Journal of Toxicological Sciences最新文献_第5页

1,2-Naphthoquinone promotes cell migration through EGFR-ERK signaling pathway in human A549 cells. 1,2-萘醌通过EGFR-ERK信号通路促进人A549细胞迁移。

IF 1.5 4区医学

Journal of Toxicological Sciences Pub Date : 2025-01-01 DOI: 10.2131/jts.50.459

Yuexuan Pan, Sho Kubota, Yuzhu Zhang, Shuang Fang, Nobumasa Takasugi, Yoshito Kumagai, Takashi Uehara

{"title":"1,2-Naphthoquinone promotes cell migration through EGFR-ERK signaling pathway in human A549 cells.","authors":"Yuexuan Pan, Sho Kubota, Yuzhu Zhang, Shuang Fang, Nobumasa Takasugi, Yoshito Kumagai, Takashi Uehara","doi":"10.2131/jts.50.459","DOIUrl":"https://doi.org/10.2131/jts.50.459","url":null,"abstract":"Hazardous environmental factors contribute to various irreversible threats to human health worldwide. Accumulating evidence suggests that exposure to particulate matter with an aerodynamic diameter of <2.5 µm (PM2.5) plays a critical role in lung carcinogenesis. Previously, we reported that 1,2-naphthoquinone (1,2-NQ), a component of atmospheric PM2.5 and diesel exhaust particles, forms a covalent bond with the epidermal growth factor receptor (EGFR) via protein N-arylation, thereby activating the downstream protein kinase B (Akt) signaling pathway. Here, we elucidate a regulatory mechanism by which 1,2-NQ modulates the migratory activity of human lung adenocarcinoma A549 cells. Specifically, exposure of A549 cells to 1,2-NQ induces phosphorylation of EGFR, leading to the activation of extracellular signal-regulated kinase 1/2 (ERK1/2). This activation is significantly suppressed by anti-EGFR antibodies (cetuximab and panitumumab) and inhibitors targeting rapidly accelerated fibrosarcoma (Raf; LY3009120) and mitogen-activated protein kinase kinase (MEK; U0126). These findings suggest that 1,2-NQ induces ERK1/2 phosphorylation by activating the Raf-MEK pathway. Notably, suppression of EGFR-ERK1/2 signaling resulted in a decrease in migratory activity. Our findings provide new insights into lung cancer carcinogenesis and may contribute to the development of novel therapeutic strategies.","PeriodicalId":17654,"journal":{"name":"Journal of Toxicological Sciences","volume":"50 9","pages":"459-469"},"PeriodicalIF":1.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144959038","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

Retraction: MZF1 alleviates oxidative stress and apoptosis induced by rotenone in SH-SY5Y cells by promoting RBM3 transcription. 收缩：MZF1通过促进RBM3转录，缓解鱼tenone诱导SH-SY5Y细胞的氧化应激和凋亡。

IF 1.5 4区医学

Journal of Toxicological Sciences Pub Date : 2025-01-01 DOI: 10.2131/jts.50.R2

Ji Zhang, Wen Chai, Zhengbing Xiang, Xinhua Zhou, Ping Zhang

{"title":"Retraction: MZF1 alleviates oxidative stress and apoptosis induced by rotenone in SH-SY5Y cells by promoting RBM3 transcription.","authors":"Ji Zhang, Wen Chai, Zhengbing Xiang, Xinhua Zhou, Ping Zhang","doi":"10.2131/jts.50.R2","DOIUrl":"10.2131/jts.50.R2","url":null,"abstract":"Editor's AnnouncementMZF1 alleviates oxidative stress and apoptosis induced by rotenone in SH-SY5Y cells by promoting RBM3 transcriptionJi Zhang, Wen Chai, Zhengbing Xiang, Xinhua Zhou, Ping Zhang(The Journal of Toxicological Sciences, 46, 477-486, 2021)This paper has been withdrawn at the request of the authors.This article was accepted for publication by the Editorial Committee of The Journal of Toxicological Sciences after a regular peer review process. However, the Editorial Committee received an email from the corresponding author, Dr. Ping Zhang, requesting that the paper be withdrawn. The Editorial Board asked him to submit a letter of consent from all co-authors, and he subsequently provided one with the signatures of all co-authors. As that letter attested to the authors' intention, we approved the withdrawal of this paper.The authors have not disclosed the reasons for the withdrawal. However, the Editorial Committee has decided to respect their decision. Therefore, this action was taken at the authors' own responsibility.Toshiyuki Kaji, Ph.D. Editor-in-ChiefThe Journal of Toxicological Sciences.","PeriodicalId":17654,"journal":{"name":"Journal of Toxicological Sciences","volume":"50 7","pages":"R2"},"PeriodicalIF":1.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144626667","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

