Reproductive toxicologyPub Date : 2026-03-01Epub Date: 2026-01-08DOI: 10.1016/j.reprotox.2026.109163
Samane Jahanabadi , Houman Alimoradi , Ali Razmi
{"title":"MicroRNAs in fetal alcohol spectrum disorders: A systematic review of prenatal exposure and molecular targets","authors":"Samane Jahanabadi , Houman Alimoradi , Ali Razmi","doi":"10.1016/j.reprotox.2026.109163","DOIUrl":"10.1016/j.reprotox.2026.109163","url":null,"abstract":"<div><h3>Background</h3><div>Fetal alcohol spectrum disorder (FASD), caused by prenatal ethanol exposure, encompasses developmental abnormalities such as craniofacial dysmorphism, sensory and motor impairments, and neurocognitive deficits. MicroRNAs have been proposed as key regulators in FASD pathophysiology, yet the specific molecular pathways they influence remain unclear.</div></div><div><h3>Methods</h3><div>To better understand the role of microRNAs in the progression of FASD, we have systematically reviewed the effects of prenatal exposure to alcohol on microRNAs. The search was performed through PubMed MEDLINE, web of science, Scopus, and Google Scholar for all articles between 2006 and 2025.</div></div><div><h3>Results</h3><div>The range of ethanol concentrations as well as exposure pattern which applied in the animal models were widely distributed. Totally, 241 differentially expressed microRNAs were identified from 36 experimentally published reports. Emerging data have implicated that special miRNAs are involved in apoptosis (e.g., miR-335, miR-21, miR-9, miR-29a), axon guidance (e.g., miR-17–5p, miR-10b-3p, let-7a-3p, let-7g-3p, let-7i-3p), cell migration/proliferation (e.g., miR760, miR-98–5p, miR-378a-3p), and up- or downregulations of proteins associated with FASD’s abnormalities.</div></div><div><h3>Conclusions</h3><div>Despite substantial heterogeneity in experimental designs, including differences in model systems, species, dosing regimens, and exposure durations, several microRNAs (miR‑9, miR‑335, miR‑15b, miR‑34a, let‑7i, miR‑200a, and miR‑326) consistently emerge as key regulators implicated in the pathophysiology of fetal alcohol spectrum disorders.</div></div>","PeriodicalId":21137,"journal":{"name":"Reproductive toxicology","volume":"140 ","pages":"Article 109163"},"PeriodicalIF":2.8,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145949028","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 role of adenosine triphosphate in the treatment of linezolid-induced ovarian damage and reproductive dysfunction in rats: An investigation into the pathogenesis","authors":"Ilhan Bahri Delibasi , Bulent Yavuzer , Bahadir Suleyman , Neset Gumusburun , Taha Abdulkadir Coban , Ali Sefa Mendil , Elif Esra Uyar , Nurinisa Yucel , Halis Suleyman","doi":"10.1016/j.reprotox.2026.109165","DOIUrl":"10.1016/j.reprotox.2026.109165","url":null,"abstract":"<div><div>Linezolid is an oxazolidinone-derived antibacterial agent that inhibits bacterial protein synthesis by binding to the peptidyl transferase center of the 50S ribosomal subunit. This study investigated whether exogenously administered adenosine triphosphate (ATP) mitigates ovarian damage and reproductive dysfunction induced by linezolid in rats. Forty-eight female albino Wistar rats were randomly assigned to four groups (n = 12 each): healthy control (HG), ATP-only (ATPG), linezolid-only (LZDG), and ATP plus linezolid (ATLDG). ATPG and ATLDG received intraperitoneal ATP (4 mg/kg), whereas HG and LZDG received saline (0.9 % NaCl). One hour later, linezolid (125 mg/kg) was administered orally to LZDG and ATLDG, and the regimen was repeated twice daily for 28 consecutive days. At study end, six rats per group were euthanized for ovarian biochemical, histopathological, and immunohistochemical evaluations; prior to euthanasia (i.p. thiopental sodium, 50 mg/kg), blood was collected for serum prolactin and anti-Müllerian hormone (AMH) analysis. For fertility assessment, the remaining six females per group were co-housed with two proven fertile males for seven days and then monitored for pregnancy for one month. Linezolid exposure increased oxidative stress, caused ovarian tissue injury, decreased AMH, elevated prolactin, and resulted in a 66.7 % infertility rate. ATP co-treatment attenuated these alterations and reduced infertility to 33.3 %. These findings suggest that ATP may provide a protective therapeutic approach against linezolid-induced ovarian toxicity and reproductive dysfunction.</div></div>","PeriodicalId":21137,"journal":{"name":"Reproductive toxicology","volume":"140 ","pages":"Article 109165"},"PeriodicalIF":2.8,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145952721","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}
