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Molecular Advances in Endocrine Toxicity

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Toxicology".

Deadline for manuscript submissions: closed (15 July 2023) | Viewed by 5047

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Dr. Anthony Archibong

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Guest Editor

Meharry Endocrine Core Lab, Department of Neuroscience & Pharmacology, Meharry Medical College, Nashville, TN 37208, USA
Interests: reproductive toxicology; reprductive endocrinology; reproductive physiology; andrology; gamete science

Special Issue Information

Dear Colleagues,

Endocrine toxicity presents a major risk for growth retardation, suppressed development, infertility, altered blood pressure, altered ion concentrations, and other substances in the blood and even behavior. Endocrine toxicity is a multifactorial disorder involving altered functions of the hypothalamus, pituitary gland, thyroid, parathyroid, adrenal gland, gonads, placenta, pancreas, and even the kidney and gastrointestinal tract. This toxicity involves interference in the synthesis, secretion, transport, metabolism, and binding action necessary for the maintenance of homeostasis. Such interference ultimately results in loss of normal tissue function, development, growth, or reproduction. Unregulated factors that contribute to congenital disorders and autoimmune response contribute to altering endocrine milieu and the onset of diseases such as cancer, metabolic disorders, and infertility. Therefore, unraveling the underlying causes of endocrine toxicity is critical to improving disease burden. Oxidative stress resulting from accumulation of reactive radicals and subsequent inflammation contributes significantly to the pathogenesis of endocrine toxicity. Thus, remediating specific sources of oxidative stress inducers can improve endocrine-regulated growth and development, metabolism, blood pressure, and infertility in affected subjects. The topic of endocrine toxicity is an alphabet soup for numerous factors that initiate and maintain the condition.

Therefore, in this Special Issue, we will discuss the role of environmental pollutants/endocrine disruptors in the mechanisms associated with the generation of oxidative stress and their role in metabolic dysregulation and inflammation. Further, we will describe the potential interventions that target specific oxidative stress and metabolic pathways that can restore homeostasis.

Dr. Anthony Archibong
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

environment
toxicity
endocrine disruptors
metabolism

Published Papers (4 papers)

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Research

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12 pages, 2772 KiB

Open AccessArticle

Testosterone and Prolactin Perturbations Possibly Associated with Reduced Levels of β-Arrestin1 in Mononuclear Leukocytes of Women with Premenstrual Dysphoric Disorder

by Sanket Nayyar, Anthony Archibong and Tultul Nayyar

Int. J. Mol. Sci. 2023, 24(20), 15449; https://doi.org/10.3390/ijms242015449 - 22 Oct 2023

Viewed by 1006

Abstract

Previously, we reported that a reduction in β-Arrestin1 protein levels in peripheral blood mononuclear leukocytes (PBMC) significantly correlated with the severity of depression symptoms in women with premenstrual dysphoric disorder (PMDD). This study aimed to determine whether the reduced premenstrual β-Arrestin1 protein levels were associated with changes in the regulator for late luteal phase progesterone secretion. The study participants (n = 25) were non-pregnant women between 18 and 42 years of age not taking any antidepressants or receiving therapy and experiencing the luteal phase of menstruation. ELISA determined the β-Arrestin1 protein in PBMC; testosterone and prolactin levels from the plasma were determined by radioimmunoassay. Reduced levels of β-Arrestin1 protein in women with Hamilton Rating Scale for Depression (HAM-D) scores above 19 were observed alongside significantly higher plasma testosterone and prolactin concentrations. Understanding the mechanism underlying the initiation of PMDD will allow for identification of a key perturbed metabolic enzyme that can serve as a target for drug development to ensure the alleviation of PMDD, which has been suggested earlier as a risk factor for developing major depressive disorders. Full article

(This article belongs to the Special Issue Molecular Advances in Endocrine Toxicity)

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16 pages, 1721 KiB

Open AccessArticle

Antioxidant Defense Capacity Is Reduced in Thyroid Stem/Precursor Cells Compared to Differentiated Thyrocytes

by Fiorenza Gianì, Fabio Allia, Maria Antonietta Trovato, Roberta Masto, Gabriella Pellegriti and Riccardo Vigneri

Int. J. Mol. Sci. 2023, 24(14), 11509; https://doi.org/10.3390/ijms241411509 - 15 Jul 2023

