Unravelling the Mechanism of N-Acetylcysteine in Alleviating Smoke-Induced Hypoxia-Driven Ocular Defects in Drosophila melanogaster

Abstract

Smoke that includes particulate matter (PM), carbon monoxide (CO), sulfur dioxide (SO2), and nitrogen dioxide (NO2) has a substantial negative impact on human health. PM, which can vary from tiny dust to coarse particles, enters the respiratory system and reduces the amount of oxygen taken in by the lungs, leading to hypoxia. Drosophila was employed as the model organism to study the effects of smoke-induced hypoxia on eye development and to evaluate N-Acetylcysteine (NAC) as a potential protective agent. In this study, Drosophila eggs were exposed to 0.1 g of coconut husk smoke . Furthermore, different size fractions of particulate matter (PM) (10, 2.5, and 1.0 mu m) and concentrations of different gases were monitored to correlate the inference of PM and gases on the tracheal terminal tube. To determine whether CO and PM (10, 2.5, and 1 mu m) contribute to hypoxia, quantitative PCR analysis of sima and tango was performed, revealing a significant upregulation of sima expression. Impairment of the tracheal terminal branches results in reduced oxygen delivery to tissues, which affects the development of photoreceptor cells. Biochemical estimation disclosed the presence of reactive oxygen species, which led to cellular injury and DNA damage. The marked downregulation of NinaE (Rh1), Rh3, and Rh6 causes internal defect in the eye. Treatment with NAC restored all these abnormalities to normal levels. This research provides insight into how smoke-induced hypoxia disrupts eye development, while NAC shows potential as an effective therapeutic agent in counteracting its harmful effects.