Reproductive toxicologyPub Date : 2026-03-01Epub Date: 2026-01-11DOI: 10.1016/j.reprotox.2026.109167
Yaling Wu , Yi Chen , Shixuan Wang , Tong Wu , Jinjin Zhang
{"title":"Guarding the ovarian reserve: Maternal methyl donor supplementation protects against propylparaben-induced ovarian aging in offspring","authors":"Yaling Wu , Yi Chen , Shixuan Wang , Tong Wu , Jinjin Zhang","doi":"10.1016/j.reprotox.2026.109167","DOIUrl":"10.1016/j.reprotox.2026.109167","url":null,"abstract":"<div><div>Prenatal exposure to endocrine-disrupting chemicals is increasingly recognized as a contributing factor to female reproductive aging. Propylparaben (PRP), a widely used preservative with estrogenic activity, is ubiquitously detected in human biological samples, raising concern regarding gestational exposure. However, how prenatal PRP exposure affects ovarian development and whether nutritional interventions confer protection remain unclear. Here, pregnant mice were exposed to PRP from embryonic day 7.5 to E13.5, with or without maternal methyl donor (MD) supplementation. Prenatal PRP exposure was associated with impaired primordial follicle pool establishment as early as postnatal day 7 and reduced ovarian reserve and fertility in adult offspring. These effects were associated with increased oxidative stress, inflammation, fibrotic remodeling, hyperactivation of PI3K/AKT/mTOR signaling, and aberrant DNA methylation, collectively contributing to premature follicle activation and depletion. Maternal MD supplementation partially mitigated PRP-induced ovarian injury, helped preserve follicle homeostasis, and improved reproductive outcomes, accompanied by partial restoration of DNA methylation and moderation of aberrant pathway activation. These findings suggest that maternal MD intake may offer a potential nutritional approach to mitigating long-term reproductive risks associated with prenatal PRP exposure.</div></div>","PeriodicalId":21137,"journal":{"name":"Reproductive toxicology","volume":"140 ","pages":"Article 109167"},"PeriodicalIF":2.8,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145966939","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":"A mouse model of busulfan-induced ovarian toxicity and evidence for attenuation with mTOR inhibition","authors":"Mari Deguchi, Yuji Tanaka, Akiko Nakamura, Tsukuru Amano, Ayako Inatomi, Hiroyuki Yamanaka, Akimasa Takahashi, Tetsuro Hanada, Yutaka Yoneoka, Shunichiro Tsuji","doi":"10.1016/j.reprotox.2025.109153","DOIUrl":"10.1016/j.reprotox.2025.109153","url":null,"abstract":"<div><div>Busulfan, an alkylating agent used in hematopoietic stem cell transplantation conditioning, is associated with a high risk of ovarian toxicity. We established a time-resolved in vivo model of busulfan-induced ovarian injury and tested whether sapanisertib, an mTOR inhibitor, mitigates damage. Mice received busulfan (30 mg/kg, intraperitoneally) or saline; ovaries were assessed at 12, 24, and 72 h and 7 days by hematoxylin and eosin histology, follicle counting, TUNEL, and Ki-67 immunohistochemistry. A separate cohort received daily oral sapanisertib (0.3 mg/kg) from 7 days before busulfan through euthanasia; proliferation was assessed at 24 h, and follicle counts at 7 days. In the busulfan-only group, Ki-67 staining showed an early proliferative surge at 24 h in growing follicles, including primary follicles, whereas loss of primordial follicles and an increased primary-to-primordial follicle ratio were evident by 7 days. Primordial follicles showed no TUNEL-positive cells through 72 h, whereas growing follicles were frequently TUNEL-positive. Relative to busulfan alone, the mTOR inhibitor preserved primordial follicles, shifted the primary-to-primordial ratio toward control values, and reduced the proportion of primary follicles with extensive proliferation at 24 h. These findings are consistent with premature activation of primordial follicles as a proximate contributor to busulfan-induced loss of ovarian reserve and suggest that mTOR inhibition may mitigate this process. A two-time-point assay (24 h for proliferation, 7 days for morphology) provides a practical framework for future studies and translation.</div></div>","PeriodicalId":21137,"journal":{"name":"Reproductive toxicology","volume":"140 ","pages":"Article 109153"},"PeriodicalIF":2.8,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145857566","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}
