Preprint Review Version 1 Preserved in Portico This version is not peer-reviewed

The Impact of Oxidative Stress on the Epigenetics of Fetal Alcohol Spectrum Disorders

Sergio Terracina
ORCID logo ,
Luigi Tarani
ORCID logo ,
Mauro Ceccanti
ORCID logo ,
Mario Vitali
,
Silvia Francati
,
Marco Lucarelli
ORCID logo ,
Sabrina Venditti
,
Loredana Verdone
,
Giampiero Ferraguti
ORCID logo ,
Marco Fiore
*
Version 1 : Received: 7 March 2024 / Approved: 7 March 2024 / Online: 7 March 2024 (12:06:43 CET)

A peer-reviewed article of this Preprint also exists.

Terracina, S.; Tarani, L.; Ceccanti, M.; Vitali, M.; Francati, S.; Lucarelli, M.; Venditti, S.; Verdone, L.; Ferraguti, G.; Fiore, M. The Impact of Oxidative Stress on the Epigenetics of Fetal Alcohol Spectrum Disorders. Antioxidants 2024, 13, 410. Terracina, S.; Tarani, L.; Ceccanti, M.; Vitali, M.; Francati, S.; Lucarelli, M.; Venditti, S.; Verdone, L.; Ferraguti, G.; Fiore, M. The Impact of Oxidative Stress on the Epigenetics of Fetal Alcohol Spectrum Disorders. Antioxidants 2024, 13, 410.

Abstract

Fetal Alcohol Spectrum Disorders (FASD) represent a continuum of lifelong impairments resulting from prenatal exposure to alcohol, with significant global impact. The “spectrum” of disorders includes a continuum of physical, cognitive, behavioral, and developmental impairments, which can have profound and lasting effects on individuals throughout their lives impacting their health, social interactions, psychological well-being and every aspect of their lives. This narrative paper explores the intricate relationship between oxidative stress and epigenetics in FASD pathogenesis and its therapeutic implications. Oxidative stress, induced by alcohol metabolism, disrupts cellular components, particularly in the vulnerable fetal brain, leading to aberrant development. Furthermore, oxidative stress is implicated in epigenetic changes, including alterations in DNA methylation, histone modifications, and microRNA expression, which influence gene regulation in FASD patients. Moreover, mitochondrial dysfunction and neuroinflammation contribute to epigenetic changes associated with FASD. Understanding these mechanisms holds promise for targeted therapeutic interventions. This includes antioxidant supplementation and lifestyle modifications to mitigate FASD-related impairments. While preclinical studies show promise, further clinical trials are needed to validate these interventions' efficacy in improving clinical outcomes for individuals affected by FASD. This comprehensive understanding of the role of oxidative stress on epigenetics in FASD underscores the importance of multidisciplinary approaches for diagnosis, management, and prevention strategies. Continued research in this field is crucial for advancing our knowledge and developing effective interventions to address this significant public health concern.

Keywords

FASD; Epigenetics; Oxidative Stress; Antioxidants; Alcohol

Subject

Biology and Life Sciences, Neuroscience and Neurology

Copyright: This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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