Reproductive toxicology最新文献_第2页

Unveiling the transcriptional pattern of epithelial ovarian carcinoma-related microRNAs-mRNAs network after mouse exposure to 2,3,7,8-Tetrachlorodibenzo-p-dioxin

IF 3.3 4区医学 Q2 REPRODUCTIVE BIOLOGY

Reproductive toxicology

Pub Date : 2025-02-18 DOI: 10.1016/j.reprotox.2025.108863

Nour Aldeli , Abdulsamie Hanano

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), the most potent organic environmental contaminant known to date, is recognized as a human carcinogen. Despite the documented link between TCDD exposure and epithelial ovarian cancer (EOC) in mammalian females, the molecular mechanisms underlying cancer initiation remain elusive. Emerging evidence suggests aberrant miRNA expression in various human malignancies, including OC. This work was performed to examine whether TCDD exposure in female mice disrupts the expression of miRNAs, particularly those known as OC-modulators. We conducted an extensive search in the PubMed database to identify miRNAs experimentally implicated in OC. Fifty-two miRNAs were identified as potential OC modulators and classified into two groups based on their abundance in OC. Group I comprised 24 miRNAs upregulated in OC, while Group II included 28 miRNAs downregulated in OC. Subsequently, we analyzed the expression of both groups in BALB/c mice ovaries following a single TCDD dose. Our findings revealed significant upregulation of 10 miRNAs from Group I (miR-21, miR-27a, miR-30a, miR-99a, miR-141, miR-182, miR-183, miR-200a, miR-200b, and miR-429) and significant downregulation of 12 miRNAs from Group II (let-7d, miR-15a, miR-19a, miR-23b, miR-34a, miR-34c, miR-125b-1, miR-133, miR-140, miR-199a, miR-210, and miR-383) in TCDD-exposed mouse ovaries. Furthermore, we identified OC-related genes targeted by miRNAs from both groups through an extensive search in PubMed databases. Using TR-qPCR, we evaluated the downstream impact of TCDD-dysregulated miRNAs on their target genes. Our results indicate that TCDD-induced upregulation of oncogenic miRNAs negatively regulates target genes associated with EOC, while downregulation of cancer-suppressor miRNAs positively regulates genes linked to EOC.

{"title":"Unveiling the transcriptional pattern of epithelial ovarian carcinoma-related microRNAs-mRNAs network after mouse exposure to 2,3,7,8-Tetrachlorodibenzo-p-dioxin","authors":"Nour Aldeli , Abdulsamie Hanano","doi":"10.1016/j.reprotox.2025.108863","DOIUrl":"10.1016/j.reprotox.2025.108863","url":null,"abstract":"<div><div>2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), the most potent organic environmental contaminant known to date, is recognized as a human carcinogen. Despite the documented link between TCDD exposure and epithelial ovarian cancer (EOC) in mammalian females, the molecular mechanisms underlying cancer initiation remain elusive. Emerging evidence suggests aberrant miRNA expression in various human malignancies, including OC. This work was performed to examine whether TCDD exposure in female mice disrupts the expression of miRNAs, particularly those known as OC-modulators. We conducted an extensive search in the PubMed database to identify miRNAs experimentally implicated in OC. Fifty-two miRNAs were identified as potential OC modulators and classified into two groups based on their abundance in OC. Group I comprised 24 miRNAs upregulated in OC, while Group II included 28 miRNAs downregulated in OC. Subsequently, we analyzed the expression of both groups in BALB/c mice ovaries following a single TCDD dose. Our findings revealed significant upregulation of 10 miRNAs from Group I (miR-21, miR-27a, miR-30a, miR-99a, miR-141, miR-182, miR-183, miR-200a, miR-200b, and miR-429) and significant downregulation of 12 miRNAs from Group II (let-7d, miR-15a, miR-19a, miR-23b, miR-34a, miR-34c, miR-125b-1, miR-133, miR-140, miR-199a, miR-210, and miR-383) in TCDD-exposed mouse ovaries. Furthermore, we identified OC-related genes targeted by miRNAs from both groups through an extensive search in PubMed databases. Using TR-qPCR, we evaluated the downstream impact of TCDD-dysregulated miRNAs on their target genes. Our results indicate that TCDD-induced upregulation of oncogenic miRNAs negatively regulates target genes associated with EOC, while downregulation of cancer-suppressor miRNAs positively regulates genes linked to EOC.</div></div>","PeriodicalId":21137,"journal":{"name":"Reproductive toxicology","volume":"132 ","pages":"Article 108863"},"PeriodicalIF":3.3,"publicationDate":"2025-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143445585","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Antidepressant aripiprazole induces adverse effects on neural development during cortex organoid generation

