生命早期暴露全氟丁烷磺酸对SD大鼠的神经发育毒性及其机制

doi:10.3969/j.issn.1004-616x.2025.01.004

Abstract

Abstract: OBJECTIVE： This study aimed to investigate the effects from exposure to perfluorobutanesulfonic acid (PFBS) on the neurodevelopment of rat offspring. METHODS： Maternal rats were divided into PFBS low (5 mg/kg)，medium (50 mg/kg)，high (500 mg/kg) dose groups and control group (saline). The rats were dosed from the second day of pregnancy (GD1) until weaning. At 90 days after birth，10 offspring from each group were randomly selected for sacrificing，and the hippocampal tissue was collected for pathological，Western blot，and real-time qPCR tests. Pathological test was used to observe the impair of CA1 of hippocampus by subjecting to hematoxylin-eosin (HE) staining. Protein expression of BDNF，TRKB，PI3K，AKT and P-AKT in hippocampus were detected by Western blot. The expression level of Syn1 and Syp mRNA in hippocampus were detected by quantitative reverse transcription PCR. RESULTS： The pathological test showed that early-life exposure to PFBS resulted in the nuclear condensation，blurred cell boundaries，and irregular cell morphology in the CA1 region of hippocampus in each dose groups，most significant in the high dose group. Compared to the control group，protein expression of BDNF，TRKB，PI3K，P-AKT and the ratio of P-AKT/AKT were decreased in each dose group (P<0.01). Expression levels of Syn1 and Syp mRNA decreased in the medium and high dose groups，compared to control group (P<0.05). CONCLUSION： Exposed to PFBS during early life damaged the hippocampus. Damage from PFBS on the BDNF/TRKB/CREB and PI3K/AKT signaling pathways might be the mechanisms for induction of developmental neurotoxicity in rats.

Key words: PFASs, PFBS, neurotoxicity, early life, BDNF/CREB signaling pathway

CLC Number:

R994.6

TAN Qitao, ZHU Hangyu, SUN Yan. Developmental neurotoxicity and its mechanism of perfluorobutane sulfonate exposure in early life in SD rats[J]. Carcinogenesis, Teratogenesis & Mutagenesis, 2025, 37(1): 21-26.

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Developmental neurotoxicity and its mechanism of perfluorobutane sulfonate exposure in early life in SD rats

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