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A workflow for human health hazard evaluation using transcriptomic data and key Characteristics-Based gene sets.
IF 3.4 3区 医学
Toxicological Sciences Pub Date : 2025-03-20 DOI: 10.1093/toxsci/kfaf036
Han-Hsuan D Tsai, King David Oware, Fred A Wright, Weihsueh A Chiu, Ivan Rusyn
{"title":"A workflow for human health hazard evaluation using transcriptomic data and key Characteristics-Based gene sets.","authors":"Han-Hsuan D Tsai, King David Oware, Fred A Wright, Weihsueh A Chiu, Ivan Rusyn","doi":"10.1093/toxsci/kfaf036","DOIUrl":"10.1093/toxsci/kfaf036","url":null,"abstract":"<p><p>Key Characteristics (KCs) are properties of chemicals that are associated with different types of human health hazard. KCs are used for systematic reviews in support of hazard identification. Transcriptomic data are a rich source of mechanistic data and are frequently interpreted through \"enriched\" pathways/gene sets. Such analyses may be challenging to interpret in regulatory science because of redundancy among pathways, complex data analyses, and unclear relevance to hazard identification. We hypothesized that by cross-mapping pathways/gene sets and KCs, the interpretability of transcriptomic data can be improved. We summarized 72 published KCs across 7 hazard traits into 34 umbrella KC terms. Gene sets from Reactome and Kyoto Encyclopedia of Genes and Genomes (KEGG) were mapped to these, resulting in \"KC gene sets\". These sets exhibit minimal overlap and vary in the number of genes. Comparisons of the same KC gene sets mapped from Reactome and KEGG revealed low similarity, indicating complementarity. Performance of these KC gene sets was tested using publicly available transcriptomic datasets of chemicals with known organ-specific toxicity: Benzene and 2,3,7,8-tetrachlorodibenzo-p-dioxin tested in mouse liver, and drugs sunitinib and amoxicillin tested in human induced pluripotent stem cell-derived cardiomyocytes. We found that KC terms related to the mechanisms affected by tested compounds were highly enriched, while the negative control (amoxicillin) showed limited enrichment with marginal significance. This study's impact is in presenting a computational approach based on KCs for the analysis of toxicogenomic data and facilitating transparent interpretation of these data in the process of chemical hazard identification.</p>","PeriodicalId":23178,"journal":{"name":"Toxicological Sciences","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143670973","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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
Effects of Dopamine Agonists on the Estradiol-Induced Prolactin Surge in Ovariectomized Female Wistar Han Rats.
IF 3.4 3区 医学
Toxicological Sciences Pub Date : 2025-03-12 DOI: 10.1093/toxsci/kfaf027
Atish Patel, Travis L Calkins, Justin D Vidal, Pragati S Coder, Scott Carrier, Giri Gokulrangan, Ananth Srinivas R Chakilam, Sandeep sAkare, Richard J Briscoe, Madhu S Mondal
{"title":"Effects of Dopamine Agonists on the Estradiol-Induced Prolactin Surge in Ovariectomized Female Wistar Han Rats.","authors":"Atish Patel, Travis L Calkins, Justin D Vidal, Pragati S Coder, Scott Carrier, Giri Gokulrangan, Ananth Srinivas R Chakilam, Sandeep sAkare, Richard J Briscoe, Madhu S Mondal","doi":"10.1093/toxsci/kfaf027","DOIUrl":"https://doi.org/10.1093/toxsci/kfaf027","url":null,"abstract":"<p><p>Dopamine agonists (DAs) are approved for the treatment of hypodopaminergic pathologies, including Parkinson's disease, restless legs syndrome, and periodic limb movement disorder. During drug development, drugs acting on dopaminergic receptors are often associated with a rat-specific endocrine tumor response, including changes in fertility, which are ascribed to DA-induced suppression of pituitary prolactin release. Although these effects are not observed in or relevant to humans, given species differences in the effects of prolactin on reproductive organs, modeling DA-mediated changes in prolactin and the reproductive system remains important for preclinical drug development. We investigated the effects of 2 D2/D3 DAs, pergolide and rotigotine, on the estradiol (E2)-induced prolactin surge in ovariectomized (OVX) female Wistar Han rats. Daily treatment with DAs over 7 days led to a reduction in the prolactin surge in E2-implanted OVX rats. Specifically, pergolide induced a significant decrease in prolactin levels at all time points compared with the OVX-E2 control group. Similarly, rotigotine dose-dependently suppressed plasma prolactin levels compared with the OVX-E2 control group. This study demonstrates the utility of the OVX rat model in evaluating the effects of DAs on the E2-induced prolactin surge. These results support the use of rotigotine, a DA with a long history of safe human use without significant endocrine-related adverse events, as a positive control at a dose level of 5.0 mg/kg/day for future nonclinical toxicity studies investigating the effects of novel DAs on reproductive hormones in rats.</p>","PeriodicalId":23178,"journal":{"name":"Toxicological Sciences","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143606431","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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
NAPQI is absent in the mouse brain after Sub-hepatotoxic and hepatotoxic doses of acetaminophen.
