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Reproductive and Developmental Toxicology 2023
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Reproductive and Developmental Toxicology 2023

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 (31 January 2023) | Viewed by 9076

Special Issue Editor

Prof. Dr. Louise C. Abbott

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

  • 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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19 pages, 14984 KiB  
Article
Hexavalent Chromium Disrupts Oocyte Development in Rats by Elevating Oxidative Stress, DNA Double-Strand Breaks, Microtubule Disruption, and Aberrant Segregation of Chromosomes
by Liga Wuri, Robert C. Burghardt, Joe A. Arosh, Charles R. Long and Sakhila K. Banu
Int. J. Mol. Sci. 2023, 24(12), 10003; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms241210003 - 11 Jun 2023
Cited by 3 | Viewed by 1596
Abstract
Environmental and occupational exposure to hexavalent chromium, Cr(VI), causes female reproductive failures and infertility. Cr(VI) is used in more than 50 industries and is a group A carcinogen, mutagenic and teratogenic, and a male and female reproductive toxicant. Our previous findings indicate that [...] Read more.
Environmental and occupational exposure to hexavalent chromium, Cr(VI), causes female reproductive failures and infertility. Cr(VI) is used in more than 50 industries and is a group A carcinogen, mutagenic and teratogenic, and a male and female reproductive toxicant. Our previous findings indicate that Cr(VI) causes follicular atresia, trophoblast cell apoptosis, and mitochondrial dysfunction in metaphase II (MII) oocytes. However, the integrated molecular mechanism of Cr(VI)-induced oocyte defects is not understood. The current study investigates the mechanism of Cr(VI) in causing meiotic disruption of MII oocytes, leading to oocyte incompetence in superovulated rats. Postnatal day (PND) 22 rats were treated with potassium dichromate (1 and 5 ppm) in drinking water from PND 22–29 and superovulated. MII oocytes were analyzed by immunofluorescence, and images were captured by confocal microscopy and quantified by Image-Pro Plus software, Version 10.0.5. Our data showed that Cr(VI) increased microtubule misalignment (~9 fold), led to missegregation of chromosomes and bulged and folded actin caps, increased oxidative DNA (~3 fold) and protein (~9–12 fold) damage, and increased DNA double-strand breaks (~5–10 fold) and DNA repair protein RAD51 (~3–6 fold). Cr(VI) also induced incomplete cytokinesis and delayed polar body extrusion. Our study indicates that exposure to environmentally relevant doses of Cr(VI) caused severe DNA damage, distorted oocyte cytoskeletal proteins, and caused oxidative DNA and protein damage, resulting in developmental arrest in MII oocytes. Full article
(This article belongs to the Special Issue Reproductive and Developmental Toxicology 2023)
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17 pages, 2328 KiB  
Article
Pre- and Postnatal Dietary Exposure to a Pesticide Cocktail Disrupts Ovarian Functions in 8-Week-Old Female Mice
by Léonie Dopavogui, Florence Cadoret, Gaspard Loison, Sara El Fouikar, François-Xavier Frenois, Frank Giton, Sandrine Ellero-Simatos, Frédéric Lasserre, Arnaud Polizzi, Clémence Rives, Nicolas Loiseau, Roger D. Léandri, Nicolas Gatimel and Laurence Gamet-Payrastre
Int. J. Mol. Sci. 2022, 23(14), 7525; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23147525 - 07 Jul 2022
Cited by 2 | Viewed by 1685
Abstract
Female infertility has a multifactorial origin, and exposure to contaminants, including pesticides, with endocrine-disrupting properties is considered to be involved in this reproductive disorder, especially when it occurs during early life. Pesticides are present in various facets of the environment, and consumers are [...] Read more.
Female infertility has a multifactorial origin, and exposure to contaminants, including pesticides, with endocrine-disrupting properties is considered to be involved in this reproductive disorder, especially when it occurs during early life. Pesticides are present in various facets of the environment, and consumers are exposed to a combination of multiple pesticide residues through food intake. The consequences of such exposure with respect to female fertility are not well known. Therefore, we aimed to assess the impact of pre- and postnatal dietary exposure to a pesticide mixture on folliculogenesis, a crucial process in female reproduction. Mice were exposed to the acceptable daily intake levels of six pesticides in a mixture (boscalid, captan, chlorpyrifos, thiacloprid, thiophanate and ziram) from foetal development until 8 weeks old. Female offspring presented with decreased body weight at weaning, which was maintained at 8 weeks old. This was accompanied by an abnormal ovarian ultrastructure, a drastic decrease in the number of corpora lutea and progesterone levels and an increase in ovary cell proliferation. In conclusion, this study shows that this pesticide mixture that can be commonly found in fruits in Europe, causing endocrine disruption in female mice with pre- and postnatal exposure by disturbing folliculogenesis, mainly in the luteinisation process. Full article
(This article belongs to the Special Issue Reproductive and Developmental Toxicology 2023)
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Review

