Naringin supplementation during pregnancy alters rat offspring’s brain redox system and mitochondrial function

• Published in: Brain research 2025-01, Vol.1847, p.149317, Article 149317
• Main Authors: dos Santos, B.G., Klein, C.P., August, P.M., Crestani, M.S., Hozer, R.M., Saccomori, A.B., Dal Magro, B.M., Rodrigues, K.S., Matté, C.
• Format: Article
• Language: English
• Subjects: Animals; Animals, Newborn; Brain - drug effects; Brain - metabolism; Dietary Supplements; DOHaD; Female; Flavanones - pharmacology; Flavonoids; Male; Mitochondria; Mitochondria - drug effects; Mitochondria - metabolism; Naringin; Oxidation-Reduction - drug effects; Oxidative Stress - drug effects; Pregnancy; Prenatal Exposure Delayed Effects - metabolism; Rats; Rats, Wistar; Redox status
• ISSN: 0006-8993; 1872-6240; 1872-6240
• DOI: 10.1016/j.brainres.2024.149317

[Display omitted] •Naringin intake during pregnancy alters the offspring’s brain redox status.•Maternal naringin intake induces mitochondrial deficits in the offspring’s brain.•Offspring’s cerebellum is the most affected area. Naringin supplementation is known to ameliorate oxidative stress in the central nervous system (CNS) and improve cognitive function in disease models using adult rodents. However, if this supplementation is applied during critical periods of development, would it still be beneficial? To address this question, we used pregnant Wistar rats that were supplemented daily with naringin (100 mg/kg) during gestation. After delivery, pups were euthanized on postnatal day (PND) 1, 7, and 21. The prefrontal cortex, hippocampus, striatum, and cerebellum were dissected for redox system and mitochondrial function evaluation. Our data demonstrated that naringin supplementation to pregnant rats during gestation differentially affected the brain structures analyzed, inducing a dysregulation in the redox homeostasis, mainly on PND1. Redox and mitochondrial alterations found in offspring’s cerebellum on PND1 were also observed on PND7, and persisted up to PND21, indicating a higher susceptibility of this structure to the effects triggered by maternal naringin supplementation. In contrast to what was observed in the cerebellum, we found a progressive decline in the number of alterations in the prefrontal cortex, hippocampus, and striatum from PND1 up to PND21, suggesting that these brain structures are not as susceptible as the cerebellum to the naringin’s effects. Thus, our findings demonstrate a possible negative programming effect triggered by maternal naringin supplementation during pregnancy in the offspring’s brain, especially in the cerebellum.