Protocatechuic acid suppresses diethylnitrosamine-induced hepatic preneoplastic lesions by inhibiting phase I enzymes, reducing cell proliferation, and promoting apoptosis. 原儿茶酸通过抑制I期酶、减少细胞增殖和促进细胞凋亡来抑制二乙基亚硝胺诱导的肝脏肿瘤前病变。

IF 1.5 4区医学

Journal of Toxicological Sciences Pub Date : 2025-01-01 DOI: 10.2131/jts.50.387

Charatda Punvittayagul, Sirinya Taya, Theerapat Luangsuphabool, Rawiwan Wongpoomchai

{"title":"Protocatechuic acid suppresses diethylnitrosamine-induced hepatic preneoplastic lesions by inhibiting phase I enzymes, reducing cell proliferation, and promoting apoptosis.","authors":"Charatda Punvittayagul, Sirinya Taya, Theerapat Luangsuphabool, Rawiwan Wongpoomchai","doi":"10.2131/jts.50.387","DOIUrl":"https://doi.org/10.2131/jts.50.387","url":null,"abstract":"Protocatechuic acid (PCA) is a phenolic compound naturally occurring in various plants. Although numerous studies have reported on its various biological activities, information on the anti-carcinogenic potential and its molecular mechanisms in animal models has never been conclusively determined. Therefore, this study aimed to study the inhibitory effect of PCA against diethylnitrosamine (DEN)-induced rat hepatocarcinogenesis. Rats received three intraperitoneal injections of 100 mg kg-1 body weight of DEN to initiate hepatic preneoplastic lesions, and glutathione S-transferase placental form (GST-P)-positive foci were used as the end-point marker. Rats were treated with PCA at 40 mg kg-1 body weight by oral gavage administration for 15 weeks to study its chemopreventive effect on the early stages of hepatocarcinogenesis. PCA treatment decreased the number and the area of hepatic GST-P-positive foci in DEN-induced rats. It inhibits the activity of cytochrome P450 reductase and reduces the expression of cytochrome P450 2E1 protein. It also suppresses cell proliferation by down-regulation of Cyclin D1 expression. Additionally, it induces apoptosis, as indicated by the up-regulation of pro-apoptotic genes, Bax and Bad, in DEN-induced rats. These findings suggest that PCA is an anti-cancer agent that inhibits hepatocarcinogenesis in DEN-treated rats.","PeriodicalId":17654,"journal":{"name":"Journal of Toxicological Sciences","volume":"50 8","pages":"387-397"},"PeriodicalIF":1.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144775755","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

Potential of connexin 32 as a predictive marker for drug-induced cholestatic liver injury in a collagen vitrigel-culture model of HepG2-NIAS cells, a new subline of HepG2 cells, with bile canaliculus-like structures. 连接蛋白32在HepG2- nias细胞（一种具有胆管样结构的HepG2细胞亚系）胶原培养模型中作为药物性胆汁淤积性肝损伤预测标志物的潜力