IF 3.3 4区医学 Q2 REPRODUCTIVE BIOLOGY

Reproductive toxicology

Pub Date : 2025-02-17 DOI: 10.1016/j.reprotox.2025.108862

Youngin Jeong , Suil Son , Jiyun Park , C-Yoon Kim , Jin Kim

A significant number of women experience anxiety and depressive symptoms during pregnancy, leading to the prescription of antidepressants, including aripiprazole. However, although a few animal studies have reported its developmental toxicity, there is a lack of research on the potential risks aripiprazole may pose to the fetus, particularly regarding neural development, as well as an absence of appropriate models to verify these effects. Therefore, this study investigates the impact of aripiprazole on neural development using cortex organoids, which can effectively model human brain development and function while overcoming interspecies differences. Cortex organoids were generated and exposed to aripiprazole at concentrations of 0.3–9 µM over 4 weeks. We assessed morphological changes, cell viability, gene expression, immunofluorescence staining, and electrophysiological function. The results revealed that aripiprazole led to significant reductions in organoid size and increased cell death, particularly at higher concentrations. Immunofluorescence analysis showed abnormalities in the expression patterns of neural stem cells and neuronal markers. Additionally, real-time PCR demonstrated decreased expression of genes related to neural stem cells, neural differentiation and migration, maturation, synaptogenesis, and gliogenesis, along with increased apoptosis-related gene expression. Electrophysiological recordings indicated impaired neural activity, evidenced by reduced mean firing rates. Our study is the first to demonstrate that aripiprazole induces adverse effects on neural development across functional, molecular, and morphological aspects. The findings will aid in a better understanding of the risks associated with antidepressant use during pregnancy in terms of neural development and suggest that cortex organoids are a valuable model for evaluating potential neurodevelopmental toxicants.

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引用次数: 0

The potential role of ascorbic acid in attenuating infertility induced by emamectin benzoate via suppressing oxidative stress and ameliorating sperm count in male rats

IF 3.3 4区医学 Q2 REPRODUCTIVE BIOLOGY

Reproductive toxicology

Pub Date : 2025-02-15 DOI: 10.1016/j.reprotox.2025.108852

Assia Kamel-Chouider , Meriem Hariti , Samira Akdader-Oudahamne , Zohra Hamouli-Said

Pesticides are chemical compounds with toxicological properties. Emamectin benzoate (EMB) is a macrolytic lactone belonging to the avermectin class, produced naturally by the actinomycetes Streptomyces avermitilis. Ascorbic acid (AA) is used in many therapeutic areas, in particular for its antioxidant properties. The objective of this study is to evaluate the potential role of ascorbic acid (AA) against the reproductive toxicity induced by emamectin benzoate (EMB). In this experimental study, 24 adult male rats were used. The animals were divided into 4 groups (n = 6). Control group (C) treated with distilled water, an EMB group received 20 mg EMB/kg body weight (bw) by gavage, AA group received ascorbic acid intraperitoneally (200 mg/kg bw) and an EMB + AA group received 20 mg EMB/kg bw and ascorbic acid intraperitoneally (200 mg/kg bw). The duration of the treatment was 15 days. Our results showed that the administration of EMB increased (MDA, proteins carbonyl), decreased antioxidant (SOD, CAT, GSH). Microscopic analysis revealed histological damage in the EMB group, which were represented by alteration of normal architecture, inflammatory cell infiltration, multifocal vacuolation of Sertoli cell cytoplasm, congested blood vessels, a large area of low spermatozoa density in epididymal lumen and increased collagen fibers in the muscle layer, which implicated fibrosis. However, co-treatment with ascorbic acid reduced EMB-related testis, epididymis toxicity, corrected the imbalance between oxidants and antioxidants, ameliorated sperm production, moderated amount of collagen fiber. We note that treatment with ascorbic acid (AA) only did not result in any significant change compared to controls. In conclusion, ascorbic acid has beneficial effects by attenuating the toxicity of Emamectin benzoate.