Reproductive toxicologyPub Date : 2026-03-01Epub Date: 2025-12-12DOI: 10.1016/j.reprotox.2025.109138
Madison T. Stewart, Gu Zhou, Danielle P.M. LeBlanc, Annette E. Dodge, Matthew J. Meier, Andrew Williams, Alexandra S. Long, Paul A. White, Carole L. Yauk, Francesco Marchetti
{"title":"CORRIGENDUM, Long Term Exposure to Benzo[b]fluoranthene Does Not Induce Mutations in MutaMouse Male Germ Cells. Reprod Toxicol, 2025, 137:108985 http://doi.org/10.1016/j.reprotox.2025.108985","authors":"Madison T. Stewart, Gu Zhou, Danielle P.M. LeBlanc, Annette E. Dodge, Matthew J. Meier, Andrew Williams, Alexandra S. Long, Paul A. White, Carole L. Yauk, Francesco Marchetti","doi":"10.1016/j.reprotox.2025.109138","DOIUrl":"10.1016/j.reprotox.2025.109138","url":null,"abstract":"","PeriodicalId":21137,"journal":{"name":"Reproductive toxicology","volume":"140 ","pages":"Article 109138"},"PeriodicalIF":2.8,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145757481","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}
Reproductive toxicologyPub Date : 2026-03-01Epub Date: 2025-11-27DOI: 10.1016/j.reprotox.2025.109117
Lei Yin , Zoey Hsuan Hsiao , Chelin Hu , Xiaozhong (John) Yu
{"title":"Development of canine testicular organoid for assessing the effects of environmental exposure","authors":"Lei Yin , Zoey Hsuan Hsiao , Chelin Hu , Xiaozhong (John) Yu","doi":"10.1016/j.reprotox.2025.109117","DOIUrl":"10.1016/j.reprotox.2025.109117","url":null,"abstract":"<div><div>Modeling the male reproductive system in vitro remains challenging due to its complex structure and function such as spermatogenesis. To enhance translational relevance and adhere to the 3 R principles -Replacement, Reduction, Refinement, we developed a three-dimensional (3D) canine testicular organoid model using testes ethically obtained from routine neutering procedures. Testicular cells were isolated via enzymatic digestion, seeded into agarose micro-molds, embedded in extracellular matrix, and cultured for up to 21 days. Organoids increased in diameter (500–1072 μm) and developed complex branching morphologies. Immunofluorescence confirmed the presence of key testicular cell types, including germ cells (GCNA1), Sertoli cells (SOX9), and Leydig cells (HSD3B1), as well as germ cell populations expressing stage-specific differentiation markers, SALL4, DPPA3, PRMT7, and SCP3. Temporal gene expression analysis revealed dynamic regulation of markers involved in testicular function and spermatogenesis, including significant upregulation of GATA4. To evaluate toxicological responsiveness, organoids were exposed to cadmium chloride (CdCl₂). Treatment with 1 μM CdCl₂ significantly reduced cell viability, and 5 μM exposure induced γ-H2AX expression, indicating DNA damage and cellular stress. These findings demonstrate the successful generation and functional validation of a canine testicular organoid model that supports germ cell maintenance and enables mechanistic assessment of reproductive toxicants. This system represents a scientifically robust and ethically sourced alternative to traditional in vivo approaches for evaluating male reproductive toxicity.