Reproductive toxicology最新文献

{"title":"Effects of bisphenol A and bisphenol S on human fallopian tube contractions: An in vitro and in silico study","authors":"Richa Singh ,&nbsp;Parul Sharma ,&nbsp;Sakshi Agarwal ,&nbsp;Shristi Modanwal ,&nbsp;Sushmitha Paulraj ,&nbsp;Sanjeev Kumar Mahto","doi":"10.1016/j.reprotox.2026.109211","DOIUrl":"10.1016/j.reprotox.2026.109211","url":null,"abstract":"<div><div>Bisphenol A (BPA), a widely used industrial compound, and its structural analogue Bisphenol S (BPS) are known to exert reproductive toxicity. However, their direct impact on human fallopian tube contractility remains unexplored. This study aimed to investigate the effects of BPA and BPS on spontaneous smooth muscle contractions of the human fallopian tube. Fallopian tube samples from the proliferative phase were used for in vitro contractility assays. The effects of BPA and BPS (1–20 µM) on maximum contractile strength (MCS), basal tone (BT), and contraction frequency (CF) were recorded and analyzed using ANOVA. Cytotoxicity of both compounds was assessed in MCF-7 cells using the MTT assay. Molecular docking examined BPA and BPS binding affinities to key receptors. Both BPA and BPS significantly reduced contractile activity in a concentration-dependent manner (p &lt; 0.001), with BPA exhibiting a stronger inhibitory effect than BPS. MTT assays demonstrated a significant dose- and time-dependent decrease in cell viability for both compounds. Molecular docking indicated comparable binding affinities of BPA and BPS toward estrogen, progesterone, oxytocin, prostaglandin, and calcium channel receptors. BPA and BPS impair human fallopian tube contractility and exhibit cytotoxicity. These findings highlight potential reproductive risks associated with exposure to bisphenol compounds and underscore the need for subsequent extensive studies.</div></div>","PeriodicalId":21137,"journal":{"name":"Reproductive toxicology","volume":"142 ","pages":"Article 109211"},"PeriodicalIF":2.8,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147388303","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}

{"title":"Identifying and reporting dystocia in laboratory rodents","authors":"Paul Barrow ,&nbsp;Prägati S. Coder ,&nbsp;Rashin Ghaffari ,&nbsp;Leah Zorrilla ,&nbsp;Christopher J. Bowman ,&nbsp;Curtis E. Grace ,&nbsp;Jason Manton ,&nbsp;Alan Hoberman ,&nbsp;Narinder Barraclough ,&nbsp;Isabelle Leconte ,&nbsp;Nicola Powles-Glover ,&nbsp;Connie Chen ,&nbsp;Shermaine Mitchell-Ryan","doi":"10.1016/j.reprotox.2026.109206","DOIUrl":"10.1016/j.reprotox.2026.109206","url":null,"abstract":"<div><div>Dystocia (prolonged, difficult, and/or delayed parturition) results from a variety of potential clinical conditions including uterine inertia, hormonal imbalances, oversized fetuses, abnormal orientation of fetuses in the birth canal, etc. In the laboratory, dystocia frequently results in euthanasia. In 2020, the Health and Environmental Sciences Institute’s Developmental and Reproductive Toxicology committee formed a working group to discuss anecdotal reports of increased incidence of dystocia amongst laboratory rodents. Based on an initial survey completed by contributing laboratories, it became apparent that there is significant disparity in how various laboratories define, record, report, and interpret dystocia in laboratory animals. This report highlights the key findings from a survey of performing laboratories conducted by this working group and proposes best practices and recommendations for the monitoring and recording of parturition and dystocia in reproductive toxicity studies in rodents. Implementing consistent definitions, observation strategies, and documentation standards will strengthen data comparability and enhance the scientific foundation on which regulatory decisions are made. Furthermore, consistent reporting of dystocia across industry laboratories will improve the transparency and reliability of evidence used in hazard identification and risk assessment and thereby help reduce discrepancies in regulatory outcomes and facilitate regulatory decision-making for chemicals, plant protection products, biocides, and pharmaceuticals.</div></div>","PeriodicalId":21137,"journal":{"name":"Reproductive toxicology","volume":"142 ","pages":"Article 109206"},"PeriodicalIF":2.8,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147326976","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}