杀虫剂是具有毒理学特性的化合物。苯甲酸埃马菌素（EMB）是一种属于阿维菌素类的大分解内酯，由放线菌 Streptomyces avermitilis 天然产生。抗坏血酸（AA）被用于许多治疗领域，特别是其抗氧化特性。本研究旨在评估抗坏血酸（AA）对苯甲酸阿维菌素（EMB）引起的生殖毒性的潜在作用。本实验研究使用了 24 只成年雄性大鼠。动物分为 4 组（n = 6）。对照组（C）用蒸馏水处理，EMB 组每公斤体重灌胃 20 毫克 EMB，AA 组腹腔注射抗坏血酸（每公斤体重 200 毫克），EMB + AA 组每公斤体重注射 20 毫克 EMB，腹腔注射抗坏血酸（每公斤体重 200 毫克）。疗程为 15 天。我们的研究结果表明，服用 EMB 会增加（MDA、蛋白质羰基），降低抗氧化剂（SOD、CAT、GSH）。显微镜分析显示，EMB 组的组织学损伤表现为正常结构改变、炎症细胞浸润、Sertoli 细胞胞浆多灶空泡化、血管充血、附睾管腔内精子密度大面积降低以及肌肉层胶原纤维增加，这意味着纤维化。然而，与抗坏血酸联合治疗可降低与 EMB 相关的睾丸、附睾毒性，纠正氧化剂和抗氧化剂之间的失衡，改善精子生成，减少胶原纤维的数量。我们注意到，与对照组相比，仅使用抗坏血酸（AA）治疗并没有导致任何显著变化。总之，抗坏血酸具有减轻苯甲酸埃马菌素毒性的有益作用。

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引用次数: 0

Hormonal mechanism and pathogenetic therapy of citalopram-induced infertility in female rats

IF 3.3 4区医学 Q2 REPRODUCTIVE BIOLOGY

Reproductive toxicology

Pub Date : 2025-02-14 DOI: 10.1016/j.reprotox.2025.108859

Ilhan Bahri Delibasi , Neset Gumusburun , Seval Bulut , Renad Mammadov , Betul Kalkan Yilmaz , Bahadir Suleyman , Nuri Bakan , Ali Sefa Mendil , Halis Suleyman , Durdu Altuner

Citalopram is a selective serotonin reuptake inhibitor (SSRI) and has been associated with reproductive dysfunction in women. In this study, the effects of citalopram on reproductive health in female rats were investigated. Albino Wistar rats was divided into six groups (each group/n = 12): healthy (HG), citalopram (CTP), cabergoline (CBR), metyrapone (MTP), cabergoline+citalopram (CBR+CTP), and metyrapone+citalopram (MTP+CTP). Initially, cabergoline 0.1 mg/kg and metyrapone 50 mg/kg were administered orally. A dose of 10 mg/kg of citalopram was given orally one hour later. For 30 days, the treatment protocol was applied once a day. Then, blood samples were taken from the tail veins of six rats from each group for prolactin and corticosterone analyses and ovaries were removed after euthanasia. The ovaries were examined for oxidants and antioxidants and histopathologically. During two months, the remaining animals were kept with male rats. The rats that did not deliver during this period were considered infertile. In terms of oxidants and antioxidants, there was no significant difference between the groups (p > 0.05). In half of the female rats, citalopram caused infertility, increased levels of prolactin and corticosterone, and damaged the ovaries histopathologically (p < 0.05). Cabergoline suppressed the elevation of prolactin by citalopram (p < 0.001) but did not prevent infertility. In contrast, metyrapone significantly prevented the citalopram-induced increase in corticosterone, infertility, and tissue damage induced by citalopram (p < 0.05). According to the results of our study, the preventive effect of drugs that suppress excessive corticosterone on citalopram-induced infertility in rats may be encouraging for further clinical studies.

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引用次数: 0

The impact of triadimenol on male fertility: An in vitro study and molecular docking examination