</div></div>","PeriodicalId":21137,"journal":{"name":"Reproductive toxicology","volume":"140 ","pages":"Article 109117"},"PeriodicalIF":2.8,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145638092","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":"Atrazine and diazinon inhibit oocyte maturation and ovulation in zebrafish","authors":"Md Hasan Ali , Maisum Sarwar Jyoti , Mrityunjoy Acharjee , Shakhawat Hossain , Saokat Ahamed , Md. Forhad Hossain , Toshinobu Tokumoto","doi":"10.1016/j.reprotox.2026.109172","DOIUrl":"10.1016/j.reprotox.2026.109172","url":null,"abstract":"<div><div>Oocyte maturation and ovulation are well characterized biological processes in fish that are induced by progestins through the coordination of nongenomic actions via the membrane progesterone receptor (mPR) and genomic actions via the nuclear progesterone receptor (Pgr). In zebrafish, the effects of chemicals on these processes can be elucidated using <em>in vitro</em> and <em>in vivo</em> oocyte maturation and ovulation assays. The binding affinity of chemicals for mPR and Pgr can be analyzed using a recently established graphene quantum dot (GQD)-labeled mPR and Pgr binding assay. Combining these physiological and biochemical analyses makes it possible to investigate whether the effects of chemical substances on oocyte maturation and ovulation are mediated by mPR and Pgr. In this study, the effects of herbicides and pesticides on fish oocyte maturation and ovulation were evaluated using <em>in vitro</em> and <em>in vivo</em> assays. The findings revealed that at concentrations greater than 0.1 μM, atrazine (ATZ) and diazinon (DZN) substantially reduced oocyte maturation, whereas 2,4-D exposure did not have a similar effect. ATZ and DZN reduced oocyte maturation and ovulation <em>in vivo</em>. However, the concentrations of these compounds required to inhibit ovulation were significantly lower than those required to inhibit oocyte maturation. The binding affinity of endocrine-disrupting chemicals (EDCs) was analyzed using GQD-labeled mPR and Pgr binding assays. All three EDCs—ATZ, DZN, and 2,4-D—exhibited binding affinity for mPR. For Pgr, DZN and 2,4-D exhibited binding affinity, but ATZ did not. These results suggest that ATZ and DZN prevent fish oocyte maturation and ovulation by binding to mPR.</div></div>","PeriodicalId":21137,"journal":{"name":"Reproductive toxicology","volume":"140 ","pages":"Article 109172"},"PeriodicalIF":2.8,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146041566","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}
Reproductive toxicologyPub Date : 2026-03-01Epub Date: 2025-12-22DOI: 10.1016/j.reprotox.2025.109147
Z.G. Yurtgezen , M. Sapmaz-Metin , D. Ercetin
{"title":"Endocrine-disrupting effects of titanium dioxide nanoparticles on the female reproductive system: Evidence from an ovariectomized rat model","authors":"Z.G. Yurtgezen , M. Sapmaz-Metin , D. Ercetin","doi":"10.1016/j.reprotox.2025.109147","DOIUrl":"10.1016/j.reprotox.2025.109147","url":null,"abstract":"<div><h3>Background</h3><div>Titanium dioxide nanoparticles (TiO₂NPs) are widely used metal nanoparticles capable of accumulating in tissues and exerting endocrine-disrupting effects. Their impact on female reproductive physiology remains largely unclear. This study aimed to elucidate the endocrine-disrupting properties of TiO₂NPs by assessing ovarian and uterine histology, serum hormone levels, estrous cycle changes, and receptor expression patterns in both intact and ovariectomized female rats.</div></div><div><h3>Methods</h3><div>Thirty-two Sprague Dawley rats were randomly divided into four groups (n = 8/group): intact control, intact TiO₂NP (10 mg/kg/day, oral, 30 days), ovariectomized control (OvX), and OvX + TiO₂NP (10 mg/kg/day, oral). Vaginal cytology was monitored for 10 days. ELISA measured serum estradiol, luteinizing hormone (LH), and follicle-stimulating hormone (FSH) levels. Ovarian and uterine tissues were examined histologically and immunohistochemically for estrogen-receptor alpha (ERα), estrogen-receptor beta (ERβ), luteinizing hormone receptor (LHR), and follicle-stimulating hormone receptor (FSHR) expression.</div></div><div><h3>Results</h3><div>TiO₂NP exposure elevated estradiol levels in both intact and ovariectomized rats. While ovariectomy significantly increased LH and FSH, TiO₂NP treatment normalized these levels in OvX rats. Ovarian changes included an increase in atretic follicles and a reduction in hormone receptor expression, whereas uterine tissues showed greater gland number, endometrial thickness, and receptor positivity. Estrous cycles were absent in OvX rats but reappeared with prolonged length and estrus frequency in the OvX + TiO₂NP group.</div></div><div><h3>Conclusion</h3><div>TiO₂NPs exert estrogen-like effects and modulate gonadotropin release through the hypothalamic–pituitary axis, even without ovarian estrogen, indicating pronounced endocrine-disrupting effects on the female reproductive system.</div></div>","PeriodicalId":21137,"journal":{"name":"Reproductive toxicology","volume":"140 ","pages":"Article 109147"},"PeriodicalIF":2.8,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145828205","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}