IF 3.4 3区 医学
Toxicological Sciences Pub Date : 2025-03-10 DOI: 10.1093/toxsci/kfaf034
Nyera A Ali, Stefanie Kennon-McGill, Larry D Parker, Laura P James, William E Fantegrossi, Mitchell R McGill
{"title":"NAPQI is absent in the mouse brain after Sub-hepatotoxic and hepatotoxic doses of acetaminophen.","authors":"Nyera A Ali, Stefanie Kennon-McGill, Larry D Parker, Laura P James, William E Fantegrossi, Mitchell R McGill","doi":"10.1093/toxsci/kfaf034","DOIUrl":"https://doi.org/10.1093/toxsci/kfaf034","url":null,"abstract":"<p><p>Acetaminophen (APAP) is the most-used over-the-counter analgesic among pregnant women. However, concerns have arisen over the safety of APAP exposure during gestation. In particular, it's been speculated that the hepatotoxic metabolite of APAP, N-acetyl-p-benzoquinone imine (NAPQI), forms in the brain after maternal use of therapeutic APAP doses and leads to neurodevelopmental disorders (NDDs). However, APAP metabolism in the brain is understudied. Here, we tested the hypothesis that NAPQI can be generated in the brain by overdosing BTBR T+Itpr3tf/J (common model of the NDD autism) and C57Bl/6J mice with APAP and measuring glutathione loss and APAP-protein adducts as two of the best markers of NAPQI available. Despite glutathione depletion and adducts in the liver, we saw none in the brain. We conclude NAPQI is unlikely to contribute to the pathophysiology of NDDs. IMPACT STATEMENT: It has been hypothesized that NAPQI formation in the brain provides biological plausibility for the purported link between APAP and NDDs. Our results cast doubt on that hypothesis.</p>","PeriodicalId":23178,"journal":{"name":"Toxicological Sciences","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143597839","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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
Deciphering PFAS Mode of Action: Comparative Gene Expression Analysis in Human Liver Spheroids.
IF 3.4 3区 医学
Toxicological Sciences Pub Date : 2025-03-04 DOI: 10.1093/toxsci/kfaf023
A Rowan-Carroll, M Meier, C L Yauk, A Williams, K Leingartner, L Bradford, L Lorusso, E Atlas
{"title":"Deciphering PFAS Mode of Action: Comparative Gene Expression Analysis in Human Liver Spheroids.","authors":"A Rowan-Carroll, M Meier, C L Yauk, A Williams, K Leingartner, L Bradford, L Lorusso, E Atlas","doi":"10.1093/toxsci/kfaf023","DOIUrl":"https://doi.org/10.1093/toxsci/kfaf023","url":null,"abstract":"<p><p>Understanding the mechanisms by which environmental chemicals cause toxicity is necessary for effective human health risk assessment. High-Throughput Transcriptomics (HTTr) can be used to inform risk assessment on toxicological mechanisms, hazards, and potencies. We applied HTTr to elucidate the molecular mechanisms by which Per- and Polyfluoroalkyl Substances (PFAS) cause liver perturbations. We contrasted transcriptomic profiles of PFOA, PFBS, PFOS, and PFDS against transcriptomic profiles from established liver-toxic and non-toxic reference compounds, alongside peroxisome proliferator-activated receptors (PPARs) agonists. Our analysis was conducted on metabolically competent 3-D human liver spheroids produced from primary cells from 10 donors. Pathway analysis showed that PFOS and PFDS perturb many of the same pathways as the known liver-toxic compounds in the spheroids, and that the cholesterol biosynthesis pathways are significantly affected by exposure to these compounds. PFOA alters lipid metabolism-related pathways but its expression profile does not closely match reference compounds. PFBS upregulates many degradation-related pathways and targets many of the same pathways as the PPAR agonists and acetaminophen. Our transcriptional analysis does not support that these PFAS are DNA damaging in this model. A multidimensional scaling analysis revealed that PFOS, PFOA, and PFDS cluster together in the same multidimensional space as liver-damaging compounds; whereas, PFBS clusters more closely with the non-liver-damaging compounds. Benchmark concentration-response modeling predicts that all the PFAS are bioactive in the liver. Overall, our results show that these PFAS produce unique transcriptional changes but also alter pathways associated with established liver-toxic chemicals in this liver spheroid model.