IF 1.8 4区医学

Journal of Toxicological Sciences Pub Date : 2025-01-01 DOI: 10.2131/jts.50.135

Miaki Uzu, Toshiaki Takezawa

{"title":"Potential of connexin 32 as a predictive marker for drug-induced cholestatic liver injury in a collagen vitrigel-culture model of HepG2-NIAS cells, a new subline of HepG2 cells, with bile canaliculus-like structures.","authors":"Miaki Uzu, Toshiaki Takezawa","doi":"10.2131/jts.50.135","DOIUrl":"10.2131/jts.50.135","url":null,"abstract":"Cholestatic drug-induced liver injury (DILI) is caused by the aberrant excretion of bile acids (BAs) from hepatocytes via bile canaliculus-like structures (BCLSs) into the bile ducts. The precise in vitro evaluation method for cholestatic DILI has not been established due to a lack of specific markers and cell resources. We previously reported that HepG2-NIAS cells cultured on a collagen vitrigel (CV) membrane formed BCLSs with high protein expression of transporters involved in the excretion of BAs, including bile salt export pump (BSEP). In this study, the potential of connexin (Cx) 32, a component of gap junction, as a predictive marker for cholestatic DILI was investigated using a CV-culture model of HepG2-NIAS cells. The cells were treated with 7 drugs with different DILI-risk levels, and cell toxicity and Cx32 expression were evaluated. Cell toxicity was significantly increased not only by high DILI-risk drugs (troglitazone and cyclosporine A) but also by chlorpromazine with low DILI-risk. Furthermore, cell toxicity of troglitazone was not enhanced by a co-treatment with taurocholate, suggesting the low involvement of inhibition of BA excretion via BSEP in cholestatic DILI. In contrast, the total protein expression of Cx32 and co-localization of Cx32 and F-actin, which is composed of BCLSs, were significantly increased only by high DILI-risk drugs. Treatment with high DILI-risk drugs also induced the increased protein expression of zonula occludens (ZO)-1, which supports BCLSs concerted with Cx32. These results suggest that Cx32 expression in the CV-culture model of HepG2-NIAS cells may be a prominent predictive marker for cholestatic DILI.","PeriodicalId":17654,"journal":{"name":"Journal of Toxicological Sciences","volume":"50 3","pages":"135-145"},"PeriodicalIF":1.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143537434","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

The Journal of Toxicological Sciences and Fundamental Toxicological Sciences to become open access journals. 《毒理学科学杂志》和《基础毒理学科学》成为开放获取期刊。

IF 1.8 4区医学

Journal of Toxicological Sciences Pub Date : 2025-01-01 DOI: 10.2131/jts.50.R1

Toshiyuki Kaji, Akira Naganuma

{"title":"The Journal of Toxicological Sciences and Fundamental Toxicological Sciences to become open access journals.","authors":"Toshiyuki Kaji, Akira Naganuma","doi":"10.2131/jts.50.R1","DOIUrl":"https://doi.org/10.2131/jts.50.R1","url":null,"abstract":"We would like to express our gratitude for your contributions to our official scientific journals, The Journal of Toxicological Sciences and Fundamental Toxicological Sciences.We have decided to make both journals open access in order to internationalize them and expand their reach to a broader audience. Articles will be published under the Creative Commons license with the highest degree of freedom, CC BY (4.0). As a result of this change, article copyright will belong to the authors, and secondary use, including copying, distribution, display, storage, modification, and commercial use, can be carried out without the relevant society's permission.The new Instructions for Authors will be published on the journal websites in advance. These new submission guidelines \u2028will apply to papers submitted on or after June 1, 2025 (Japan time). Please note that the previous Instructions for Authors will apply to papers submitted until May 31, 2025 (Japan time).We hope that this change will encourage you to submit more of your excellent papers to The Journal of Toxicological Sciences and Fundamental Toxicological Sciences.Toshiyuki Kaji, Ph.D.Editor-in-ChiefThe Journal of Toxicological SciencesAkira Naganuma, Ph.D.Editor-in-ChiefFundamental Toxicological Sciences.","PeriodicalId":17654,"journal":{"name":"Journal of Toxicological Sciences","volume":"50 5","pages":"R1"},"PeriodicalIF":1.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143971045","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

Perfluorooctane sulfonate induces hepatotoxicity through promoting inflammation, cell death and autophagy in a rat model. 在大鼠模型中，全氟辛烷磺酸通过促进炎症、细胞死亡和自噬诱导肝毒性。

