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[Effect of maternal BDE-209 exposure on the learning and memory ability of offspring rats and the dose-effect
Ying Wu1, Yan-Hong Yu, Dun-Jin Chen
1Department of Gynecology and Obstetrics, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China. wuyingwin @hotmail.com
Insights
Maternal exposure to brominated diphenyl ethers-209 (BDE-209) impaired offspring rat learning and memory. Higher BDE-209 doses caused significant hippocampus damage, indicating a dose-dependent effect on cognitive function.
Area of Science:
- Environmental Toxicology
- Neuroscience
- Developmental Biology
Context:
- Brominated diphenyl ethers (BDEs) are flame retardants with potential neurotoxic effects.
- Prenatal and lactational exposure to environmental contaminants can impact offspring neurodevelopment.
- Brominated diphenyl ether-209 (BDE-209) is a prevalent congener of concern.
Purpose:
- To evaluate the impact of maternal BDE-209 exposure on the learning and memory capabilities of Wistar rat offspring.
- To investigate potential dose-dependent effects of BDE-209 on cognitive function and hippocampal histology.
Summary:
- Female Wistar rats were exposed to varying doses of BDE-209 (100-1200 mg/kg) or peanut oil (control) during gestation and lactation.
- Offspring cognitive performance was assessed using the Morris water maze, and hippocampal tissues were examined histologically.
- Higher BDE-209 doses (600 and 1200 mg/kg) significantly prolonged escape latency and caused hippocampal neural cell reduction and pathological changes.
Impact:
- Maternal BDE-209 exposure negatively affects offspring learning and memory, with effects becoming pronounced at higher doses.
- The study reveals a dose-response relationship between BDE-209 exposure and neurodevelopmental deficits.
- Findings highlight the potential risks of BDE-209 to cognitive development and hippocampal integrity.
Objective:
To investigate the effect of maternal brominated diphenyl ethers-209 (BDE-209) exposure on the learning and memory ability of the offspring rats in prenatal and lactational periods.
Methods:
After confirmation of successful mating, female Wistar rats were randomized into 5 groups and subjected to daily oral gavage of peanut oil suspensions containing BDE-209 at the doses of 100 mg/kg (group A), 300 mg/kg (group B), 600 mg/kg (group C), and 1200 mg/kg (group D), or only peanut oil (group E, as control). From each group, 20 male weaning rats of the first generation were randomly selected to examine their learning and memorizing ability using Morris water maze. The histological alterations of the hippocampus were observed microscopically with HE staining after the test.
Results:
During the initial one or two days of water maze test, no significant difference was noted in the escape latency between the groups (P=0.068, P=0.104). On days 3 to 5, groups B, C, and D showed prolonged escape latency as compared with the control group (P<0.05), but group A showed no such changes (P>0.05). Under optical microscope, the hippocampus in groups A and B exhibited no significant variation from that of the control group, but in groups C and D, the neural cells were obviously reduced and presented disorderly alignment, with substantial cell nuclear shrinkage and interstitial edema.
Conclusion:
Maternal BDE-209 exposure induces disturbance of the learning and memorizing ability and pathological changes of the hippocampus in the offspring rats, and these changes show a dose-effect relation.