Viewed by 982

Abstract

There is much evidence linking oxidative stress to thyroid cancer, and stem cells are thought to play a key role in the tumor-initiating mechanism. Their vulnerability to oxidative stress is unexplored. This study aimed to comparatively evaluate the antioxidant capacity of stem/precursor thyroid cells and mature thyrocytes. Human stem/precursor cells and mature thyrocytes were exposed to increasing concentrations of menadione, an oxidative-stress-producing agent, and reactive oxygen species (ROS) production and cell viability were measured. The expression of antioxidant and detoxification genes was measured via qPCR as well as the total antioxidant capacity and the content of glutathione. Menadione elevated ROS generation in stem/precursor thyroid cells more than in mature thyrocytes. The ROS increase was inversely correlated (p = 0.005) with cell viability, an effect that was partially prevented by the antioxidant curcumin. Most thyroid antioxidant defense genes, notably those encoding for the glutathione-generating system and phase I detoxification enzymes, were significantly less expressed in stem/precursor thyroid cells. As a result, the glutathione level and the total antioxidant capacity in stem/precursor thyroid cells were significantly decreased. This reduced antioxidant defense may have clinical implications, making stem/precursor thyroid cells critical targets for environmental conditions that are not detrimental for differentiated thyrocytes. Full article

(This article belongs to the Special Issue Molecular Advances in Endocrine Toxicity)

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17 pages, 1547 KiB

Open AccessArticle

Resumption of Spermatogenesis and Fertility Post Withdrawal of Hydroxyurea Treatment

by Carlos Virgous, Letitia Lyons, Amos Sakwe, Tultul Nayyar, Shawn Goodwin, James Hildreth, Kevin Osteen, Kaylon Bruner-Tran, Oluwatobi Alawode, Phillip Bourne, Edward Richard Hills and Anthony E. Archibong

Int. J. Mol. Sci. 2023, 24(11), 9374; https://doi.org/10.3390/ijms24119374 - 27 May 2023

Cited by 1 | Viewed by 1488

Abstract

Hydroxyurea (HU), a drug for treating cancers of the blood and the management of sickle cell anemia, induces hypogonadism in males. However, the impact of HU on testicular architecture and function, as well as its effects on the resumption of male fertility following treatment withdrawal, remain poorly understood. We used adult male mice to determine whether HU-induced hypogonadism is reversible. Fertility indices of mice treated with HU daily for ~1 sperm cycle (2 months) were compared with those of their control counterparts. All indices of fertility were significantly reduced among mice treated with HU compared to controls. Interestingly, significant improvements in fertility indices were apparent after a 4-month withdrawal from HU treatment (testis weight: month 1 post-HU withdrawal (M1): HU, 0.09 ± 0.01 vs. control, 0.33 ± 0.03; M4: HU, 0.26 ± 0.03 vs. control, 0.37 ± 0.04 g); sperm motility (M1: HU,12 vs. 59; M4: HU, 45 vs. control, 61%; sperm density (M1: HU, 1.3 ± 0.3 vs. control, 15.7 ± 0.9; M4: HU, 8.1 ± 2.5 vs. control, 16.8 ± 1.9 million). Further, circulating testosterone increased in the 4th month following HU withdrawal and was comparable to that of controls. When a mating experiment was conducted, recovering males sired viable offspring with untreated females albeit at a lower rate than control males (p < 0.05); therefore, qualifying HU as a potential candidate for male contraception. Full article

(This article belongs to the Special Issue Molecular Advances in Endocrine Toxicity)

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Review

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18 pages, 816 KiB

Open AccessReview

Imprinting and Reproductive Health: A Toxicological Perspective

by Ritu Chauhan, Anthony E. Archibong and Aramandla Ramesh

Int. J. Mol. Sci. 2023, 24(23), 16559; https://doi.org/10.3390/ijms242316559 - 21 Nov 2023

Cited by 2 | Viewed by 1113

Abstract

This overview discusses the role of imprinting in the development of an organism, and how exposure to environmental chemicals during fetal development leads to the physiological and biochemical changes that can have adverse lifelong effects on the health of the offspring. There has been a recent upsurge in the use of chemical products in everyday life. These chemicals include industrial byproducts, pesticides, dietary supplements, and pharmaceutical products. They mimic the natural estrogens and bind to estradiol receptors. Consequently, they reduce the number of receptors available for ligand binding. This leads to a faulty signaling in the neuroendocrine system during the critical developmental process of ‘imprinting’. Imprinting causes structural and organizational differentiation in male and female reproductive organs, sexual behavior, bone mineral density, and the metabolism of exogenous and endogenous chemical substances. Several studies conducted on animal models and epidemiological studies provide profound evidence that altered imprinting causes various developmental and reproductive abnormalities and other diseases in humans. Altered metabolism can be measured by various endpoints such as the profile of cytochrome P-450 enzymes (CYP450’s), xenobiotic metabolite levels, and DNA adducts. The importance of imprinting in the potentiation or attenuation of toxic chemicals is discussed. Full article

(This article belongs to the Special Issue Molecular Advances in Endocrine Toxicity)

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