IF 1.8 4区医学

Journal of Toxicological Sciences Pub Date : 2025-01-01 DOI: 10.2131/jts.50.45

Leilei Tang, Jianjun Zhu, Sheng Zhuge, Jiawen Yu, Guojun Jiang

{"title":"Perfluorooctane sulfonate induces hepatotoxicity through promoting inflammation, cell death and autophagy in a rat model.","authors":"Leilei Tang, Jianjun Zhu, Sheng Zhuge, Jiawen Yu, Guojun Jiang","doi":"10.2131/jts.50.45","DOIUrl":"10.2131/jts.50.45","url":null,"abstract":"Perfluorooctane sulfonate (PFOS) is reported to cause hepatotoxicity in animals and humans. However, the underlying mechanism by which it affects organelle toxicity in the liver are not well elucidated yet. This study aimed to investigate the mechanisms underlying PFOS-induced hepatic toxicity, focusing on inflammation, cell death, and autophagy. We established a PFOS-exposed Sprague-Dawley (SD) rat liver injury model by intraperitoneal injection of PFOS (1 mg/kg and 10 mg/kg body weight) every alternate day for 15 days. Our findings indicated that PFOS increased liver weight, caused lipid disorder and hepatic steatosis in rats. Meanwhile, PFOS disrupted the structure of mitochondria, increased accumulation of reactive oxygen species (ROS), repressed superoxide dismutase (SOD) and glutathione peroxidase (GSH-PX) levels, and elevated malondialdehyde (MDA) and nitric oxide synthase (NOS) amounts. We found PFOS induced inflammation as evidenced by activation of NOD-like receptor protein 3 (NLRP3), Cleaved cysteine-aspartic acid protease (caspase)1, tumor necrosis factor (TNF)α and interleukin (IL)-1β levels. Moreover, PFOS exposure significantly decreased B-cell lymphoma2 (Bcl2)/Bcl2 associated X (Bax) ratio and increased the protein expression of Cleaved caspase-3. Compared with the control group, PFOS upregulated the protein expression of necroptotic markers and autophagy-related proteins. In conclusion, PFOS induced inflammation, cell death, and autophagy through oxidative stress by ROS overload, thereby providing a mechanistic explanation for PFOS-induced hepatotoxicity.","PeriodicalId":17654,"journal":{"name":"Journal of Toxicological Sciences","volume":"50 2","pages":"45-55"},"PeriodicalIF":1.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143080637","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

Alteration of bile acid composition is a possible risk factor for antibiotics-induced liver injury. 胆汁酸组成的改变是抗生素引起肝损伤的一个可能的危险因素。

IF 1.5 4区医学

Journal of Toxicological Sciences Pub Date : 2025-01-01 DOI: 10.2131/jts.50.379

Akinori Takemura, Shotaro Suminoe, Tomoya Hirai, Keito Nakasone, Kotaro Hayasaki, Binbin Song, Kousei Ito

{"title":"Alteration of bile acid composition is a possible risk factor for antibiotics-induced liver injury.","authors":"Akinori Takemura, Shotaro Suminoe, Tomoya Hirai, Keito Nakasone, Kotaro Hayasaki, Binbin Song, Kousei Ito","doi":"10.2131/jts.50.379","DOIUrl":"https://doi.org/10.2131/jts.50.379","url":null,"abstract":"Drug-induced liver injury (DILI), in rare instances, can become severe and lead to fatal outcomes; therefore, it is crucial to clarify the mechanisms underlying DILI. Antibiotics are well known to induce a high frequency of DILI. We hypothesized that alterations in the bile acid composition, owing to the destruction of enterobacteria, is one factor frequently associated with antibiotics-induced liver injury. To verify this hypothesis, we constructed and evaluated a mouse model of antibiotic-induced liver injury. Although no liver injury was observed upon administering three antibiotics (vancomycin, flucloxacillin, and ampicillin) alone, oral administration of antibiotics (vancomycin and flucloxacillin) with cholic acid (CA) increased levels of alanine transaminase (ALT). In the high ALT group, plasma taurocholic acid (TCA) levels were significantly increased, with a positive correlation detected between ALT and blood TCA levels (Spearman's ρ = 0.839). Overall, we constructed a mouse model of antibiotic-induced livery injury and confirmed our hypothesis that elevated blood levels of conjugated bile acids (increased TCA levels in this mouse model) can induce DILI.","PeriodicalId":17654,"journal":{"name":"Journal of Toxicological Sciences","volume":"50 8","pages":"379-386"},"PeriodicalIF":1.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144775753","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

