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Updated: Aug 19, 2026
Human Pluripotent Stem Cell Based Developmental Toxicity Assays for Chemical Safety Screening and Systems Biology Data Generation
Published on: June 17, 2015
[Relation between methylmercury chloride-induced programmed cell death and the development of nervous system in rats]
1National Center for Maternal and Infant Health, Beijing Medical University, China.
Abstract:
The study was designed to reveal the role of programmed cell death (PCD, or apoptosis) induced by methylmercury chloride (MMC) in SD rat embryos, wish TdT-mediated dUTP nick end labeling (TUNEL), Nile blue sulfate (NBS) vital stailing electron microscopy (SEM) and in vivo teratogenic methods (TEM). Pregnant rats were intraperitoneally injected at gestation day 9.5 with doses of 0, 0.2, 0.4, 0.8, 1.6 and 3.2 mg/kg MMC and killed at 11.5 day later. Results showed that the PCD of embryonic nervous system was apparently dose dependent with MMC during rat head-fold stage. Observations under SEM and TEM showed that MMC caused pathologic changes of epithelia and organellae in embryonic brain such as atrophied or decreased microvilli cavernous damages and mitochondrial swelling and so on. Though MMC could result in developmental anomalies of embryonic brain and other organs, the main defect was open neural tube. The experiment study suggested that over PCD may be one of the teratogenic mechanisms of MMC on rat embryos, developing brain in particular.
Insights
Methylmercury chloride (MMC) induces programmed cell death (PCD) in developing rat embryos, leading to brain abnormalities and open neural tubes. This PCD is dose-dependent, highlighting a key teratogenic mechanism.
Area of Science:
- Developmental toxicology
- Neuroscience
- Cell biology
Context:
- Methylmercury chloride (MMC) is a known teratogen.
- Understanding the mechanisms of MMC-induced birth defects is crucial for public health.
- Programmed cell death (PCD), or apoptosis, plays a role in embryonic development.
Purpose:
- To investigate the role of PCD in methylmercury chloride (MMC)-induced teratogenesis in Sprague-Dawley (SD) rat embryos.
- To elucidate the dose-dependent effects of MMC on embryonic development and identify specific pathological changes.
Summary:
- MMC exposure at gestation day 9.5 induced a dose-dependent increase in PCD in the embryonic nervous system.
- Scanning electron microscopy (SEM) and transmission electron microscopy (TEM) revealed pathological changes in embryonic brain epithelia and organellae, including mitochondrial swelling and damaged microvilli.
- The primary developmental anomaly observed was an open neural tube, indicating significant teratogenic effects on brain development.
Impact:
- This study suggests that excessive PCD is a significant mechanism underlying MMC's teratogenic effects, particularly on the developing brain.
- Findings contribute to understanding the neurodevelopmental risks associated with mercury exposure during pregnancy.
- Provides a basis for further research into protective strategies against environmental teratogens.
