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Special Issue "Reproductive and Developmental Toxicology 2.0"

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: 31 December 2021.

Special Issue Editor

Prof. Dr. Louise C. Abbott
E-Mail Website
Guest Editor
Department of Veterinary Integrative Biosciences (VIBS), College of Veterinary Medicine and Biomedical Sciences, Texas A&M University, College Station, TX 77843-4458, USA
Interests: toxicology; reproductive toxicology; developmental toxicology
Special Issues and Collections in MDPI journals

Special Issue Information

Dear Colleagues,

The fields of reproductive and developmental toxicology are complex areas of considerable importance and intense study, not just for the human population, but also for all animal species. Reproductive systems and developing embryos and fetuses exhibit increased risks of adverse effects due to exposure to a broad range of toxicants, from pharmaceuticals to environmental contaminants. New information concerning risk levels, as well as ways to mitigate risk, are gained using in vitro, in silico, and in vivo toxicity model studies. Research about the effects of toxicants on the process of reproduction and on developing individuals requires investigation at all levels of scientific inquiry—molecular, physiological and anatomical—and the importance of genetic makeup in response to toxicant exposure is just being realized. Individuals may encounter substances that have potentially harmful effects on reproductive health or the developing embryo and fetus anywhere in the environment, through water, air, soil, dust, food, or consumer products. The goal of all toxicology research is to utilize reliable and predictive toxicity testing to understand and prevent exposure to potentially harmful toxicants of reproducing animals and humans, as well as developing individuals. This Special Issue focuses on reproductive and developmental toxicology. We invite authors to submit manuscripts that study the molecular mechanism of any toxicant with adverse effects on male and female reproductive systems or the developing embryo or fetus.

Prof. Dr. Louise Abbott
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 papers will be 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

  • reproductive toxicity
  • reproductive toxicology
  • developmental toxicology
  • embryo toxicity
  • fetal toxicity
  • environmental exposures

Published Papers (4 papers)

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Research

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Article
GSH and Zinc Supplementation Attenuate Cadmium-Induced Cellular Stress and Stimulation of Choline Uptake in Cultured Neonatal Rat Choroid Plexus Epithelia
Int. J. Mol. Sci. 2021, 22(16), 8857; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22168857 - 17 Aug 2021
Viewed by 453
Abstract
Choroid plexus (CP) sequesters cadmium and other metals, protecting the brain from these neurotoxins. These metals can induce cellular stress and modulate homeostatic functions of CP, such as solute transport. We previously showed in primary cultured neonatal rat CP epithelial cells (CPECs) that [...] Read more.
Choroid plexus (CP) sequesters cadmium and other metals, protecting the brain from these neurotoxins. These metals can induce cellular stress and modulate homeostatic functions of CP, such as solute transport. We previously showed in primary cultured neonatal rat CP epithelial cells (CPECs) that cadmium induced cellular stress and stimulated choline uptake at the apical membrane, which interfaces with cerebrospinal fluid in situ. Here, in CPECs, we characterized the roles of glutathione (GSH) and Zinc supplementation in the adaptive stress response to cadmium. Cadmium increased GSH and decreased the reduced GSH-to-oxidized GSH (GSSG) ratio. Heat shock protein-70 (Hsp70), heme oxygenase (HO-1), and metallothionein (Mt-1) were induced along with the catalytic and modifier subunits of glutamate cysteine ligase (GCL), the rate-limiting enzyme in GSH synthesis. Inhibition of GCL by l-buthionine sulfoximine (BSO) enhanced stress protein induction and stimulation of choline uptake by cadmium. Zinc alone did not induce Hsp70, HO-1, or GCL subunits, or modulate choline uptake. Zinc supplementation during cadmium exposure attenuated stress protein induction and stimulation of choline uptake; this effect persisted despite inhibition of GSH synthesis. These data indicated up-regulation of GSH synthesis promotes adaptation to cadmium-induced cellular stress in CP, but Zinc may confer cytoprotection independent of GSH. Full article
(This article belongs to the Special Issue Reproductive and Developmental Toxicology 2.0)
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Article
Co-Treatment of Copper Oxide Nanoparticle and Carbofuran Enhances Cardiotoxicity in Zebrafish Embryos
Int. J. Mol. Sci. 2021, 22(15), 8259; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22158259 - 31 Jul 2021
Viewed by 622
Abstract
The use of chemicals to boost food production increases as human consumption also increases. The insectidal, nematicidal and acaricidal chemical carbofuran (CAF), is among the highly toxic carbamate pesticide used today. Alongside, copper oxide nanoparticles (CuO) are also used as pesticides due to [...] Read more.
The use of chemicals to boost food production increases as human consumption also increases. The insectidal, nematicidal and acaricidal chemical carbofuran (CAF), is among the highly toxic carbamate pesticide used today. Alongside, copper oxide nanoparticles (CuO) are also used as pesticides due to their broad-spectrum antimicrobial activity. The overuse of these pesticides may lead to leaching into the aquatic environments and could potentially cause adverse effects to aquatic animals. The aim of this study is to assess the effects of carbofuran and copper oxide nanoparticles into the cardiovascular system of zebrafish and unveil the mechanism behind them. We found that a combination of copper oxide nanoparticle and carbofuran increases cardiac edema in zebrafish larvae and disturbs cardiac rhythm of zebrafish. Furthermore, molecular docking data show that carbofuran inhibits acetylcholinesterase (AChE) activity in silico, thus leading to impair cardiac rhythms. Overall, our data suggest that copper oxide nanoparticle and carbofuran combinations work synergistically to enhance toxicity on the cardiovascular performance of zebrafish larvae. Full article
(This article belongs to the Special Issue Reproductive and Developmental Toxicology 2.0)
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Review

