Effect of Toxicants on Oocyte Quality and Embryo Development

A special issue of Genes (ISSN 2073-4425). This special issue belongs to the section "Toxicogenomics".

Deadline for manuscript submissions: closed (31 May 2022) | Viewed by 8515

Special Issue Editor


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Guest Editor
Reproductive and Health Biotechnology Lab (RHBL), Department of Biomedical Sciences, Ontario Veterinary College, University of Guelph, Guelph, ON, Canada
Interests: toxicants; oocyte quality; embryo development; gene expression; molecular mechanisms

Special Issue Information

Dear Colleagues,

Oocyte competence is a determinant in attaining viable zygotes, which is fundamental for correct preimplantation embryonic development and is ultimately responsible for achieving a viable pregnancy. Man-made chemicals and drugs for therapeutic and/or recreational use can significantly affect the correct maturation of an oocyte and irreversibly compromise the early stages of embryonic development, significantly decreasing the chances of attaining a potential offspring by impacting the genomic and epigenetic profiles of gametes and embryos at specific key stages of maturation/development. Correct and timely genomic and transcriptional activation during oocyte maturation and embryo development is crucial to attaining a viable pregnancy. Understanding the genomic and epigenetic mechanisms of action of toxicants, such as endocrine disrupting compounds, during early development is a necessary step to fully comprehend their possible impact on fertility, leading to further regulation of the use of man-made chemicals and drugs—such as pesticides, plasticizers and unregulated substances, in women of reproductive age as well as in farm animals—that have been shown to be more sensitive to the exposure to such persistent and spread toxicants in the environment.

This Special Issue aims to present a collection of articles showcasing novel and international research in the field of reproductive toxicology, spanning from the direct genomic, genetic and epigenetic effects of toxicants on gametes, on preimplantation embryo stages of development and on the follicular environment responsible for oocyte competence and, ultimately, on achieving a viable pregnancy.

Manuscripts on the following topics are encouraged and will be considered for publication: toxicant effects at the genomic and epigenetic levels in gametes and early embryo; effects of endocrine disrupting compounds on oocyte competence and embryo development; effects of recreational and therapeutic drugs on fertility and early development; effects of man-made and natural chemicals on gene expression, genomic activation, transcriptome profile and epigenetic modifications in gametes, embryos and reproductive tissues; effects of oxidative and/or heat stress during development; and mechanistic articles on the genomic function of toxicants during early development.

Dr. Laura A. Favetta
Guest Editor

Manuscript Submission Information

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Keywords

  • endocrine disrupting compounds
  • recreational and therapeutic drugs
  • genomic and epigenetic modifications
  • transcriptome
  • gene expression
  • maternal embryonic transition
  • oxidative stress
  • preimplantation embryonic development
  • oocyte competence
  • oocyte maturation

Published Papers (3 papers)