{"title":"Co-exposure to arsenic and nickel alters the morphology and oxidative status of the ventral prostate of Wistar rats","authors":"João Victor Leles Faria ,&nbsp;Luiz Otávio Guimarães-Ervilha ,&nbsp;Thainá Iasbik-Lima ,&nbsp;John Lennon de Paiva Coimbra ,&nbsp;Tungstênio Lima de Souza ,&nbsp;Guilherme Mattos Jardim Costa ,&nbsp;Renê Chagas da Silva ,&nbsp;Mônica Morais Santos ,&nbsp;Mariana Machado-Neves","doi":"10.1016/j.reprotox.2026.109182","DOIUrl":"10.1016/j.reprotox.2026.109182","url":null,"abstract":"<div><div>Arsenic and nickel are toxic chemicals with the capability to accumulate in tissues and cause various health problems, including reproductive disorders. There is no information on whether the mixture of those two chemicals may intensify prostate damage in rats. Therefore, this study aimed to verify the effects of arsenic and nickel exposure on the rat ventral prostate, using histological, biochemical, molecular, and hormonal approaches. Forty Wistar rats were divided into four groups (<em>n</em> = 10/group). Control rats received saline solution in drinking water, whereas rats from the exposed groups ingested arsenic (1 mg L⁻¹), nickel (7 mg L⁻¹), and the two metals simultaneously at the same concentrations. After 70 days of treatment, the ventral prostate was collected, dissected, and processed for microscopic and biochemical analyses. Arsenic-exposed rats showed high estradiol and protein carbonyl levels, arsenic and iron content, and low percentage of collagen fiber I in their ventral prostate. Nickel-exposed rats presented high nickel and iron content, cell and cytoplasmic area, epithelial height, and low zinc proportion. Co-exposed rats exhibited most of the alterations observed here, involving oxidative imbalance, protein oxidation, low collagen fiber content, and high mast cell count. The co-exposure induced inflammatory foci, hyperplasia, and glandular atrophy in the ventral prostate. The <em>in silico</em> analysis revealed metal interactions with cancer, cell cycle, and oxidative stress proteins. Summarizing, co-exposure to arsenic and nickel intensified prostate damage, evidencing an oxidative process and tissue damage that confirms the prostate’s sensitiveness to metal mixture after a subchronic exposure.</div></div>","PeriodicalId":21137,"journal":{"name":"Reproductive toxicology","volume":"141 ","pages":"Article 109182"},"PeriodicalIF":2.8,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146135691","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}

{"title":"Early-life BPS exposure induces reproductive toxicity in offspring mice via ferroptosis","authors":"Yan Su ,&nbsp;Xinxin Guo ,&nbsp;Nuo Xu ,&nbsp;Mengfen Pan ,&nbsp;Kaixing Lin ,&nbsp;Huaicai Zeng ,&nbsp;Qingzhi He","doi":"10.1016/j.reprotox.2026.109175","DOIUrl":"10.1016/j.reprotox.2026.109175","url":null,"abstract":"<div><div>Bisphenol S (BPS), a widely utilized environmental endocrine disruptor, poses significant risks to environmental pollution and human health. While the reproductive toxicity of BPS is recognized, its transgenerational consequences, particularly from early-life exposure, remain poorly defined. In this study, we established a mouse model of early-life BPS exposure to assess its effects on male reproductive development in offspring. Our findings demonstrate that early-life BPS (0.2, 2, 20 mg/L) exposure impairs testicular architecture, diminishes sperm quantity, elevates sperm morphological abnormalities, and dysregulates the expression of CYP11A1, CYP17A1, STAR, and HSD17B3. These changes collectively result in suppressed testosterone production and disrupted spermatogenesis in offspring mice. Additionally, early-life BPS exposure triggered oxidative stress, elevating malondialdehyde levels while reducing superoxide dismutase and glutathione. In offspring mice, BPS induced testicular iron accumulation and mitochondrial damage. This was accompanied by elevated expression of ACSL4 and TFR1, alongside reduced levels of GPX4 and SLC7A11. In TM3 Leydig cells, Fer-1 (1 µM) effectively restored BPS (80 µM)-induced testosterone deficiency and normalized the expression of key ferroptosis-related proteins. Collectively, this study establishes ferroptosis as a critical mechanism in the transgenerational male reproductive damage induced by BPS, thereby providing novel insights into the toxicological effects of environmental endocrine disruptors.</div></div>","PeriodicalId":21137,"journal":{"name":"Reproductive toxicology","volume":"140 ","pages":"Article 109175"},"PeriodicalIF":2.8,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146077531","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}

