Hormones and Oxidative Stress

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: closed (30 October 2024) | Viewed by 1098

Special Issue Editor


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Guest Editor
Department of Experimental and Clinical Medicine, Research Unit of Histology and Embryology, University of Florence, Viale G. Pieraccini 6, 50139 Florence, Italy
Interests: hormone; human health; oxidative stress; endocrinology

Special Issue Information

Dear Colleagues,

Reactive oxygen species (ROS) are generated as normal products of aerobic cellular metabolism. ROS produced at low concentrations have beneficial effects on a variety of physiological processes, including cellular signaling, proliferation, and growth. However, when present at high levels, ROS can react with lipids, proteins, and DNA, causing cell damage with consequent biochemical and biophysical deleterious effects. Therefore, all aerobic organisms have evolved both enzymatic and nonenzymatic antioxidant defense mechanisms to counteract the deleterious impact of ROS on cells and tissues. An imbalance between the production of ROS and the capability of the antioxidant defense system results in the induction of oxidative stress, which is involved in different pathological events, including cardiovascular disease, obesity, diabetes, and cancer. The regulation of cellular antioxidant defenses may be influenced by different factors, such as age, organ specificity, and hormonal state. Some hormones, such as melatonin, insulin, and estrogen, act as antioxidants and/or exert an impact on the various enzymatic and non-enzymatic components of the defense system, while others, including thyroid hormones, corticosteroids, and catecholamines, promote the generation of ROS and oxidative stress. Moreover, any alterations in the hormonal milieu can exhibit significant effects on ROS production and oxidative stress, possibly leading to pathological conditions. The intricate interplay between the endocrine system, redox equilibrium, and oxidative stress is a topic that deserves to be elucidated given its potential impact on human health. 

For this Special Issue, “Hormones and Oxidative Stress”, we invite you to submit your original research papers and reviews with the aim of better understanding the complex relationship between hormonal conditions, redox states, and oxidative stress in living systems in both physiological and pathological conditions.

Dr. Silvia Nistri
Guest Editor

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Keywords

  • reactive oxygen species
  • oxidative stress
  • hormones
  • antioxidants
  • melatonin
  • insulin
  • estrogen

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Published Papers (1 paper)

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Research

18 pages, 18799 KiB  
Article
Protective Effects of Beta-3 Adrenoceptor Agonism on Mucosal Integrity in Hyperoxia-Induced Ileal Alterations
by Patrizia Nardini, Virginia Zizi, Marta Molino, Camilla Fazi, Maura Calvani, Francesco Carrozzo, Giorgia Giuseppetti, Laura Calosi, Daniele Guasti, Denise Biagini, Fabio Di Francesco, Luca Filippi and Alessandro Pini
Antioxidants 2024, 13(7), 863; https://doi.org/10.3390/antiox13070863 - 18 Jul 2024
Viewed by 734
Abstract
Organogenesis occurs in the uterus under low oxygen levels (4%). Preterm birth exposes immature newborns to a hyperoxic environment, which can induce a massive production of reactive oxygen species and potentially affect organ development, leading to diseases such as necrotizing enterocolitis. The β3-adrenoreceptor [...] Read more.
Organogenesis occurs in the uterus under low oxygen levels (4%). Preterm birth exposes immature newborns to a hyperoxic environment, which can induce a massive production of reactive oxygen species and potentially affect organ development, leading to diseases such as necrotizing enterocolitis. The β3-adrenoreceptor (β3-AR) has an oxygen-dependent regulatory mechanism, and its activation exerts an antioxidant effect. To test the hypothesis that β3-AR could protect postnatal ileal development from the negative impact of high oxygen levels, Sprague–Dawley rat pups were raised under normoxia (21%) or hyperoxia (85%) for the first 2 weeks after birth and treated or not with BRL37344, a selective β3-AR agonist, at 1, 3, or 6 mg/kg. Hyperoxia alters ileal mucosal morphology, leading to increased cell lipid oxidation byproducts, reduced presence of β3-AR-positive resident cells, decreased junctional protein expression, disrupted brush border, mucin over-production, and impaired vascularization. Treatment with 3 mg/kg of BRL37344 prevented these alterations, although not completely, while the lower 1 mg/kg dose was ineffective, and the higher 6 mg/kg dose was toxic. Our findings indicate the potential of β3-AR agonism as a new therapeutic approach to counteract the hyperoxia-induced ileal alterations and, more generally, the disorders of prematurity related to supra-physiologic oxygen exposure. Full article
(This article belongs to the Special Issue Hormones and Oxidative Stress)
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