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22 pages, 909 KiB  
Review
The Threat Posed by Environmental Contaminants on Neurodevelopment: What Can We Learn from Neural Stem Cells?
by Raj Bose, Stefan Spulber and Sandra Ceccatelli
Int. J. Mol. Sci. 2023, 24(5), 4338; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms24054338 - 22 Feb 2023
Cited by 1 | Viewed by 1931
Abstract
Exposure to chemicals may pose a greater risk to vulnerable groups, including pregnant women, fetuses, and children, that may lead to diseases linked to the toxicants’ target organs. Among chemical contaminants, methylmercury (MeHg), present in aquatic food, is one of the most harmful [...] Read more.
Exposure to chemicals may pose a greater risk to vulnerable groups, including pregnant women, fetuses, and children, that may lead to diseases linked to the toxicants’ target organs. Among chemical contaminants, methylmercury (MeHg), present in aquatic food, is one of the most harmful to the developing nervous system depending on time and level of exposure. Moreover, certain man-made PFAS, such as PFOS and PFOA, used in commercial and industrial products including liquid repellants for paper, packaging, textile, leather, and carpets, are developmental neurotoxicants. There is vast knowledge about the detrimental neurotoxic effects induced by high levels of exposure to these chemicals. Less is known about the consequences that low-level exposures may have on neurodevelopment, although an increasing number of studies link neurotoxic chemical exposures to neurodevelopmental disorders. Still, the mechanisms of toxicity are not identified. Here we review in vitro mechanistic studies using neural stem cells (NSCs) from rodents and humans to dissect the cellular and molecular processes changed by exposure to environmentally relevant levels of MeHg or PFOS/PFOA. All studies show that even low concentrations dysregulate critical neurodevelopmental steps supporting the idea that neurotoxic chemicals may play a role in the onset of neurodevelopmental disorders. Full article
(This article belongs to the Special Issue Reproductive and Developmental Toxicology 2023)
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13 pages, 1099 KiB  
Review
Carbamate Pesticides: Shedding Light on Their Impact on the Male Reproductive System
by Sílvia Moreira, Ricardo Silva, David F. Carrageta, Marco G. Alves, Vicente Seco-Rovira, Pedro F. Oliveira and Maria de Lourdes Pereira
Int. J. Mol. Sci. 2022, 23(15), 8206; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23158206 - 26 Jul 2022
Cited by 14 | Viewed by 2887
Abstract
Carbamates are widely used and known around the world as pesticides in spite of also having medical applications. This class of chemicals is classified as acetylcholinesterase inhibitors, blocking acetylcholine hydrolyzation in a reversible manner. Their lack of species selectivity and their reported high [...] Read more.
Carbamates are widely used and known around the world as pesticides in spite of also having medical applications. This class of chemicals is classified as acetylcholinesterase inhibitors, blocking acetylcholine hydrolyzation in a reversible manner. Their lack of species selectivity and their reported high toxicity can induce, upon exposure, adverse outcomes in male fertility that may lead to infertility. In addition, they are also considered endocrine-disrupting chemicals and can interfere with the hypothalamic–pituitary–testicular axis, essential for the normal function of the male reproductive system, thus being able to provoke male reproductive dysfunctions. Although the molecular mechanisms are not fully understood, various signaling pathways, such as those mediated by acetylcholine or kisspeptin, are affected by exposure to carbamates, thus compromising steroidogenesis and spermatogenesis. Over the last decades, several studies, both in vitro and in vivo, have reported a myriad of negative effects of carbamates on the male reproductive system. In this review, an up-to-date overview of the impact of carbamates on the male reproductive system is discussed, with an emphasis on the role of these compounds on acetylcholine regulation and the male endocrine system. Full article
(This article belongs to the Special Issue Reproductive and Developmental Toxicology 2023)
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