</p>","PeriodicalId":23178,"journal":{"name":"Toxicological Sciences","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143558142","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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
Distribution of polybrominated diphenyl ethers (PBDEs) in placental tissues of maternal and fetal origin in exposed Wistar rats and associations with thyroid hormone levels. 多溴联苯醚(PBDEs)在Wistar大鼠胎盘组织中的分布及其与甲状腺激素水平的关系
IF 3.4 3区 医学
Toxicological Sciences Pub Date : 2025-03-01 DOI: 10.1093/toxsci/kfae151
Shaza Gaballah, Brian Hormon, Genavieve St Armour Mason Nelson, Jinyan Cao, Kate Hoffman, Heather B Patisaul, Heather M Stapleton
{"title":"Distribution of polybrominated diphenyl ethers (PBDEs) in placental tissues of maternal and fetal origin in exposed Wistar rats and associations with thyroid hormone levels.","authors":"Shaza Gaballah, Brian Hormon, Genavieve St Armour Mason Nelson, Jinyan Cao, Kate Hoffman, Heather B Patisaul, Heather M Stapleton","doi":"10.1093/toxsci/kfae151","DOIUrl":"10.1093/toxsci/kfae151","url":null,"abstract":"<p><p>In utero exposure to polybrominated diphenyl ethers (PBDEs) is linked to adverse pregnancy and fetal health outcomes, including altered thyroid hormone (TH) levels. Despite their phase-out, PBDEs are still commonly detected in newborn cord blood. While PBDEs can cross the placenta, few studies have separately assessed PBDEs or THs in the maternal and fetal placental tissues. Additionally, no studies have separately assessed THs in these tissues across mid- and late gestation, during the onset of fetal TH synthesis. To address these gaps, we conducted a study with Wistar rats and examined PBDE accumulation in the maternal and fetal placenta. Pregnant dams were exposed daily to sesame oil vehicle, a low dose, or high dose PBDE mixture. At GD15 and 20, dams were sacrificed and placental tissues were collected. Tissues were analyzed for PBDEs, T3, rT3, and T4 using mass spectrometry. BDE-47, -99, -100, and -209 were frequently detected in both the fetal and maternal placenta. At GD15, higher concentrations of BDE-99, -100, and -209 were measured in the fetal placenta; however, this trend reversed by GD20, with higher maternal placental concentrations. Placental T3 and T4 were significantly impacted by exposure, tissue, and exposure × tissue at GD15, with significant reductions in both THs following low-dose exposure in the maternal placenta. By GD20, maternal placental T3 was only significantly reduced in the high exposure groups and there was no effect on placental T4. Overall, these results highlight the rapid developmental changes that occur throughout gestation between the maternal and fetal placenta, and the differential impacts of gestational PBDE exposure on placental T3 and T4 across mid- and late gestation.</p>","PeriodicalId":23178,"journal":{"name":"Toxicological Sciences","volume":" ","pages":"20-30"},"PeriodicalIF":3.4,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11879049/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142772596","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Diet-induced obesity alters the ovarian chemical biotransformation and oxidative stress response proteins both basally and in response to 7,12-dimethylbenz[a]anthracene exposure.