{"title":"Uterine artery transcriptomic signatures of e-cigarette aerosol exposure in pregnancy","authors":"Alexander L. Carabulea ,&nbsp;Vishal D. Naik ,&nbsp;Joseph D. Janeski ,&nbsp;Hong Jiang ,&nbsp;Saravanan Venkatachalam ,&nbsp;Jayanth Ramadoss","doi":"10.1016/j.reprotox.2025.109133","DOIUrl":"10.1016/j.reprotox.2025.109133","url":null,"abstract":"<div><div>Electronic cigarette (e-cig) use among U.S. adults has shifted notably, with increased adoption among younger adults and middle-aged individuals transitioning from traditional cigarettes. We herein investigated the impact of gestational e-cig aerosol exposure on uterine artery (UA) transcriptome. Timed-pregnant Sprague-Dawley rats were randomly assigned to either the pair-fed Control or the E-cig group before initiation of vaping (4 s e-cig vapor every 2 min, two episodes of 1.5 h each; gestational day (GD) 5 until GD 20). Maternal weight and placental efficiency were not altered, whereas there was a significant deficit in fetal body weight and crown-rump length in the E-cig group on GD 21. Twenty three genes were significantly upregulated, while 40 genes were downregulated in the uterine artery of the E-cig group when compared with the Control group uterine artery. The top significantly downregulated genes in the uterine artery include genes involved in extracellular matrix and Wnt signaling regulation (Smoc2, Gpc3, Frzb, Sfrp2), immune and inflammatory response (C1qtTNF3, Tmem82, Clec21), muscle contraction (Actc1) and cell migration ( Gas2l3, Ret, Robo2). Top upregulated genes in the uterine artery (Vsig4, Agt, Cntn2, Kcnk5, Fhad1, Fgf13, Ctxn1, Prg4, and Pln) included genes involved in immune response and regulation (Vsig4, Kcnk5), and uterine artery vasodilation (Agt). Significant differences between the Control and E-cig groups were validated using Principal Component Analysis (PCA) and k-means clustering. These findings reveal how e-cig aerosol exposure during pregnancy may disrupt key biological processes in the uterine artery that delivers O₂ and nutrients to the fetoplacental compartment.</div></div>","PeriodicalId":21137,"journal":{"name":"Reproductive toxicology","volume":"140 ","pages":"Article 109133"},"PeriodicalIF":2.8,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145692209","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}

{"title":"Quantitative analysis and toxicological mechanisms of various male infertility inducers: A network meta-analysis and pharmacological approach","authors":"Muhammad Arif Asghar ,&nbsp;Ao Zhang ,&nbsp;Shixin Tang ,&nbsp;Hang Han ,&nbsp;Bing Wan ,&nbsp;Jingwei Wu ,&nbsp;Li Ping Wong ,&nbsp;Xiao Zhang ,&nbsp;Qinjian Zhao","doi":"10.1016/j.reprotox.2025.109134","DOIUrl":"10.1016/j.reprotox.2025.109134","url":null,"abstract":"<div><h3>Background</h3><div>Male infertility is a global health concern, accounting for nearly half of all infertility cases. This study evaluates the toxicological effects of key infertility inducers in rodent models and explores underlying molecular mechanisms.</div></div><div><h3>Methods</h3><div>A systematic review and network meta-analysis (NMA) compared nine widely studied inducers: environmental toxicants (Bisphenol-A, Lead acetate, microplastics), pharmacological agents (Cyclophosphamide, Streptozotocin, Valproic acid, Tripterygium glycosides), and metabolic/physical stressors (High-Fat Diet, heat stress). Key endpoints included sperm count, motility, morphology, testis weight, and hormone levels. Network pharmacology and enrichment analyses identified molecular pathways, focusing on oxidative stress. Clinical relevance was assessed based on mechanistic alignment with human infertility.</div></div><div><h3>Results</h3><div>A total of 201 studies involving 3412 rodents were analyzed. NMA revealed significant differences in reproductive toxicity among inducers. Cyclophosphamide, STZ, and microplastics caused the most severe impairments, reducing sperm counts to 30.08 ± 19.1, 38.13 ± 8.2, and 18.97 ± 11.1 × 10⁶/mL, and motility to 31.73 ± 6.1 %, 30.74 ± 4.1 %, and 31.32 ± 10.2 %, respectively. Overall, sperm count, motility, and testosterone decreased by 1.46-, 1.21-, and 1.16-fold. Network pharmacology identified oxidative stress-related genes (NFE2L2, SOD1, HMOX1) as common targets, with oxidative stress emerging as shared mechanistic pathways. Trend analysis (2009–2024) revealed rising research on microplastics, HFD, and Lead acetate.</div></div><div><h3>Conclusions</h3><div>This first integrated toxicological and mechanistic analysis elucidates how diverse inducers impair male reproductive health. Oxidative stress contributes to toxicity, highlighting potential molecular targets for therapy. Findings support the translational relevance of rodent infertility models and guide risk assessment and mitigation strategies for stressors.</div></div>","PeriodicalId":21137,"journal":{"name":"Reproductive toxicology","volume":"140 ","pages":"Article 109134"},"PeriodicalIF":2.8,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145692158","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}

