D-galactose dose-dependently exerts differential effects on life history traits and redox modulation in early adulthood in Drosophila melanogaster

D-galactose, a common component of staple foods, induces oxidative stress and inflammageing when taken in excess, making it a widely used model for ageing studies. However, its dose-dependent effects on early life development remain poorly characterized, particularly whether low-dose beneficial effects exist at early adulthood following drug withdrawal. This study assessed the dose-dependent impact of D-galactose on life history traits, behaviour, and redox homeostasis in D. melanogaster , determining whether developmental exposure (confined to pre-eclosion) produces alterations in early adulthood. Eggs were exposed throughout development to distilled water (control) or D-galactose (10, 20, or 25 mg/g). Treatment ended at eclosion; adults were maintained on untreated food. Larval behaviour, pupation, eclosion, and adult locomotor performance (day five) were assessed. Biochemical analyses (thiols, H₂O₂, nitric oxide, MAO-B activity) were conducted on five-day-old adults. The 10 mg/g dose significantly improved pupation ( p < 0.001), eclosion ( p < 0.05), larval feeding ( p < 0.05), and crawling ( p = 0.01). In five-day-old adults, this low dose decreased H₂O₂ ( p < 0.001) and increased total and non-protein thiols ( p < 0.001), indicating redox modulation despite drug withdrawal. The 25 mg/g dose impaired pupation, elevated H₂O₂ and nitrite/nitrate ( p < 0.001), and reduced thiols. Adult climbing activity was unaffected across all groups ( p > 0.05), revealing dissociation between redox changes and behavioural outcomes. D-galactose exerts dose-dependent biphasic effects. The low dose was associated with beneficial developmental effects and redox changes consistent with a hormetic response, while higher doses induced oxidative/nitrosative stress and impairment. The absence of corresponding enhancement in adult behaviour despite altered redox status highlights a biochemical-functional dissociation following developmental exposure.