Toxicology and applied pharmacology最新文献

{"title":"Sodasulphanecobalamin provides rapid cyanide detoxification and hemodynamic rescue in a rat model of acute cyanide poisoning.","authors":"Olatunji N Salako, Ioannis Sarris, Frank Anayo Orji, Vincent Chukuemaka Eze, Kaliyapillai Vijayakumar, Levent Kenar","doi":"10.1016/j.taap.2026.118027","DOIUrl":"https://doi.org/10.1016/j.taap.2026.118027","url":null,"abstract":"<p><p>Current cyanide antidotes have limitations including delayed onset, methemoglobinemia, or the need for multiple agents. We developed Sodasulphanecobalamin (SSC), a cobalt‑sulfur complex integrating rapid cyanide chelation with sulfur-donor detoxification. SSC was synthesized from hydroxocobalamin and sulfur-based precursors, characterized by HPLC, HR-MS, NMR, IR, and elemental analysis, with the coordination geometry pending X-ray crystallography. In rats, SSC given 1 or 5 min after intravenous KCN (2.5 mg/kg) restored mean arterial pressure (MAP) within 5 ± 1 and 9 ± 2 min, respectively, with 100% survival in both groups (n = 9). At a higher cyanide dose (3.5 mg/kg, ~1.7× LD₅₀), SSC given after 5 min maintained 100% survival (n = 6), whereas hydroxocobalamin resulted in 83% survival. SSC (78% yield, >98% purity) restored MAP significantly faster than hydroxocobalamin (11 ± 2 min, p = 0.032) and standard nitrite-thiosulfate therapy (28 ± 3 min, p = 0.0004). At 3.5 mg/kg, SSC achieved 100% survival vs. 83% for hydroxocobalamin and 67% for standard therapy. Blood cyanide declined 85% within 5 min with corresponding thiocyanate rise, and methemoglobin remained below 3% (p > 0.05 vs. controls). Naive rats showed no toxicity over 28 days. Pharmacokinetics revealed a half-life of 4.2 ± 0.6 h. SSC is a fast-acting, well-tolerated cyanide antidote outperforming current therapies. Further studies are needed for dosing optimization and intramuscular administration.</p>","PeriodicalId":23174,"journal":{"name":"Toxicology and applied pharmacology","volume":" ","pages":"118027"},"PeriodicalIF":3.6,"publicationDate":"2026-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148892327","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}

{"title":"Toxicity of tungsten and molybdenum disulphide particles after acute and subacute exposure in vitro.","authors":"Daniela Perroni Frias, Maria Konstantinou, Alicia Arriaza, Anastasiia Snigireva, Sarah McCarrick, Karin Broberg, Niels Hadrup, Ulla Vogel, Anda Gliga","doi":"10.1016/j.taap.2026.118029","DOIUrl":"https://doi.org/10.1016/j.taap.2026.118029","url":null,"abstract":"<p><p>Tungsten (W) and molybdenum disulphide (MoS₂) particles are increasingly used industrially, but may pose potential health risks, particularly following inhalation in occupational settings. Existing data is inconsistent but there is evidence that these particles are genotoxic. Therefore, there is a need to further increase our understanding on their toxicity and underlying mechanisms. To this end, we tested W and MoS₂ particles in two human cell models, in vitro bronchial epithelial cells (BEAS-2B) and monocyte-derived macrophages (dTHP-1) after acute exposure (24 h), but we also investigated effects after subacute (2-week) exposure of BEAS-2B cells. We evaluated cellular metal content (by ICP-MS), cytotoxicity (by Alamar Blue and Trypan Blue), DNA damage (by alkaline comet assay) and secretion of pro-inflammatory cytokines (IL-6, IL-8/CXCL8, IL-1ß, TNF-α by multiplex electrochemiluminescence) into cell media. After acute exposure, both particles induced dose-dependent DNA damage in BEAS-2B and dTHP-1 cells. In addition, W particles also increased secretion of cytokines from dTHP1, while none were significantly increased in BEAS-2B cells. After subacute exposure both particles increased IL-6 secretion from BEAS-2B cells and induced dose-dependent DNA damage, which remained persistent at 1 week of recovery. Overall, our data indicate that MoS₂ and W are genotoxic, likely via different mechanisms. The data suggest that exposure duration did not influence genotoxicity in BEAS-2B, but was important for inflammatory responses. When compared with in vivo data, our cell models predicted genotoxicity in bronchoalveolar lavage cells well and, to some extent, also lung inflammation. Finally, these findings stress the importance of limiting occupational exposure to W and MoS₂ to protect workers' health.</p>","PeriodicalId":23174,"journal":{"name":"Toxicology and applied pharmacology","volume":" ","pages":"118029"},"PeriodicalIF":3.6,"publicationDate":"2026-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148888430","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}