In silico model to predict dermal absorption of chemicals in finite dose conditions. 在有限剂量条件下预测皮肤吸收化学物质的硅模型。

IF 1.8 4区医学

Journal of Toxicological Sciences Pub Date : 2025-01-01 DOI: 10.2131/jts.50.171

Ibuki Narita, Hiroaki Todo, Chihiro Fujiwara, Hiroyuki Teramae, Takeshi Oshizaka, Shoko Itakura, Syuuhei Komatsu, Kozo Takayama, Kenji Sugibayashi

{"title":"In silico model to predict dermal absorption of chemicals in finite dose conditions.","authors":"Ibuki Narita, Hiroaki Todo, Chihiro Fujiwara, Hiroyuki Teramae, Takeshi Oshizaka, Shoko Itakura, Syuuhei Komatsu, Kozo Takayama, Kenji Sugibayashi","doi":"10.2131/jts.50.171","DOIUrl":"10.2131/jts.50.171","url":null,"abstract":"The development of in silico approaches that can estimate the dermal absorption of chemicals exposed in practical conditions is highly anticipated. In the present study, an in silico model to estimate both the dermal absorption rate and dermal permeation profile was developed for the application of chemicals in finite dose conditions. Forty-three chemicals with molecular weights in the range 116-362 and logKo/w in the range 1.1-4.5 were used to develop an in silico model. A gradient boosting tree approach was applied to estimate permeation parameters for diffusion and partition coefficients of the chemicals in skin using physicochemical parameters of the chemicals such as molecular weight, lipophilicity, and the highest and lowest occupied molecular orbitals as the descriptor. In addition, 11 chemicals with different molecular weights and lipophilicities were applied on excised human skin in a finite dose condition, and dermal absorption profiles were obtained. Consideration of donor-solvent evaporation time, saturated concentrations of the chemicals, and donor-solvent coverage area on the skin surface, in addition to estimated skin permeation parameters of the chemicals, showed comparatively good dermal absorption profiles, although some cases of underestimation of dermal absorption were identified. It will be necessary to verify the accuracy of this model through experiments using more chemicals. However, the obtained results suggested that the established model may be valid to estimate the dermal absorption of chemicals in practical conditions.","PeriodicalId":17654,"journal":{"name":"Journal of Toxicological Sciences","volume":"50 4","pages":"171-186"},"PeriodicalIF":1.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143772434","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

miRNA-214-3p targets BNIP3 to affect autophagy and thus drive gastric cancer progression. miRNA-214-3p通过靶向BNIP3影响自噬从而驱动胃癌进展。

IF 1.8 4区医学

Journal of Toxicological Sciences Pub Date : 2025-01-01 DOI: 10.2131/jts.50.235

Changjiang Chen, Shen Guan, Yong Zhuang, Mingming Xie, Qingxia Huang, Xiaoling Li, Chunkang Yang, Jinliang Jian

