Environmental Hypoxia Can Alter the Eye Development of Drosophila melanogaster

Abstract

Environmental hypoxia, defined as reduced oxygen availability, arises from both natural and anthropogenic factors. Naturally, it occurs at high altitudes, whereas human-driven hypoxia is primarily associated with particulate matter and trace gases. Emissions of trace gases including carbon monoxide, nitrogen oxides, sulfur dioxide, and volatile organic compounds together with fine particulate matter (PM2.5, PM10, and smaller fractions), intensify oxygen depletion and impair air quality, creating persistent localized hypoxic environments. To model these conditions, Drosophila melanogaster was subjected to hypobaric pressure (120 mbar) and smoke exposure generated from 0.1 g of coconut husk. In smoke-induced hypoxia, various PM size fractions (10, 2.5, and 1.0 μm) and gas concentrations were monitored to assess their effects on the tracheal terminal tubes. Both hypoxic conditions led to developmental eye defects in Drosophila, as demonstrated by histological staining. Biochemical analyses revealed elevated reactive oxygen species, indicating cellular injury and DNA damage. Gene expression analysis by qPCR showed upregulation of Puf, Wge, Twr, and Sima, along with downregulation of photoreceptor-specific genes Rh1, Rh3, and Rh6 which are critical for eye development. Importantly, treatment with alpha-tocopherol and N-acetylcysteine (NAC) restored these molecular and morphological defects to near-normal levels. This study highlights the detrimental impact of oxygen deprivation on ocular development and identifies alpha-tocopherol and NAC as potential therapeutic agents for mitigating hypobaric and smoke-induced hypoxia.