Reproductive toxicologyPub Date : 2026-03-01Epub Date: 2026-01-07DOI: 10.1016/j.reprotox.2025.109154
Nelly Banda , Kanami Watanabe , John Yabe , Rio Doya , Yared Beyene Yohannes , Yoshinori Ikenaka , Mayumi Ishizuka , Shouta M.M. Nakayama
{"title":"Intergenerational sex-specific transcriptomic alterations in gonads of mice after parental lead exposure","authors":"Nelly Banda , Kanami Watanabe , John Yabe , Rio Doya , Yared Beyene Yohannes , Yoshinori Ikenaka , Mayumi Ishizuka , Shouta M.M. Nakayama","doi":"10.1016/j.reprotox.2025.109154","DOIUrl":"10.1016/j.reprotox.2025.109154","url":null,"abstract":"<div><div>Lead (Pb) exposure is known to influence gene expression across multiple tissues, potentially affecting germline biology and offspring development. This study investigated transcriptomic alterations in the gonads of F1 mice following four weeks of parental exposure to Pb‑contaminated soil. After exposure, breeding generated four experimental groups: ① exposed dams with unexposed sires, ② exposed sires with unexposed dams, ③both parents exposed, and ④ unexposed controls. Testes and ovaries were collected from 9‑week‑old offspring, and RNA sequencing was performed using Qiagen CLC Genomics Workbench to characterise transcriptional changes. Principal component analysis revealed distinct transcriptomic profiles in Groups 1–3 relative to controls, indicating that parental Pb exposure, whether maternal, paternal, or combined, shaped offspring gonadal gene expression. Heatmap clustering showed partial overlap between Male Group 3 and controls, although unique expression features remained evident. All exposed groups exhibited reduced overall transcript abundance when compared to controls. Males with maternal Pb exposure displayed the highest number of differentially expressed genes (DEGs), with gene ontology analysis highlighting alterations in immune‑related and enzymatic pathways. In contrast, males with both maternal and paternal exposure showed the fewest DEGs, though a greater proportion were located on the Y chromosome. These sex‑specific transcriptional patterns, particularly those observed in the offspring of exposed sires, suggest that Pb‑related molecular effects may arise independently of direct maternal transfer. While the underlying mechanisms remain uncertain, the findings raise the possibility that some effects could be transmitted through heritable pathways.</div></div>","PeriodicalId":21137,"journal":{"name":"Reproductive toxicology","volume":"140 ","pages":"Article 109154"},"PeriodicalIF":2.8,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145925772","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}
Reproductive toxicologyPub Date : 2026-03-01Epub Date: 2025-12-26DOI: 10.1016/j.reprotox.2025.109144
George Daston , Matthew Burbank , Florian Gautier , Barbara F. Hales , Amer Jamalpoor , Yasunari Kanda , Susan Makris , Aldert H. Piersma , Nicola Powles-Glover , Sonya Sobrian , Vicki Sutherland , Steven Van Cruchten , Ronald L. Wange , Connie L. Chen
{"title":"Corrigendum to “Hypothesis-driven approach to developmental toxicity assessment: Using mechanistic information to inform testing” [Reprod. Toxicol. 140 (2026) 109119]","authors":"George Daston , Matthew Burbank , Florian Gautier , Barbara F. Hales , Amer Jamalpoor , Yasunari Kanda , Susan Makris , Aldert H. Piersma , Nicola Powles-Glover , Sonya Sobrian , Vicki Sutherland , Steven Van Cruchten , Ronald L. Wange , Connie L. Chen","doi":"10.1016/j.reprotox.2025.109144","DOIUrl":"10.1016/j.reprotox.2025.109144","url":null,"abstract":"","PeriodicalId":21137,"journal":{"name":"Reproductive toxicology","volume":"140 ","pages":"Article 109144"},"PeriodicalIF":2.8,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145846785","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}