{"title":"miRNA-214-3p targets BNIP3 to affect autophagy and thus drive gastric cancer progression.","authors":"Changjiang Chen, Shen Guan, Yong Zhuang, Mingming Xie, Qingxia Huang, Xiaoling Li, Chunkang Yang, Jinliang Jian","doi":"10.2131/jts.50.235","DOIUrl":"https://doi.org/10.2131/jts.50.235","url":null,"abstract":"With a fourth-place death rate among all malignancies, gastric cancer (GC) is one of the most prevalent tumors globally. As a primary malignant characteristic of GC, metastasis contributes substantially to a high death rate and unfavorable prognosis. miRNA-214-3p can influence cell apoptosis since it is an autophagy-regulating molecule. Its significance in GC malignant development has not, however, been investigated in terms of mechanism. qRT-PCR was utilized to confirm expression of miRNA-214-3p in GC tissues and cells. Bioinformatics analysis was then implemented to examine BNIP3 expression in GC as well as binding interaction between BNIP3 and miRNA-214-3p. The targeting capability of miRNA-214-3p on BNIP3 was confirmed using the dual-luciferase assay. Capacities of cells to proliferate, migrate, and invade were assayed using Transwell assays and colony formation. In order to determine if GC cells were capable of autophagy, immunofluorescence and western blot were employed. In GC, miRNA-214-3p was substantially expressed in GC tissues and cells, but BNIP3 was downregulated, as shown by bioinformatics analysis and verified by cell tests. MiRNA-214-3p targeted BNIP3, as shown by further bioinformatics analysis, and dual-luciferase experiment verified this binding connection. MicroRNA-214-3p facilitated cell invasion, migration, and proliferation, as shown by Transwell tests and colony formation. MiRNA-214-3p accelerated malignant development of GC by targeting BNIP3 to impact autophagy, as demonstrated by immunofluorescence and western blot analyses. By targeting BNIP3 to affect autophagy, miRNA-214-3p aided in the malignant growth of GC. This suggested that miRNA-214-3p may function as a likely therapeutic target or biomarker for the disease, with significant implications for early diagnosis and treatment of patients.","PeriodicalId":17654,"journal":{"name":"Journal of Toxicological Sciences","volume":"50 5","pages":"235-244"},"PeriodicalIF":1.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144000714","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

Differential effects of different time windows of postnatal perfluorooctane sulfonate exposure on cognitive development in mouse hippocampus. 出生后全氟辛烷磺酸暴露不同时间窗对小鼠海马认知发育的差异影响。

IF 1.8 4区医学

Journal of Toxicological Sciences Pub Date : 2025-01-01 DOI: 10.2131/jts.50.223

Ayane Ninomiya, Asahi Haijima, Yuki Fujiwara, Reika Kawabata-Iwakawa, Izuki Amano, Noriyuki Koibuchi

{"title":"Differential effects of different time windows of postnatal perfluorooctane sulfonate exposure on cognitive development in mouse hippocampus.","authors":"Ayane Ninomiya, Asahi Haijima, Yuki Fujiwara, Reika Kawabata-Iwakawa, Izuki Amano, Noriyuki Koibuchi","doi":"10.2131/jts.50.223","DOIUrl":"https://doi.org/10.2131/jts.50.223","url":null,"abstract":"Perinatal perfluorooctane sulfonate (PFOS) exposure of the next generation through placenta and breast milk has been of high concern. Epidemiological and animal studies have reported that perinatal PFOS exposure is associated with neurodevelopmental disorders such as learning and autism spectrum disorders in children. However, the sensitive time window of perinatal PFOS exposure for neurodevelopment has yet to be elucidated. Here we examined differential effects of different time windows of postnatal PFOS exposure (postnatal day (PD) 1-7 or 8-14) on cognitive development and gene expression profiles in the hippocampus. Pups were exposed to PFOS from PD 1 to 7 (PD 1-7 group) or from PD 8-14 (PD 8-14 group) through breastfeeding by dams who received a daily gavage of 1 mg/kg body weight PFOS per day during each period. An object location test and an object recognition test revealed the impairment in spatial memory in PD 1-7 group at PD 70. Learning ability was also retarded in a visual discrimination test. According to RNA-seq analysis and real-time PCR, Serpina3g and Tmem91 were significantly downregulated in the hippocampus of PD 1-7 group at PD 21. These results suggest that the first 7 days after birth are critically vulnerable to PFOS exposure and consequent neurodevelopmental deficits rather than the late phase of postpartum. Our work puts a strong emphasis on the importance of monitoring PFOS concentration in pregnant women and potential impact on retardation of neurodevelopment in children.","PeriodicalId":17654,"journal":{"name":"Journal of Toxicological Sciences","volume":"50 5","pages":"223-233"},"PeriodicalIF":1.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143999748","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