The Mechanism Behind the Therapeutic Role of Alpha-Tocopherol in Mitigating Hypobaric Hypoxia-Induced Eye Defect in Drosophila melanogaster.

Hypoxia, or low oxygen levels, is linked to several pathological disorders, including retinopathies. Retina being a metabolically active tissue, low oxygen levels resulted in retinal degradation. The developmental perspective of hypobaric hypoxia (HBH)-induced eye development remains elusive. Drosophila is used as our model organism to investigate the impact of HBH on eye development and alpha-tocopherol as a potential inhibitor. To induce the hypoxic condition, we exposed the Drosophila to hypobaric pressure (120 mbar). Hypoxia induces eye defects in different developmental stages of Drosophila as revealed by histological staining. Biochemical estimation disclosed the presence of reactive oxygen species (ROS) during hypoxia, which led to cellular injury and DNA damage. Quantitative PCR reveals the upregulation of Puf, Wge, and Twr genes and the downregulation of Rh1 and Rh6 involved in eye development. All these defects are brought back to normal levels after treatment with alpha-tocopherol. This research provides a foundation for understanding ocular developmental problems caused by oxygen deprivation and alpha-tocopherol as a crucial therapeutic approach to the treatment of HBH.