IF 3.3 4区医学 Q2 REPRODUCTIVE BIOLOGY

Reproductive toxicology

Pub Date : 2025-02-13 DOI: 10.1016/j.reprotox.2025.108861

Arici Merve , Bilgehan Ayşenur , Dincel Efe Dogukan , Özhan Gül

Triadimenol, a triazole fungicide, induces various adverse effects including neurotoxicity, hepatotoxicity, and developmental/reproductive toxicity in non-target organisms. Occupational exposure generally occurs in male agricultural workers. Investigating the effects of triadimenol on three different testicular cell lines would be valuable in elucidating the mechanisms underlying male reproductive issues or infertility. This preliminary study examines the potential toxic effects of triadimenol exposure in Leydig (TM3), Sertoli (TM4), and mouse-derived Spermatogonia (GC-1) cell lines, which are representative of the male reproductive system in vitro. The median inhibitory concentration (IC₅₀) values of triadimenol were found to be 121.35 μM, 332.1 μM, and 349.49 μM in TM3, TM4, and GC-1 cells, respectively. The exposure doses were determined to range from 0 to 100 µM in TM3 cell line and 0–300 µM in TM4 and GC-1 cell lines. Reactive oxygen species (ROS) production, reduced glutathione (GSH) content, malondialdehyde (MDA) and protein carbonyl levels, and genotoxicity were examined. TM3 cell line was more resistant to oxidative damage than the other cell lines, while TM4 cell line was found to be more sensitive in terms of protein carbonyl formation. Triadimenol damaged DNA in TM3 cell line (≥16.93), TM4 cell line (≥9.18), and GC-1 cell line (≥3.28). Additionally, the docking score of triadimenol on the active site of steroid 5-α-reductase 2 (5αR2), which converts testosterone to 5α-dihydrotestosterone, was not close. The results emphasised that the toxicity of triadimenol was cell-specific. Overall, triadimenol disrupted male fertility by affecting spermatogenesis, testosterone production, germ cell support, and sperm quality.

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引用次数: 0

The biological effects of bisphenol AF in reproduction and development: What do we know so far?

IF 3.3 4区医学 Q2 REPRODUCTIVE BIOLOGY

Reproductive toxicology

Pub Date : 2025-02-13 DOI: 10.1016/j.reprotox.2025.108857

Megan V. Alexander , Archana Ayyar , Alexandra W. Gannon , Kristen E. Linares , Sara J. Vincent , Samantha Lowe , Alvin To , Chellakkan S. Blesson

Due to the established endocrine-disrupting effects of Bisphenol A (BPA), alternative bisphenols entered the market. Bisphenol AF (BPAF) is now commonly used in the industrial manufacturing of polycarbonate plastics and epoxy resins. However, BPAF’s effects on reproduction and development have not been thoroughly reviewed. We investigated the relationship between BPAF exposure and reproduction and early development. We performed a literature review of studies on BPAF and reproductive physiology. Using keywords, we searched PubMed, Medline, Cochrane Library Database, Embase, and ClinicalTrials.gov for English language literature available until December 2024; we additionally identified and included studies from bibliographies. We included 125 articles, spanning in vitro and in vivo model organism and human studies. BPAF is a selective estrogen receptor modulator and an androgen receptor antagonist and is more potent than BPA. It is detected in urine, blood products, saliva, amniotic fluid, and breast milk. In vitro and in vivo studies demonstrate a spectrum of BPAF-induced endocrine and reproductive changes in both sexes. There is strong evidence of alterations in the hypothalamic-pituitary-gonadal axis and of altered steroidogenesis pathways. Multiple studies using zebrafish, Xenopus, chickens, and rodents, show BPAF’s effects on embryogenesis, morphology, and sexual differentiation. Decreased serum testosterone and impaired spermatogenesis and oocyte viability have been demonstrated. The current literature shows clear disruptive effects of BPAF on reproductive health and embryonic development. Though further investigation is warranted, there is ample converging evidence to support limiting the use of BPAF and other similar bisphenols.

{"title":"The biological effects of bisphenol AF in reproduction and development: What do we know so far?","authors":"Megan V. Alexander , Archana Ayyar , Alexandra W. Gannon , Kristen E. Linares , Sara J. Vincent , Samantha Lowe , Alvin To , Chellakkan S. Blesson","doi":"10.1016/j.reprotox.2025.108857","DOIUrl":"10.1016/j.reprotox.2025.108857","url":null,"abstract":"<div><div>Due to the established endocrine-disrupting effects of Bisphenol A (BPA), alternative bisphenols entered the market. Bisphenol AF (BPAF) is now commonly used in the industrial manufacturing of polycarbonate plastics and epoxy resins. However, BPAF’s effects on reproduction and development have not been thoroughly reviewed. We investigated the relationship between BPAF exposure and reproduction and early development. We performed a literature review of studies on BPAF and reproductive physiology. Using keywords, we searched PubMed, Medline, Cochrane Library Database, Embase, and ClinicalTrials.gov for English language literature available until December 2024; we additionally identified and included studies from bibliographies. We included 125 articles, spanning in vitro and in vivo model organism and human studies. BPAF is a selective estrogen receptor modulator and an androgen receptor antagonist and is more potent than BPA. It is detected in urine, blood products, saliva, amniotic fluid, and breast milk. In vitro and in vivo studies demonstrate a spectrum of BPAF-induced endocrine and reproductive changes in both sexes. There is strong evidence of alterations in the hypothalamic-pituitary-gonadal axis and of altered steroidogenesis pathways. Multiple studies using zebrafish, Xenopus, chickens, and rodents, show BPAF’s effects on embryogenesis, morphology, and sexual differentiation. Decreased serum testosterone and impaired spermatogenesis and oocyte viability have been demonstrated. The current literature shows clear disruptive effects of BPAF on reproductive health and embryonic development. Though further investigation is warranted, there is ample converging evidence to support limiting the use of BPAF and other similar bisphenols.</div></div>","PeriodicalId":21137,"journal":{"name":"Reproductive toxicology","volume":"132 ","pages":"Article 108857"},"PeriodicalIF":3.3,"publicationDate":"2025-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143422370","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Blastocyst exposure to plastic during mice in vitro fertilization impacts placental development

