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<p>The developing brain requires high energy demands and metabolic efforts to regulate oxidative stress and myelination. Early insults cause mitochondrial dysfunction and compromise these pathways, potentially leading to cerebral palsy (CP), a severe and incurable neurological disorder that begins in childhood. Through a rodent preclinical study, we demonstrated that vitamin B2 (riboflavin), administered at a high dose (100&#xa0;mg/kg), is accumulated in healthy (B2C) or paralytic (B2CP) brains and participates in neurodevelopment. Redox homeostasis was maintained in B2C through decreased malondialdehyde and carbonyls and increased glutathione-S-transferase activity. In B2CP rodents, there was a reduction in carbonyls and increased superoxide dismutase activity. Mitochondrial morphometric analysis suggests that riboflavin treatment increases biogenesis in controls and reduces mitochondrial deformation in CP. Ultrastructural analysis revealed increased myelin sheath thickness in B2C. Additionally, myelin figure formation and mitochondrial and axonal disintegration in CP were reduced by B2. Our evidence supports vitamin B2 accumulation as a beneficial mechanism to support energy homeostasis and mitochondrial demands that occur during typical neurodevelopment or in the face of CP.</p>

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Riboflavin (Vitamin B2) Accumulation Modulates Neuronal Cellular Homeostasis in Typical Brain Development and Cerebral Palsy

  • 期刊论文

  • 发表日期：

    2025年9月12日

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  • Eulália Rebeca Silva-Araújo,
  • Eduardo Padrón-Hernández,
  • Ana Elisa Toscano,
  • Osmar Henrique dos Santos Júnior,
  • Joaci Pereira dos Santos Júnior,
  • Henrique José Cavalcanti Bezerra Gouveia,
  • Adriana Soares de Carvalho,
  • Janaína Viana de Melo,
  • Luiz Alberto Reis Mattos-Júnior,
  • Raul Manhães-de-Castro

摘要

The developing brain requires high energy demands and metabolic efforts to regulate oxidative stress and myelination. Early insults cause mitochondrial dysfunction and compromise these pathways, potentially leading to cerebral palsy (CP), a severe and incurable neurological disorder that begins in childhood. Through a rodent preclinical study, we demonstrated that vitamin B2 (riboflavin), administered at a high dose (100 mg/kg), is accumulated in healthy (B2C) or paralytic (B2CP) brains and participates in neurodevelopment. Redox homeostasis was maintained in B2C through decreased malondialdehyde and carbonyls and increased glutathione-S-transferase activity. In B2CP rodents, there was a reduction in carbonyls and increased superoxide dismutase activity. Mitochondrial morphometric analysis suggests that riboflavin treatment increases biogenesis in controls and reduces mitochondrial deformation in CP. Ultrastructural analysis revealed increased myelin sheath thickness in B2C. Additionally, myelin figure formation and mitochondrial and axonal disintegration in CP were reduced by B2. Our evidence supports vitamin B2 accumulation as a beneficial mechanism to support energy homeostasis and mitochondrial demands that occur during typical neurodevelopment or in the face of CP.