Journal of trace elements in medicine and biology : organ of the Society for Minerals and Trace Elements (GMS) · 2025
Paternal iron deficiency and rapamycin supplementation influence antioxidants status, autophagy and lifespan in Drosophila melanogaster.
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Faruk Saudatu, Ibrahim Kasimu Ghandi, Sulaiman Ismail, Abbas Abdullahi Yahya, Imam Mustapha Umar
Аннотация
BACKGROUND: Paternal iron deficiency (ID) is increasingly recognized for its intergenerational health effects. Rapamycin, on the other hand, is known for modulating metabolism, enhancing autophagy, and promoting longevity. This study explores the impact of paternal ID and rapamycin intervention on iron metabolism, antioxidant status, autophagy, telomere regulation, and lifespan in Drosophila melanogaster.
METHODS: Male flies (F0) were fed an iron-deficient diet for 14 days, followed by a 30-day intervention with either a normal or rapamycin-supplemented diet. F0 ID males were crossed with normal females to generate F1 offspring. Physiological, biochemical, and gene expression changes were analyzed in F0 flies post-intervention, while F1 offspring were assessed post-eclosion, with a 60-day survival study conducted for both generations.
RESULTS: In F0 ID males, iron chelation significantly (p < 0.0001) reduced body weight, iron levels, and antioxidant enzyme (SOD, CAT) activity, while increasing GSH levels. Gene expression analysis showed significant (p < 0.05) alterations in iron storage (Fer1HCH), autophagy (ATG1), and telomere maintenance (dHeT-A, dTahre, dTart) genes. Rapamycin reduced antioxidant enzyme levels and lifespan in F0 males despite improving oxidative stress markers. In F1 offspring, males on a normal diet exhibited lower iron levels but increased survival, whereas rapamycin enhanced antioxidant status in F1 females without significantly affecting lifespan.
CONCLUSION: Paternal ID exerts lasting, sex-specific effects across generations. While a normal diet mitigates some adverse outcomes, rapamycin worsens survival in F0 males and has mixed effects on F1 offspring, particularly concerning antioxidant status and longevity.
METHODS: Male flies (F0) were fed an iron-deficient diet for 14 days, followed by a 30-day intervention with either a normal or rapamycin-supplemented diet. F0 ID males were crossed with normal females to generate F1 offspring. Physiological, biochemical, and gene expression changes were analyzed in F0 flies post-intervention, while F1 offspring were assessed post-eclosion, with a 60-day survival study conducted for both generations.
RESULTS: In F0 ID males, iron chelation significantly (p < 0.0001) reduced body weight, iron levels, and antioxidant enzyme (SOD, CAT) activity, while increasing GSH levels. Gene expression analysis showed significant (p < 0.05) alterations in iron storage (Fer1HCH), autophagy (ATG1), and telomere maintenance (dHeT-A, dTahre, dTart) genes. Rapamycin reduced antioxidant enzyme levels and lifespan in F0 males despite improving oxidative stress markers. In F1 offspring, males on a normal diet exhibited lower iron levels but increased survival, whereas rapamycin enhanced antioxidant status in F1 females without significantly affecting lifespan.
CONCLUSION: Paternal ID exerts lasting, sex-specific effects across generations. While a normal diet mitigates some adverse outcomes, rapamycin worsens survival in F0 males and has mixed effects on F1 offspring, particularly concerning antioxidant status and longevity.