Reproductive toxicology (Elmsford, N.Y.) · 2025
Impact of particulate matter 2.5 on placental ultrastructure including mitochondrial damage through oxidative stress.
СтатьяПоддержка исследования: вне правительства СШАПоддержка NIH: внешняя программаНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Lee Gain, Han Jung Mi, You Young-Ah, Go Yoon-Young, Park Sunwha, Hur Young Min, Kim Soo Min, Han Ki-Hwan, Kim Young Ju
Аннотация
INTRODUCTION: Particulate matter 2.5 (PM2.5) 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 PM2.5 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 PM2.5 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 PM2.5 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.
METHODS: The placental samples were collected from the Air Pollution on Pregnancy Outcome (APPO) cohort and were classified into two groups based on PM2.5 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 PM2.5 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.