{"title":"The effect of cigarette exposure on placental epigenetics: A systematic review","authors":"Raina D. Pang ,&nbsp;Sarah A. Herrman ,&nbsp;Hannah Ruck ,&nbsp;Katrina Huynh ,&nbsp;Alexandra McGough ,&nbsp;Brian T. Nguyen ,&nbsp;Kimberly D. Siegmund ,&nbsp;Melissa L. Wilson","doi":"10.1016/j.reprotox.2026.109159","DOIUrl":"10.1016/j.reprotox.2026.109159","url":null,"abstract":"<div><div>Tobacco use during pregnancy is a modifiable risk factor contributing to adverse birth outcomes. The placenta is the master regulator of fetal growth and development and contributes to the overall health of the pregnant person and fetus throughout pregnancy. The primary aim of our systematic review was to investigate the impact of tobacco product use during pregnancy on placental epigenetics. A secondary aim of the review was to investigate how tobacco-related alterations in the placental epigenome are associated with maternal and fetal health outcomes. Twenty papers were included in the review. All studies included investigated combustible cigarette smoking only and the majority (85 %) studied full term placentas. Using data from studies that included data on methylation changes in 30 or more CpG loci and/or genes, the three most common molecular pathways identified across all the genes were binding, catalytic activity, and transcription regulator activity. However, a large proportion of the genes were not assigned to a specific category. Additional research is needed to understand whether non-cigarette tobacco products also disrupt placenta epigenetics.</div></div>","PeriodicalId":21137,"journal":{"name":"Reproductive toxicology","volume":"140 ","pages":"Article 109159"},"PeriodicalIF":2.8,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145918361","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}

{"title":"Effects of perfluorooctane sulfonate (PFOS) and tetrabromobisphenol A (TBBPA) on reproductive development in rats","authors":"Mette Stub,&nbsp;Louise Ramhøj,&nbsp;Marta Axelstad,&nbsp;Mikael Pedersen,&nbsp;Terje Svingen","doi":"10.1016/j.reprotox.2026.109170","DOIUrl":"10.1016/j.reprotox.2026.109170","url":null,"abstract":"<div><div>Perfluorooctane sulfonate (PFOS) and tetrabromobisphenol A (TBBPA) are environmental pollutants with known endocrine disrupting potential. Both substances display various thyroid hormone (TH) system disrupting effects, both <em>in vitro</em> and <em>in vivo</em>, but effects on the reproductive system following developmental exposure are less characterized. Recently, we described effects following perinatal exposure to PFOS (0.4 or 0.8 mg/kg bw/day) and TBBPA (250 or 500 mg/kg bw/day) on the TH system in rats, showing a complex effect pattern. Here, we report data on reproductive endpoints (anogenital distance (AGD), nipple retention (NR) and male reproductive organ weights) and steroid hormone levels in offspring from the same <em>in vivo</em> study. Results indicate that PFOS and TBBPA do not affect antiandrogenic endpoints such as AGD and NR at administered doses. PFOS had a modest effect on steroidogenesis, increasing estrone levels in fetuses, and in the 16-day-old pups increasing corticosterone levels in the low-dose group and progesterone levels in both dose groups, along with a small reduction in adjusted testes weight. TBBPA did not alter steroid hormone levels at the fetal stage, but hormones were disrupted in the 16-day-old pups. Here TBBPA increased progesterone levels in low-dose and testosterone levels in high-dose pups and reduced estrone levels in high-dose group to values below the limit of quantification (LOQ). These findings suggest that PFOS and TBBPA have some effects on circulating steroid hormone levels, but minimal effects on androgen-sensitive endpoints in rats.</div></div>","PeriodicalId":21137,"journal":{"name":"Reproductive toxicology","volume":"140 ","pages":"Article 109170"},"PeriodicalIF":2.8,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145998497","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}

