions but exhibit key distinctions, pointing to mitochondrial involvement in pathogenesis. Astronauts are more likely to develop cortical cataracts, which occur in the periphery of the lens where mitochondria are abundant. The most common type of cataract on Earth is the nuclear cataract, occurring in the center of the lens where there are no mitochondria. The retina has many mitochondria, and the damage imparted by spaceflight manifests as SANS, characterized by optic disc edema, globe flattening, choroidal retinal folds, and hyperopic refractive error shifts. Recent data point to mitochondrial dysfunction in photoreceptors and supporting structures due to radiation, oxidative stress, and vitamin/metabolic deficiencies as a cause of this unique condition.
Conclusion Spaceflight damages mitochondria within the eye, contributing to development of ocular diseases such as cataracts and SANS. Astronauts develop cortical cataracts due to the distribution of lens mitochondria and susceptibility to oxidative damage and ionizing radiation. Systemic oxidative stress also contributes to the development, thus antioxidant therapy may be a treatment. Cataracts and SANS development may be connected, as shown by the development of cotton-wool spots experienced by astronauts. Future missions to the Moon and Mars will exacerbate the negative effects of spaceflight experienced in low earth orbit and present novel stressors. Advanced medical care will not be readily accessible during long-duration missions. These demands warrant a greater understanding of the pathogenesis of ocular conditions associated with spaceflight for the development of appropriate countermeasures.