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Updated: Dec 17, 2025
Long-term Behavioral and Reproductive Consequences of Embryonic Exposure to Low-dose Toxicants
Published on: March 6, 2018
Chlorpyrifos-induced toxicity has no gender selectivity in the early fetal brain
Jiabin Gu1, Shuai Xu1, Yuqiong Liu1
1College of Biotechnology and Bioengineering, Zhejiang University of Technology, Hangzhou, China.
Abstract:
Organophosphorus pesticides induce gender-specific developmental neurotoxicity after birth, especially in adolescents and adults. However, whether and when the selectivity occurs in fetus remains unclear. In this study, we analyzed chlorpyrifos (CPF)-induced neurotoxicity in the early fetal brains of male and female mice. The gestational dams were administered 0, 1, 3, and 5 mg/(kg.d) CPF during gestational days (GD)7-11, and brains from the fetuses were isolated and analyzed on GD12. Fetal gender was identified by PCR technique based on male-specific Sry gene and Myog control gene. The body weight and head weight, the activity of acetylcholinesterase (AChE), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX), and the content of malondialdehyde (MDA), as well as the oxidative stress-related gene expression were examined. Our results showed that CPF pretreatment induced AChE inhibition in GD12 fetal brain. CPF treatment activated SOD and GPX but not CAT and MDA. For oxidative stress-related gene expression, CPF pretreatment increased mRNA expression of Sod1, Cat, Gpx1, and Gpx2 in the fetal brain on GD12. The statistical analysis did not show gender-selective CPF-induced toxicity. Moreover, our results showed that although the gestational exposure to CPF could elicit abnormalities in the early fetal brain, the toxicity observed was not gender-specific.
Insights
Gestational exposure to chlorpyrifos (CPF) causes neurotoxicity in fetal mouse brains. Unlike later life stages, this early-life toxicity was not found to be gender-specific in the study.
Area of Science:
- Developmental toxicology
- Neuroscience
- Environmental health
Background:
- Organophosphorus pesticides are known to cause gender-specific neurodevelopmental toxicity in adolescents and adults.
- The occurrence and timing of this gender selectivity during fetal development remain largely uninvestigated.
- Understanding early-life exposure effects is crucial for assessing developmental risks.
Purpose of the Study:
- To investigate chlorpyrifos (CPF)-induced neurotoxicity in early fetal brains of male and female mice.
- To determine if gender-specific toxicity occurs during critical windows of fetal brain development.
- To assess the impact of CPF on neurochemical markers and oxidative stress pathways in the developing fetal brain.
Main Methods:
- Gestational mice were administered varying doses of CPF during gestational days (GD) 7-11.
- Fetal brains were collected on GD12 for analysis, with gender identified via PCR (Sry gene).
- Assays included acetylcholinesterase (AChE) activity, antioxidant enzyme activities (SOD, CAT, GPX), malondialdehyde (MDA) content, and oxidative stress-related gene expression.
Main Results:
- CPF exposure led to AChE inhibition in GD12 fetal brains.
- CPF activated SOD and GPX activities, but not CAT or MDA levels.
- mRNA expression of Sod1, Cat, Gpx1, and Gpx2 was increased by CPF exposure.
- Statistical analysis revealed no significant gender-selective toxicity in the early fetal brain.
Conclusions:
- Gestational exposure to chlorpyrifos can induce neurotoxic effects and oxidative stress in the early fetal brain.
- The observed neurotoxicity in the early fetal stage was not gender-specific.
- These findings suggest that critical windows for gender-selective neurotoxicity may occur later in development.