IF 3.4 3区 医学
Toxicological Sciences Pub Date : 2025-03-01 DOI: 10.1093/toxsci/kfae150
Kelsey Timme, Imaobong Inyang, Hunter E White, Aileen F Keating
{"title":"Diet-induced obesity alters the ovarian chemical biotransformation and oxidative stress response proteins both basally and in response to 7,12-dimethylbenz[a]anthracene exposure.","authors":"Kelsey Timme, Imaobong Inyang, Hunter E White, Aileen F Keating","doi":"10.1093/toxsci/kfae150","DOIUrl":"10.1093/toxsci/kfae150","url":null,"abstract":"<p><p>7,12-Dimethylbenz[a]anthracene (DMBA) is a polycyclic aromatic hydrocarbon that causes female infertility via DNA damage, and the ovary has the capacity to mitigate DMBA exposure via the action of proteins including the glutathione S-transferase (GST) family. Due to previous findings of DNA damage and a reduced ovarian chemical biotransformation response to DMBA exposure in hyperphagia-induced obese mice, this study investigated the hypothesis that diet-induced obesity would hamper the ovarian biotransformative response to DMBA exposure. Six-week-old C57BL6/J mice were fed either a normal rodent diet (L) or a high fat high sucrose diet (O) until the O group was ∼30% heavier than the L. Both L and O mice were exposed to either corn oil (C) or DMBA (1 mg/kg) for 7 d. Liver weight was increased (P < 0.05) in obese mice exposed to DMBA but no effect on spleen weight, uterine weight, ovary weight, estrous cyclicity, or circulating 17β-estradiol and progesterone were observed. Primordial and preantral follicle numbers were higher (P < 0.05) in the obese mice and there was a tendency (P = 0.055) for higher antral follicles in DMBA-exposed obese mice. The ovarian proteome was identified by LC-MS/MS analysis to be altered both by diet-induced obesity and by DMBA exposure with changes observed in levels of proteins involved in oocyte development and chemical biotransformation, including GST isoform pi. Fewer proteins were affected by the combined exposure of diet and DMBA than by a single treatment, indicating that physiological status impacts the response to DMBA exposure.</p>","PeriodicalId":23178,"journal":{"name":"Toxicological Sciences","volume":" ","pages":"9-19"},"PeriodicalIF":3.4,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11879017/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143256822","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Haloacetamides exacerbate non-alcoholic fatty liver disease induced by a high-fat diet in C57BL/6J mice. 卤代乙酰胺加重C57BL/6J小鼠高脂饮食诱导的非酒精性脂肪性肝病
IF 3.4 3区 医学
Toxicological Sciences Pub Date : 2025-03-01 DOI: 10.1093/toxsci/kfae160
Zhiqiang Jiang, Lili Yang, Qinxin Liu, Meiyue Qiu, Yu Chen, Mengying Teng, Yubin Zhang, Xing Liu, Zhonghua Zhao, Yuxin Zheng, Melvin Andersen, Weidong Qu
{"title":"Haloacetamides exacerbate non-alcoholic fatty liver disease induced by a high-fat diet in C57BL/6J mice.","authors":"Zhiqiang Jiang, Lili Yang, Qinxin Liu, Meiyue Qiu, Yu Chen, Mengying Teng, Yubin Zhang, Xing Liu, Zhonghua Zhao, Yuxin Zheng, Melvin Andersen, Weidong Qu","doi":"10.1093/toxsci/kfae160","DOIUrl":"10.1093/toxsci/kfae160","url":null,"abstract":"<p><p>Obesity, a significant global health issue, heightens the risk of non-alcoholic fatty liver disease (NAFLD). Its interaction with environmental pollutants might exacerbate NAFLD's severity. Haloacetamides (HAcAms), a group of emerging nitrogenous disinfection byproducts (DBPs) and potent oxidative stressors, are found in chlorinated drinking water. Since oxidative stress is associated with HAcAms-DBP cytotoxicity and a key factor in NAFLD pathogenesis, we hypothesize that HAcAms-DBPs could exacerbate liver injury and NAFLD, particularly with high-fat diets. This study examined HAcAms-DBPs' impact on liver lipid metabolism in mice treated with 1 to 100 times the background drinking water level (13.05 µg/L) for up to 16 weeks of oral administration. Compared to a high-fat-only group, mice co-exposed to a high-fat diet and HAcAms-DBPs for 16 weeks had elevated serum alanine transaminase, aspartate transaminase, triglyceride, hepatic lipid aggregation, and inflammation response. Under high-fat conditions, background drinking water levels of HAcAms significantly upregulated liver Acetyl-CoA carboxylase 1, fatty acid synthase, peroxisome proliferator-activated receptor gamma (PPARγ), PPARγ coactivator-1α, glucose transporter 1 and 4 protein expression in C57BL/6J mice; 10 times background significantly increased expression of inflammatory marker tumor necrosis factor and liver fibrosis marker protein alpha-smooth muscle actin; 100 times further increased both liver damage and markers of early non-alcoholic steatohepatitis phenotypes like steatosis and lobular inflammation. HAcAms-DBPs plus high-fat conditions worsened liver damage. The possible health risks of NAFLD induced by HAcAms in obese individuals deserve further study.</p>","PeriodicalId":23178,"journal":{"name":"Toxicological Sciences","volume":" ","pages":"57-69"},"PeriodicalIF":3.4,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142847430","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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
