Developmental exposure to perifosine induces growth retardation associated with disruption of iron and copper homeostasis in Drosophila melanogaster

Developmental exposure to chemical compounds is a critical determinant of offspring health. While Perifosine has demonstrated significant cytotoxic properties, its safety profile during pregnancy remains uncharacterized. Using a Drosophila model, we evaluated the developmental toxicity of Perifosine through in vivo and in vitro approaches. Our results demonstrate that Perifosine induces cytotoxicity and offspring growth retardation by impairing iron and copper homeostasis, a process mediated through altered expression of key regulatory targets and subsequent mitochondrial dysfunction. Notably, both Quercetin and Resveratrol effectively mitigated these adverse effects by alleviating oxidative stress and restoring metal equilibrium. These findings provide mechanistic insights into the developmental toxicity of perinatal compound exposure and suggest potential therapeutic strategies for its prevention.