相关实验视频

Updated: Jan 10, 2026

A Ferret Model of Inflammation-sensitized Late Preterm Hypoxic-ischemic Brain Injury

A Ferret Model of Inflammation-sensitized Late Preterm Hypoxic-ischemic Brain Injury

Published on: November 19, 2019

周产期BPS暴露会通过SLC7A11/GPX4通路介导的铁死诱导后代的神经毒性

Xinxin Guo¹, Meilin Qin¹, Kaixing Lin¹

¹Guangxi Key Laboratory of Environmental Exposomics and Entire Lifecycle Health, Guilin Medical University, Guilin 541199, China; Department of Environmental and Occupational Health, School of Public Health, Guilin Medical University, Guilin 541199, China.

Ecotoxicology and environmental safety

|November 29, 2025

概括

围产期暴露在Bisphenol S (BPS) 中会导致后代的神经毒性,导致空间记忆和突触缺陷. 这种毒性与ferroptosis有关,ferroptosis是一种细胞死亡途径,涉及铁的积累和氧化应激.

科学领域:

环境毒理学环境毒理学
神经科学是一个神经科学.
细胞生物学细胞生物学

背景情况:

双S (BPS) 是一种BPA的替代品,具有潜在的神经毒性作用.
BPS的多代神经毒性影响仍然不清楚.
铁,一种依赖于铁的细胞死亡途径,与神经退行有关.

研究的目的:

研究BPS对后代产生的一代性神经毒性影响.
为了探索铁死在BPS诱导的神经毒性的作用.
阐明潜在的分子机制,包括SLC7A11/GPX4路径.

主要方法:

孕期小鼠和HT22细胞暴露在不同度的BPS中.
评估空间记忆,突触功能和后代的海马病理.
在体内和体外对铁亡标记物 (脂质过氧化,铁,线粒体超结构,蛋白质表达) 的分析.
对ferroptosis抑制剂 (Fer-1) 对BPS治疗细胞的影响的评估.

主要成果:

围产期BPS暴露导致后代的空间记忆和突触障碍.
观察到海马损伤,突触蛋白 (PSD95,SYP) 和BDNF的表达减少.
BPS暴露增加了铁亡的标志物,包括脂质过氧化,铁积累和与铁亡相关的蛋白质表达的改变 (SLC7A11,GPX4,FTH1,ACSL4).
铁-1治疗逆转了BPS诱导的铁亡,并恢复了HT22细胞中的突触蛋白表达.

结论:

周产期BPS暴露会导致后代多代神经毒性.
由SLC7A11/GPX4途径介导的铁亡是BPS诱导的神经毒性的关键机制.
这些发现强调了评估BPS多代毒性及其与铁亡的联系的重要性.

关键词:

双 S 是一种双醇.铁性化 (ferroptosis) 是一种神经毒性神经毒性在 SLC7A11/GPX4 信号通路中.

更多相关视频

Author Spotlight: Tracing the Ferroptotic Signatures and Cell Death Dynamics in Medulloblastoma for Advanced Therapeutics

Author Spotlight: Tracing the Ferroptotic Signatures and Cell Death Dynamics in Medulloblastoma for Advanced Therapeutics

Published on: March 15, 2024

Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats

Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats

Published on: November 20, 2015

相关概念视频

Teratogenicity

Teratogenicity

The ability of a drug to produce structural deformations and functional abnormalities in the developing embryo or the fetus is called teratogenicity, and the drug producing this effect is known as a teratogen. Teratogenic effects include stillbirth, miscarriage, intrauterine growth restriction, and neurocognitive delay. A teratogen may affect the embryo at different stages of development, which is important in determining the type and extent of the damage. During blastocyst formation, the early...

Protein Import into the Peroxisomes

Protein Import into the Peroxisomes

Cells contain membrane-bound organelles called peroxisomes that oxidize organic molecules by transferring hydrogen atoms to oxygen, producing hydrogen peroxide. Peroxisomes enzymatically convert the released hydrogen peroxide into water and oxygen.
Peroxisomal Protein Import:
Peroxisomes lack the genetic machinery required to code for their own proteins. Hence, most peroxisomal membrane, lumenal and transmembrane proteins are synthesized in the cytoplasm or ER and transported to the peroxisome...

Necrosis

Necrosis

Necrosis is considered as an “accidental” or unexpected form of cell death that ends in cell lysis. The first noticeable mention of “necrosis” was in 1859 when Rudolf Virchow used this term to describe advanced tissue breakdown in his compilation titled “Cell Pathology”.
Morphological Manifestations of Necrosis
Necrotic cells show different types of morphological appearance depending on the type of tissue and infection. In coagulative necrosis, cells become...