IF 3.3 4区医学 Q2 REPRODUCTIVE BIOLOGY

Reproductive toxicology

Pub Date : 2025-02-12 DOI: 10.1016/j.reprotox.2025.108856

Claude Saint-Ruf, Yasmine Boumerdassi, Franck Kouakou, Jean-Philippe Wolf, Florence Eustache, Daniel Vaiman, Francisco Miralles

Introduction

Pregnancies from Assisted Reproductive Technologies (ARTs) are associated with a significant prevalence of maternal, neonatal and long-term adverse health issues. These anomalies are generally attributed to the in vitro manipulations involved in these procedures. Concerns have been raised on the quality of the culture media, however the potential influence of the chemical composition of the devices used in the in vitro fertilization (IVF) has been poorly analysed. By comparing the transcriptomes of placentas from mouse blastocysts obtained by IVF on plasticware, glassware and naturally conceived, we have previously established that plasticware profoundly impacts placental development.

Methods

Transcriptomics, transcriptome deconvolution analysis, Gene Set Enrichment Analysis.

Results

Plasticware alters placental gene expression mostly in the trophoblast compartment, and alters cell composition favouring Glycogen Cells. These modifications correlate with alterations of epigenetic mechanisms (alterations of imprinted genes, microRNAs expression, methylation alterations). Also, sex-stratified analysis reveals that these effects are more drastic in female than male placentas. The effect of glassware on the transcriptome and cellular composition of the placenta is milder, and in particular has lower impact on the imprinted gene or microRNAs expression.

Conclusion

In vitro culture in plasticware during IVF procedures sex-specifically alters gene expression and/or cell composition in the placenta, possibly through factors released by the plasticware having an action on epigenetic actors (imprinted genes, miRNAs and DNA methylation).

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引用次数: 0

Fucoxanthin mitigates mercury-induced mitochondrial toxicity in the human ovarian granulosa cell line

IF 3.3 4区医学 Q2 REPRODUCTIVE BIOLOGY

Reproductive toxicology

Pub Date : 2025-02-11 DOI: 10.1016/j.reprotox.2025.108855

Ekramy M. Elmorsy , Huda A. Al Doghaither , Ayat B. Al-Ghafari , Saad Amer , Manal S. Fawzy , Eman A. Toraih

Mercury (Hg) is known to be a hazardous toxin with a significant negative impact on female reproduction through mechanisms that remain unclear. The carotenoid fucoxanthin (FX) is an antioxidant with several positive effects on human health. This study aimed to examine the potential protective role of FX in reducing the Hg-induced bioenergetic disturbances in a human ovarian granulosa cell line model. (methods briefly) Hg was found to reduce the viability of granulosa cells in a concentration-dependent manner, with an estimated 72-hour EC50 of 10 µM. In contrast, FX (10 and 20 µM) improved cell viability. Hg (1 and 10 µM) significantly reduced cellular ATP levels, mitochondrial membrane potential, oxygen consumption rates, and lactate production. Additionally, Hg impaired the activities and kinetics of mitochondrial complexes I and III and reduced the expression of mitochondrial genes ND1, ND5, cytochrome B, cytochrome C oxidase, and ATP synthase subunits 6 and 8. According to tests on mitochondrial membranes, Hg increased membrane fluidity by reducing saturated fatty acid levels and increasing those of unsaturated fatty acids. Hg also promoted mitochondrial swelling and enhanced the inner mitochondrial membrane permeability to hydrogen and potassium ions. FX (10 µM) was shown to mitigate the negative effects of Hg on the viability of treated granulosa cells, bioenergetics parameters, and mitochondrial membrane integrity in a concentration-dependent manner. Based on these findings, bioenergetic disruption may be a key underlying cause of Hg-induced ovarian dysfunction. Furthermore, FX may have a potential therapeutic role in treating ovarian disorders caused by Hg-induced disruption of granulosa cell bioenergetics.

