Frataxin is a conserved mitochondrial protein essential for cellular iron–sulfur (Fe–S) cluster biogenesis and oxidative balance, with its deficiency causing Friedreich’s ataxia in humans. The hypomagnetic field (HMF), an environmental stressor known to influence oxidative stress and neurodevelopment, may interact with such inherent metabolic vulnerabilities. This study investigated whether HMF exposure exacerbates Fe–S homeostasis and oxidative disruption in a Drosophila melanogaster model of frataxin deficiency. Using synchrotron radiation-based X-ray fluorescence (SR-XRF) spectroscopy for in situ elemental analysis in live tissues, we found that HMF significantly altered iron distribution and content in a tissue-specific manner. In frataxin-silenced brains, HMF decreased iron distribution but increased total iron content, whereas in eyes it reduced iron content. Sulfur content decreased in frataxin-deficient eyes but increased in brains under HMF, though its spatial distribution was unchanged. Critically, HMF elevated reactive oxygen species (ROS) in frataxin-deficient brains. Transcriptomic analysis identified 202 differentially expressed genes under HMF in frataxin-silenced flies, including key regulators of iron metabolism and oxidative stress pathways. These findings demonstrate that HMF disrupts tissue-specific iron and sulfur homeostasis and intensifies oxidative stress in a frataxin-deficient insect system, underscoring its role as an environmental factor capable of aggravating metabolic fragility.
Kang et al. (2026) studied this question.