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Research

12 pages, 1559 KiB  
Article
Cadmium Ecotoxic Effects on Embryonic Dmrt1 and Aromatase Expression in Chrysemys picta Turtles May Implicate Changes in DNA Methylation
by Beatriz Mizoguchi, Nicholas E. Topping, Andrew M. Lavin and Nicole Valenzuela
Genes 2022, 13(8), 1318; https://doi.org/10.3390/genes13081318 - 24 Jul 2022
Cited by 2 | Viewed by 2054
Abstract
Temperature-dependent sex determination (TSD) decides the sex fate of an individual based on incubation temperature. However, other environmental factors, such as pollutants, could derail TSD sexual development. Cadmium is one such contaminant of soils and water bodies known to affect DNA methylation, an [...] Read more.
Temperature-dependent sex determination (TSD) decides the sex fate of an individual based on incubation temperature. However, other environmental factors, such as pollutants, could derail TSD sexual development. Cadmium is one such contaminant of soils and water bodies known to affect DNA methylation, an epigenetic DNA modification with a key role in sexual development of TSD vertebrate embryos. Yet, whether cadmium alters DNA methylation of genes underlying gonadal formation in turtles remains unknown. Here, we investigated the effects of cadmium on the expression of two gene regulators of TSD in the painted turtle, Chrysemys picta, incubated at male-producing and female-producing temperatures using qPCR. Results revealed that cadmium alters transcription of Dmrt1 and aromatase, overriding the normal thermal effects during embryogenesis, which could potentially disrupt the sexual development of TSD turtles. Results from a preliminary DNA methylation-sensitive PCR assay implicate changes in DNA methylation of Dmrt1 as a potential cause that requires further testing (aromatase methylation assays were precluded). Full article
(This article belongs to the Special Issue Effect of Toxicants on Oocyte Quality and Embryo Development)
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28 pages, 5592 KiB  
Article
Effects of BPA, BPS, and BPF on Oxidative Stress and Antioxidant Enzyme Expression in Bovine Oocytes and Spermatozoa
by Mimi Nguyen, Reem Sabry, Ola S. Davis and Laura A. Favetta
Genes 2022, 13(1), 142; https://doi.org/10.3390/genes13010142 - 14 Jan 2022
Cited by 23 | Viewed by 3300
Abstract
Bisphenol A (BPA) and its analogs, bisphenol S (BPS) and bisphenol F (BPF), might impact fertility by altering oxidative stress pathways. Here, we hypothesize that bisphenols-induced oxidative stress is responsible for decreased gamete quality. In both female (cumulus-oocyte-complexes—COCs) and male (spermatozoa), oxidative stress [...] Read more.
Bisphenol A (BPA) and its analogs, bisphenol S (BPS) and bisphenol F (BPF), might impact fertility by altering oxidative stress pathways. Here, we hypothesize that bisphenols-induced oxidative stress is responsible for decreased gamete quality. In both female (cumulus-oocyte-complexes—COCs) and male (spermatozoa), oxidative stress was measured by CM-H2DCFDA assay and key ROS scavengers (SOD1, SOD2, GPX1, GPX4, CAT) were quantified at the mRNA and protein levels using qPCR and Western blot (COCs)/immunofluorescence (sperm). Either gamete was treated in five groups: control, vehicle, and 0.05 mg/mL of BPA, BPS, or BPF. Our results show elevated ROS in BPA-treated COCs but decreased production in BPS- and BPF-treated spermatozoa. Additionally, both mRNA and protein expression of SOD2, GPX1, and GPX4 were decreased in BPA-treated COCs (p < 0.05). In sperm, motility (p < 0.03), but not morphology, was significantly altered by bisphenols. SOD1 mRNA expression was significantly increased, while GPX4 was significantly reduced. These results support BPA’s ability to alter oxidative stress in oocytes and, to a lesser extent, in sperm. However, BPS and BPF likely act through different mechanisms. Full article
(This article belongs to the Special Issue Effect of Toxicants on Oocyte Quality and Embryo Development)
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17 pages, 2326 KiB  
Article
Transcriptome-Based Identification of Genes Responding to the Organophosphate Pesticide Phosmet in Danio rerio
by Bala Murali Krishna Vasamsetti, Kyongmi Chon, Juyeong Kim, Jin-A Oh, Chang-Young Yoon and Hong-Hyun Park
Genes 2021, 12(11), 1738; https://doi.org/10.3390/genes12111738 - 29 Oct 2021
Cited by 15 | Viewed by 2561
Abstract
Organophosphate pesticides (OPPs) are one of the most widely used insecticides. OPPs exert their neurotoxic effects by inhibiting acetylcholine esterase (AChE). Most of the gross developmental abnormalities observed in OPP-treated fish, on the other hand, may not be explained solely by AChE inhibition. [...] Read more.
Organophosphate pesticides (OPPs) are one of the most widely used insecticides. OPPs exert their neurotoxic effects by inhibiting acetylcholine esterase (AChE). Most of the gross developmental abnormalities observed in OPP-treated fish, on the other hand, may not be explained solely by AChE inhibition. To understand the overall molecular mechanisms involved in OPP toxicity, we used the zebrafish (ZF) model. We exposed ZF embryos to an OPP, phosmet, for 96 h, and then analyzed developmental abnormalities and performed whole transcriptome analysis. Phenotypic abnormalities, such as bradycardia, spine curvature, and growth retardation, were observed in phosmet-treated ZF (PTZF). Whole transcriptome analysis revealed 2190 differentially expressed genes (DEGs), with 822 and 1368 significantly up-and downregulated genes, respectively. System process and sensory and visual perception were among the top biological pathways affected by phosmet toxicity. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis revealed significant enrichment of metabolic pathways, calcium signaling pathway, regulation of actin cytoskeleton, cardiac muscle contraction, drug metabolism–other enzymes, and phototransduction. Quantitative real-time PCR results of six DEGs agreed with the sequencing data expression profile trend. Our findings provide insights into the consequences of phosmet exposure in ZF, as well as an estimate of the potential risk of OPPs to off-target species. Full article
(This article belongs to the Special Issue Effect of Toxicants on Oocyte Quality and Embryo Development)
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