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Updated: May 14, 2025
Mouse Round Spermatid Injection
Published on: January 26, 2024
BDE-209 toxicity: From spermiogenesis to sexual maturity in F1 male mice
Xin Gao1, Qi Zheng1, Siju Chen1
1Department of Occupational and Environmental Health, School of Public Health, Anhui Medical University, Meishan Rd 81, Hefei 230032, China.
Abstract:
Most studies of enviromental toxic chemicals focused on the meiosis stage during spermatogenesis, however, the research on the spermiogenesis damage phenotype of BDE-209 is limited. This study aimed to evaluate the processes by which BDE-209 regulates the formation of acrosomes and mitochondrial sheath (MS), key structures during spermiogenesis and fertilization. ICR mice were divided into control, low, medium, and high-dose BDE-209 groups and treated for 42 days. A comprehensive method combining ultrastructural analysis, transcriptomics, molecular biology, and fertility experiments was adopted. In mice exposed to BDE-209, testicular dysplasia, altered sex hormone concentrations, decreased semen quality, and head and tail deformities occurred. Chromatin condensation failure was present in BDE-209-exposed spermatozoa with decreased mRNA and protein levels of PRM1 and TNP1. BDE-209 disrupts the acrosome biogenesis process by disrupting the Golgi structure and the apical ectoplasmic specialization (ES) structure. BDE-209 exposure caused multiple damage to the MS and down-regulated the mRNA levels of Akap3, Akap4, Cfap44, Ccdc40, Dhah1, etc. These injuries resulted in subfertility in BDE-209 male mice, and the male offspring also exhibited gonadal dysplasia, sex hormonal changes, and decreased semen quality. Conclusively, BDE-209 exposure induced spermiogenesis defects and subfertility. F0 and F1 males showed a similar injury phenotype. This study advanced the understanding of the damage phenotype of spermiogenesis and complemented the reproductive toxicity of F1 male mice. These findings might be important for the study of related molecular mechanisms and the mitigation of BDE-209 exposure on offspring development.
Insights
Exposure to BDE-209 causes male reproductive toxicity, leading to spermiogenesis defects and subfertility in both exposed mice and their offspring. This study highlights the impact on acrosome and mitochondrial sheath formation.
Area of Science:
- Reproductive Toxicology
- Environmental Health
- Spermatogenesis Research
Background:
- Limited research exists on the spermiogenesis damage caused by the environmental toxic chemical BDE-209.
- Spermiogenesis involves critical structural formations like the acrosome and mitochondrial sheath (MS), essential for fertilization.
Purpose of the Study:
- To evaluate how BDE-209 affects acrosome and mitochondrial sheath (MS) formation during spermiogenesis.
- To investigate the reproductive toxicity of BDE-209 exposure in male mice and its transgenerational effects on offspring.
Main Methods:
- ICR mice were exposed to varying doses of BDE-209 for 42 days.
- A multi-faceted approach was used, including ultrastructural analysis, transcriptomics, molecular biology, and fertility assessments.
- Evaluated testicular histology, hormone levels, semen quality, sperm morphology, and gene/protein expression related to spermiogenesis.
Main Results:
- BDE-209 exposure led to testicular dysplasia, altered sex hormones, reduced semen quality, and sperm deformities (head and tail).
- Observed chromatin condensation failure, decreased protamine 1 (PRM1) and transition protein 1 (TNP1) levels, disrupted acrosome biogenesis (Golgi and apical ectoplasmic specialization structures), and damaged mitochondrial sheath (MS) with downregulated key genes (e.g., Akap3, Akap4).
- Exposed male mice exhibited subfertility, and their male offspring showed similar reproductive impairments.
Conclusions:
- BDE-209 exposure induces significant spermiogenesis defects and causes male subfertility.
- Both F0 and F1 generation males displayed comparable reproductive injury phenotypes.
- Findings advance understanding of spermiogenesis damage and the reproductive toxicity of BDE-209, offering insights for mitigation strategies.