{"title":"Screening potential reproductive and developmental effects of PFAS-free vs. PFAS-containing fire extinguishing agents in mice","authors":"Allison M. Narizzano ,&nbsp;Andrew G. East ,&nbsp;Caroline L. Procell ,&nbsp;Matthew A. Bazar ,&nbsp;Meredith E. Bohannon ,&nbsp;Dmitry Pervitsky ,&nbsp;Michael J. Quinn Jr.","doi":"10.1016/j.reprotox.2025.109151","DOIUrl":"10.1016/j.reprotox.2025.109151","url":null,"abstract":"<div><div>The combined repeated-dose and reproductive/developmental toxicity of six fire extinguishing agents were evaluated in mice: one legacy per- and polyfluoroalkyl substances (PFAS)-containing product and five PFAS-free products. For each product, up to 1,000 mg/kg-d was administered via oral gavage (n = 12/sex/group) before mating, for at least 42 days in males, and through gestation and lactation in females. First filial (F1) generation animals were exposed in utero and via lactation, and directly via oral gavage from postnatal day (PND) 22–42. No animals exhibited statistically significant reductions in reproductive function or pregnancy. Body weights of dams, litters, and weanlings were often decreased by high doses of fire extinguishing agents. The lowest concentration that impacted body weights was 320 mg/kg-d in a PFAS-free product. Perturbations to serum thyroid hormones (both generations) and immunoglobulin levels (F1) were rarely detected. Some hematological changes (<em>e.g.,</em> red blood cell parameters) were also detected across the products. Results from these whole-product toxicity tests are consistent with studies of well-characterized ingredients of the products, which are also common ingredients of many household and consumer products. In conclusion, PFAS-free products were not linked to any of the reproductive or developmental effects commonly seen with individual PFAS exposures at the occupationally relevant concentrations tested. Of the products tested, there was only one PFAS-free fire extinguishing agent that was more toxic than the PFAS-containing product.</div></div>","PeriodicalId":21137,"journal":{"name":"Reproductive toxicology","volume":"140 ","pages":"Article 109151"},"PeriodicalIF":2.8,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145846814","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}

{"title":"Micro- and nanoplastics in human male reproduction: Immune disruption, blood–testis barrier, and clinic-ready biomarkers","authors":"Iqra Batool","doi":"10.1016/j.reprotox.2025.109128","DOIUrl":"10.1016/j.reprotox.2025.109128","url":null,"abstract":"<div><div>Micro- and nanoplastics (MNPs) have recently been detected in the human male reproductive tract, signaling a new dimension of environmental exposure. Mass-based analyses identified polymer particles, predominantly polyethylene, in all archived human testes, while independent semen studies revealed multiple polymer types and a multicenter cohort associated higher mixed burdens in semen and urine with poorer sperm quality. Experimental models support these findings, showing that MNPs induce oxidative stress, activate toll-like receptor and nuclear factor kappa B pathways signaling, trigger NLRP3 inflammasome activity, and disrupt tight-junction proteins that maintain the blood–testis barrier, collectively impairing spermatogenesis and steroidogenesis. However, most human studies quantify particles and conventional semen parameters without simultaneous assessment of immune or barrier biomarkers. This review integrates emerging human evidence and proposes a translational framework that combines particle analytics with a clinic-feasible panel of seminal cytokines, oxidative indices, and extracellular-vesicle markers of junctional integrity. Such integration can determine whether MNP burden maps to measurable immune injury in men, bridging detection with mechanism for reproductive immunology.</div></div>","PeriodicalId":21137,"journal":{"name":"Reproductive toxicology","volume":"140 ","pages":"Article 109128"},"PeriodicalIF":2.8,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145688029","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}