颗粒物质2.5对氧化应激引起的胎盘超微结构包括线粒体损伤的影响

IF 2.8 4区医学 Q2 REPRODUCTIVE BIOLOGY

Reproductive toxicology Pub Date : 2025-06-10 DOI:10.1016/j.reprotox.2025.108973

Gain Lee , Jung Mi Han , Young-Ah You , Yoon-Young Go , Sunwha Park , Young Min Hur , Soo Min Kim , Ki-Hwan Han , Young Ju Kim

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引用次数: 0

摘要

PM2.5是指直径小于2.5μm的细颗粒物，与妊娠不良结局有关。该研究旨在确定产前PM2.5水平升高是否与胎盘和线粒体超微结构的改变有关，后者可能与氧化应激有关。方法收集来自空气污染对妊娠结局（APPO）队列的胎盘样本，并根据PM2.5暴露水平将其分为两组：高组(>；15 μg / m³;n = 9)和Low组(≤15 μg/m³；n = 8)。透射电镜观察胎盘的超微结构，尤其是合体滋养细胞区域。还分析了胎儿毛细血管中线粒体的结构。采用酶联免疫吸附法（ELISA）定量丙二醛（MDA）和超氧化物歧化酶2 （SOD2）。结果高组胎盘超微结构发生改变，包括微绒毛丢失、基底膜增厚、空泡化和内质网肿胀。High组微绒毛明显缩短和消失（P <； 0.005）。高组合体滋养细胞可见空泡肿胀、内质网应激和基底膜增厚（P <； 0.005）。High组胎儿毛细血管线粒体也出现损伤，双膜和嵴断裂（P <； 0.05）。高剂量组MDA和SOD2水平显著升高（P <； 0.05）。结论PM2.5暴露可能与胎盘超微结构改变和胎儿毛细血管线粒体损伤有关，可能由氧化应激介导，其表现为MDA和SOD2水平升高。

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Impact of particulate matter 2.5 on placental ultrastructure including mitochondrial damage through oxidative stress

Introduction

Particulate matter 2.5 (PM_2.5) refers to fine particles with a diameter of less than 2.5μm, associated with adverse pregnancy outcomes. The study aims to determine whether elevated prenatal PM_2.5 levels were associated with alterations in the ultrastructure of the placenta and mitochondria, potentially linked to oxidative stress.

Methods

The placental samples were collected from the Air Pollution on Pregnancy Outcome (APPO) cohort and were classified into two groups based on PM_2.5 exposure levels: the High group (> 15 μg/m³; n = 9) and the Low group (≤ 15 μg/m³; n = 8). Transmission electron microscopy was used to assess the ultrastructure of the placenta, specifically the syncytiotrophoblast area. The structure of the mitochondria in the fetal capillaries was also analyzed. Malondialdehyde (MDA) and superoxide dismutase 2 (SOD2) were quantified by using enzyme-linked immunosorbent assays (ELISA).

Results

The High group placenta showed ultrastructural changes including microvilli loss, basement membrane thickening, vacuolation and swollen endoplasmic reticulum (ER). Microvilli were significantly shortened and lost in the High group (P < 0.005). Swollen vacuoles, ER stress, and basement membrane thickening were observed in High group syncytiotrophoblast (P < 0.005). Mitochondria in fetal capillaries from the High group were also damaged, showing disrupted double membranes and cristae (P < 0.05). MDA and SOD2 levels were significantly upregulated in the High group (P < 0.05).

Conclusion

Prenatal exposure to PM_2.5 may be associated with alterations of placental ultrastructure and mitochondrial damage in fetal capillaries, potentially mediated by oxidative stress, as indicated by elevated levels of MDA and SOD2.

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来源期刊

Reproductive toxicology 生物-毒理学

CiteScore

6.50

自引率

3.00%

发文量

131

审稿时长

45 days

期刊介绍： Drawing from a large number of disciplines, Reproductive Toxicology publishes timely, original research on the influence of chemical and physical agents on reproduction. Written by and for obstetricians, pediatricians, embryologists, teratologists, geneticists, toxicologists, andrologists, and others interested in detecting potential reproductive hazards, the journal is a forum for communication among researchers and practitioners. Articles focus on the application of in vitro, animal and clinical research to the practice of clinical medicine. All aspects of reproduction are within the scope of Reproductive Toxicology, including the formation and maturation of male and female gametes, sexual function, the events surrounding the fusion of gametes and the development of the fertilized ovum, nourishment and transport of the conceptus within the genital tract, implantation, embryogenesis, intrauterine growth, placentation and placental function, parturition, lactation and neonatal survival. Adverse reproductive effects in males will be considered as significant as adverse effects occurring in females. To provide a balanced presentation of approaches, equal emphasis will be given to clinical and animal or in vitro work. Typical end points that will be studied by contributors include infertility, sexual dysfunction, spontaneous abortion, malformations, abnormal histogenesis, stillbirth, intrauterine growth retardation, prematurity, behavioral abnormalities, and perinatal mortality.