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Review
Toxic and Teratogenic Effects of Prenatal Alcohol Exposure on Fetal Development, Adolescence, and Adulthood
Int. J. Mol. Sci. 2021, 22(16), 8785; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22168785 - 16 Aug 2021
Cited by 1 | Viewed by 838
Abstract
Prenatal alcohol exposure (PAE) can have immediate and long-lasting toxic and teratogenic effects on an individual’s development and health. As a toxicant, alcohol can lead to a variety of physical and neurological anomalies in the fetus that can lead to behavioral and other [...] Read more.
Prenatal alcohol exposure (PAE) can have immediate and long-lasting toxic and teratogenic effects on an individual’s development and health. As a toxicant, alcohol can lead to a variety of physical and neurological anomalies in the fetus that can lead to behavioral and other impairments which may last a lifetime. Recent studies have focused on identifying mechanisms that mediate the immediate teratogenic effects of alcohol on fetal development and mechanisms that facilitate the persistent toxic effects of alcohol on health and predisposition to disease later in life. This review focuses on the contribution of epigenetic modifications and intercellular transporters like extracellular vesicles to the toxicity of PAE and to immediate and long-term consequences on an individual’s health and risk of disease. Full article
(This article belongs to the Special Issue Reproductive and Developmental Toxicology 2.0)
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Review
Mercury Toxicity and Neurogenesis in the Mammalian Brain
Int. J. Mol. Sci. 2021, 22(14), 7520; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22147520 - 14 Jul 2021
Viewed by 462
Abstract
The mammalian brain is formed from billions of cells that include a wide array of neuronal and glial subtypes. Neural progenitor cells give rise to the vast majority of these cells during embryonic, fetal, and early postnatal developmental periods. The process of embryonic [...] Read more.
The mammalian brain is formed from billions of cells that include a wide array of neuronal and glial subtypes. Neural progenitor cells give rise to the vast majority of these cells during embryonic, fetal, and early postnatal developmental periods. The process of embryonic neurogenesis includes proliferation, differentiation, migration, the programmed death of some newly formed cells, and the final integration of differentiated neurons into neural networks. Adult neurogenesis also occurs in the mammalian brain, but adult neurogenesis is beyond the scope of this review. Developing embryonic neurons are particularly susceptible to neurotoxicants and especially mercury toxicity. This review focused on observations concerning how mercury, and in particular, methylmercury, affects neurogenesis in the developing mammalian brain. We summarized information on models used to study developmental mercury toxicity, theories of pathogenesis, and treatments that could be used to reduce the toxic effects of mercury on developing neurons. Full article
(This article belongs to the Special Issue Reproductive and Developmental Toxicology 2.0)
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