Advancing systemic toxicity risk assessment: Evaluation of a NAM-based toolbox approach. 推进系统毒性风险评估:评估基于 NAM 的工具箱方法。
IF 3.4 3区 医学
Toxicological Sciences Pub Date : 2025-03-01 DOI: 10.1093/toxsci/kfae159
Sophie Cable, Maria Teresa Baltazar, Fazila Bunglawala, Paul L Carmichael, Leonardo Contreas, Matthew Philip Dent, Jade Houghton, Predrag Kukic, Sophie Malcomber, Beate Nicol, Katarzyna R Przybylak, Ans Punt, Georgia Reynolds, Joe Reynolds, Sharon Scott, Dawei Tang, Alistair M Middleton
{"title":"Advancing systemic toxicity risk assessment: Evaluation of a NAM-based toolbox approach.","authors":"Sophie Cable, Maria Teresa Baltazar, Fazila Bunglawala, Paul L Carmichael, Leonardo Contreas, Matthew Philip Dent, Jade Houghton, Predrag Kukic, Sophie Malcomber, Beate Nicol, Katarzyna R Przybylak, Ans Punt, Georgia Reynolds, Joe Reynolds, Sharon Scott, Dawei Tang, Alistair M Middleton","doi":"10.1093/toxsci/kfae159","DOIUrl":"10.1093/toxsci/kfae159","url":null,"abstract":"<p><p>For many years, a method that allowed systemic toxicity safety assessments to be conducted without generating new animal test data, seemed out of reach. However, several different research groups and regulatory authorities are beginning to use a variety of in silico, in chemico, and in vitro techniques to inform safety decisions. To manage this transition to animal-free safety assessments responsibly, it is important to ensure that the level of protection offered by a safety assessment based on new approach methodologies (NAMs), is at least as high as that provided by a safety assessment based on traditional animal studies. To this end, we have developed an evaluation strategy to assess both the level of protection and the utility offered by a NAM-based systemic safety \"toolbox.\" The toolbox comprises physiologically based kinetic models to predict internal exposures, and bioactivity NAMs designed to give broad coverage across many different toxicity modes of action. The output of the toolbox is the calculation of a bioactivity:exposure ratio (analogous to a margin of internal exposure), which can be used to inform decision-making. In this work, we have expanded upon an initial pilot study of 10 chemicals with an additional 38 chemicals and 70 consumer exposure scenarios. We found that, for the majority of these (>90%), the NAM-based workflow is protective of human health, enabling us to make animal-free safety decisions for systemic toxicity and preventing unnecessary animal use. We have also identified critical areas for improvement to further increase our confidence in the robustness of the approach.</p>","PeriodicalId":23178,"journal":{"name":"Toxicological Sciences","volume":" ","pages":"79-95"},"PeriodicalIF":3.4,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11879040/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142847994","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Reader comment on: "Comprehensive genotoxicity and carcinogenicity assessment of molnupiravir". 读者评论:“莫诺匹拉韦的综合遗传毒性和致癌性评价”。
IF 3.4 3区 医学
Toxicological Sciences Pub Date : 2025-03-01 DOI: 10.1093/toxsci/kfae156
Clay B Frederick, Raymond F Schinazi, Ronald Swanstrom
{"title":"Reader comment on: \"Comprehensive genotoxicity and carcinogenicity assessment of molnupiravir\".","authors":"Clay B Frederick, Raymond F Schinazi, Ronald Swanstrom","doi":"10.1093/toxsci/kfae156","DOIUrl":"10.1093/toxsci/kfae156","url":null,"abstract":"","PeriodicalId":23178,"journal":{"name":"Toxicological Sciences","volume":" ","pages":"116-117"},"PeriodicalIF":3.4,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142847601","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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
2023-2024 Toxicological Sciences Paper of the Year.
IF 3.4 3区 医学
Toxicological Sciences Pub Date : 2025-03-01 DOI: 10.1093/toxsci/kfae153
Deborah Cory-Slechta, Jeffrey M Peters
{"title":"2023-2024 Toxicological Sciences Paper of the Year.","authors":"Deborah Cory-Slechta, Jeffrey M Peters","doi":"10.1093/toxsci/kfae153","DOIUrl":"https://doi.org/10.1093/toxsci/kfae153","url":null,"abstract":"","PeriodicalId":23178,"journal":{"name":"Toxicological Sciences","volume":"204 1","pages":"1"},"PeriodicalIF":3.4,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143558062","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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
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