ArticleBiological trace element research2025
Rapamycin and Post-Deficiency Dietary Recovery Reshape Antioxidant Response and Survival in Offspring of Iron-Deficient Mothers.
Article in Biological trace element research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Maternal iron deficiency (ID) disrupts maternal and offspring health by impairing iron status and antioxidant defenses. Rapamycin is known to promote autophagy, enhance antioxidant activity, and extend lifespan. This study investigates the intergenerational effects of post-deficiency dietary interventions using normal and rapamycin-treated diets on Drosophila melanogaster. Female flies (F0) were subjected to an iron-deficient diet for 14 days, followed by a 30-day recovery period on either a normal diet or a rapamycin-supplemented diet. Some F0 females were subsequently mated with normal males to produce F1 offspring. Physiological, biochemical, and gene expression analyses were conducted on F0 flies post-chelation and post-intervention. Post-eclosion evaluations, including a 60-day survival study, were performed on both generations. In F0 females, iron chelation significantly reduced (p < 0.0001) body weight, iron levels, and antioxidant enzyme activity, while increasing glutathione (GSH) levels. Gene expression analysis revealed significant changes (p < 0.05) in iron storage (Fer1HCH), autophagy (ATG1), and telomere-related genes (dHeT-A, dTahre, dTart). While a normal diet partially restored iron levels and survival, the rapamycin-treated diet improved antioxidant defenses but had mixed effects on survival and gene expression. In the F1 generation, male and female offspring from mothers on a normal diet exhibited reduced and increased iron levels, respectively, alongside improved median survival. Rapamycin increased body weight and iron levels in female offspring but reduced their median survival. Post-deficiency dietary interventions significantly shape antioxidant responses and survival in both iron-deficient mothers and their offspring. While normal diets support recovery of iron status, rapamycin enhances antioxidant defenses but compromises survival, particularly in female offspring.
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