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Developmental and Reproductive Toxicology

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

Deadline for manuscript submissions: 20 June 2025 | Viewed by 2345

Special Issue Editor


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Guest Editor
Department of Animal Biotechnology, College of Life Science, Sangji University, Wonju-si, Republic of Korea
Interests: spermatogenesis; mouse models; reproduction biology; assisted reproductive technology; cellular biology; developmental biology

Special Issue Information

Dear Colleagues,

The study of gamete development, differentiation, and toxicity plays a pivotal role in reproductive biology and environmental health. Gamete development, encompassing spermatogenesis and oogenesis, involves intricate cellular processes that are critical for fertility. Understanding the molecular mechanisms guiding these processes is essential for addressing reproductive disorders and improving assisted reproductive technologies. The differentiation of reproductive organs is another crucial facet, exploring the genetic and epigenetic factors shaping male and female reproductive systems. Simultaneously, research in reproductive toxicity investigates the impact of environmental pollutants, chemicals, and endocrine disruptors on gamete health and embryonic development. This interdisciplinary field bridges reproductive biology and toxicology, shedding light on the potential hazards that substances pose to fertility. The igained from this research not only inform clinical practices for treating infertility but also contribute to regulatory measures promoting environmental sustainability and reproductive health awareness. Overall, this research is instrumental in safeguarding reproductive well-being and understanding the intricate processes governing life's initiation.

We are sure that this collection will be a useful guide for scientists and clinicians. Data on molecular mechanisms or pathophysiology are essential, and papers that only contain clinical trials/data are not within the scope of this Special Issue.

Dr. Hyun-Jung Park
Guest Editor

Manuscript Submission Information

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Keywords

  • spermatogenesis
  • mouse models
  • reproduction biology
  • assisted reproductive technology
  • cell signaling
  • cellular biology
  • developmental biology

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Published Papers (1 paper)

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Research

15 pages, 2589 KiB  
Article
Tebuconazole Induces Mouse Fetal Testes Damage via ROS Generation in an Organ Culture Method
by Won-Young Lee, Ran Lee and Hyun-Jung Park
Int. J. Mol. Sci. 2024, 25(13), 7050; https://doi.org/10.3390/ijms25137050 - 27 Jun 2024
Viewed by 1529
Abstract
The fungicide tebuconazole (TEB) poses risks to human and animal health via various exposure routes. It induces toxicity in multiple organs and disrupts reproductive health by affecting steroid hormone synthesis and fetal development. In this study, we investigated the impact of TEB on [...] Read more.
The fungicide tebuconazole (TEB) poses risks to human and animal health via various exposure routes. It induces toxicity in multiple organs and disrupts reproductive health by affecting steroid hormone synthesis and fetal development. In this study, we investigated the impact of TEB on fetal testes using in vitro models, focusing on germ, Sertoli, and Leydig cells, and explored the mechanisms underlying cellular damage. The results revealed significant damage to germ cells and disruption of Leydig cell development. TEB exposure led to a decrease in germ cell numbers, as indicated by histological and immunostaining analyses. TEB induced the up- and down-regulation of the expression of fetal and adult Leydig cell markers, respectively. Additionally, TEB-treated fetal testes exhibited increased expression of oxidative-stress-related genes and proteins. However, co-treatment with the antioxidant N-acetylcysteine mitigated TEB-induced germ cell damage and prevented abnormal Leydig cell development. These findings suggest that administration of antioxidants can prevent the intratesticular damage typically caused by TEB exposure. Full article
(This article belongs to the Special Issue Developmental and Reproductive Toxicology)
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