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引用次数: 0

Prenatal exposure to an environmentally relevant phthalate mixture alters oxidative stress, apoptosis, cell cycle regulators, and steroidogenic factors in the ovaries of F1 mice

IF 3.3 4区医学 Q2 REPRODUCTIVE BIOLOGY

Reproductive toxicology

Pub Date : 2025-02-11 DOI: 10.1016/j.reprotox.2025.108858

Endia J. Fletcher, Winter S. Stubblefield, Taylor A. Seaton, Adira M. Safar, Angela E. Dean, Mary J. Laws, Emily Brehm, Jodi A. Flaws

Phthalates are synthetic chemical compounds found in consumer products and known endocrine-disrupting chemicals. However, it is not well known if prenatal exposure to phthalate mixtures can affect reproductive health in female offspring. Thus, this study tested the hypothesis that prenatal exposure to an environmentally relevant phthalate mixture disrupts long-term ovarian function in adult F1 mice. Pregnant CD-1 dams were dosed orally with vehicle control (corn oil) or phthalate mixture (20 μg/kg/day-500 mg/kg/day) from gestational day 10 until birth. After birth, the F1 female ovaries and sera were collected on postnatal day (PND) 60, 3 months, and 6 months. F1 ovaries were used for evaluation of the proliferative marker, Ki67, and to quantify gene expression of steroidogenic regulators, antioxidant enzymes, apoptotic factors and cell cycle regulators. Sera were collected to measure sex steroid hormone levels. At PND60, prenatal exposure to the mixture decreased the expression of Star, Cyp11a1, Bad, and Casp3 in F1 females at PND60 compared to controls. At 3 months, the mixture decreased expression of Cyp11a1, Hsd3b1, Sod1, Casp3, Casp8, and Fas and increased gene expression of Star and Gpx in F1 ovaries compared to the controls. At 6 months, the mixture decreased testosterone levels and expression of Gsr, Bad, Bok, Casp8, Fas and Traf3, and it increased expression of Star in F1 females compared to the controls. Collectively, these data suggest that the prenatal exposure to an environmentally relevant phthalate mixture may have long-term consequences on ovarian health and function in F1 females long after initial exposure.

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引用次数: 0

Association between maternal exposure to air pollution and intrapartum fetal distress: A retrospective cohort study

IF 3.3 4区医学 Q2 REPRODUCTIVE BIOLOGY

Reproductive toxicology

Pub Date : 2025-02-11 DOI: 10.1016/j.reprotox.2025.108860

Alireza Khajavi , Ehsan Zahmatkesh , Maedeh Raznahan , Ali Shafaghat , Amir Hussein Noohi , Mohammad E. Khamseh , Laily Najafi , Farid Zayeri

This study aimed to investigate the association between maternal exposure to ambient air pollution and intrapartum fetal distress. The retrospective data were obtained for 150 parturients, ages 19–45, referred to Kamali Teaching Hospital, Karaj, Iran, in 2016. To assess the impact of the 2, 4, and 8 weeks exposure windows before the delivery of particulate matter ≤ 10 micrometers (PM₁₀) and sulfur dioxide (SO₂) on fetal distress incidence, logistic regression models were fitted, crudely and adjusted for maternal covariates. The parturients' ages owned a mean (standard deviation) of 30.4 (5.4). Moreover, 17 fetal distress cases were detected (11.3 %), demonstrating higher proportions of cousin marriage and family history of diabetes than the non-fetal distress group. Adjusted for body mass index, cousin marriage, abortion, and family history of diabetes, and over the eight weeks exposure window, a five µg/m³ increase of SO₂ and PM₁₀ provided odds ratios of 2.12 (95 % CI: 1.04–4.30) and 1.61 (95 % CI: 1.08–2.40), respectively, for fetal distress incidence. To conclude, we found the long-term impacts of SO₂ and PM₁₀ on the incidence of fetal distress based on the exposure level during the last eight weeks of pregnancy.

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引用次数: 0