{"title":"Tannic acid protects against lapatinib-induced hepatotoxicity by inhibiting cathepsin activity and repairing lysosomal membrane permeabilization.","authors":"Yuan Mu, Zengyue Pan, He Zhao, Xiangliang Huang, Nini Zhang, Zhifei Xu, Bo Yang, Qiaojun He, Xiaochun Yang, Peihua Luo, Hao Yan","doi":"10.1016/j.taap.2026.118028","DOIUrl":"https://doi.org/10.1016/j.taap.2026.118028","url":null,"abstract":"<p><p>Lapatinib is an important targeted drug used to treat HER2-positive breast cancer. However, its hepatotoxicity restricts its clinical efficacy. This study aims to elucidate the molecular mechanism of lapatinib's hepatotoxicity. Through in vivo models, we found that lapatinib treatment led to significant increases in serum ALT/AST levels and pathological damage to liver tissue in mice. It also induced a decrease in mitochondrial membrane potential and cell apoptosis in AML12 liver cells in vitro. Furthermore, this study revealed that lapatinib causes damage to both the mitochondria and the lysosomes. This led to lysosomal membrane permeabilization (LMP) and blocked mitochondrial autophagy, resulting in cathepsin leakage into the cytoplasm. Based on these findings, we discovered that the FDA-approved food additive tannic acid (TA) as a cathepsin inhibitor can effectively protect liver cells and alleviate liver damage in mice without affecting lapatinib's ability to kill SKBR3 breast cancer cells. This study has revealed a new mechanism of lapatinib hepatotoxicity involving the lysosome for the first time, providing a new target and an experimental basis for developing selective liver protection strategies in clinical practice.</p>","PeriodicalId":23174,"journal":{"name":"Toxicology and applied pharmacology","volume":" ","pages":"118028"},"PeriodicalIF":3.6,"publicationDate":"2026-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148881580","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}

{"title":"Loss of MEG3 promotes migration and invasion of nickel-transformed cells, partially via upregulation of RUNX2.","authors":"Bo Yan, Zhuo Zhang, Jingxia Li, Max Costa","doi":"10.1016/j.taap.2026.118026","DOIUrl":"https://doi.org/10.1016/j.taap.2026.118026","url":null,"abstract":"<p><p>Nickel is a transition metal that is widely distributed in the environment. Nickel compounds are classified as Group 1 carcinogens (human carcinogens) by the International Agency for Research on Cancer (IARC). Despite extensive studies, the molecular mechanisms underlying nickel-induced carcinogenesis remain incompletely understood. Maternally Expressed Gene 3 (MEG3) is the first long non-coding RNA (lncRNA) identified as a tumor suppressor. Previous studies have shown that downregulation of MEG3 increases HIF-1α expression in human bronchial epithelial BEAS-2B cells chronically exposed to nickel. In the present study, we observed that MEG3 expression is markedly reduced in nickel-transformed cells. Dysregulation of Runt-Related Transcription Factor 2 (RUNX2) has also been implicated in multiple cancer types. Previous studies have demonstrated that RUNX2 is upregulated in nickel-induced malignantly transformed BEAS-2B cells. Consistent with these findings, we observed that chronic exposure of BEAS-2B cells to low-dose nickel increases both RUNX2 mRNA and protein expression, accompanied by elevated expression of mesenchymal markers and enhanced migratory and invasive capacities. Overexpression of MEG3 in nickel-transformed cells reduces RUNX2 protein levels and reverses the alterations of epithelial-mesenchymal transition (EMT) markers, resulting in decreased cell migration and invasion in nickel-transformed cells. Similarly, silencing RUNX2 reverses the expression of EMT markers and suppresses the migratory and invasive capacities of nickel-transformed cells. Notably, shRNA-mediated RUNX2 knockdown increases MEG3 expression, indicating reciprocal regulation between MEG3 and RUNX2 in nickel-transformed cells. Collectively, our findings demonstrate that MEG3 and RUNX2 form a reciprocally regulated signaling axis that contributes to EMT, thereby promoting migration and invasion in nickel-transformed cells. These results identify MEG3 and RUNX2 as interconnected biomarkers and potential therapeutic targets for cancer prevention and treatment, warranting further mechanistic investigation.</p>","PeriodicalId":23174,"journal":{"name":"Toxicology and applied pharmacology","volume":" ","pages":"118026"},"PeriodicalIF":3.6,"publicationDate":"2026-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148866865","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}

{"title":"Surface modification as a strategy to mitigate TiO₂ NPs-induced neurotoxicity in rats.","authors":"Israa Elhussein, Eman I Hassanen, Khaled Y Farroh, Rehab A Azouz, Basma M Bawish, Marwa A Ibrahim, Azza Hassan","doi":"10.1016/j.taap.2026.118024","DOIUrl":"10.1016/j.taap.2026.118024","url":null,"abstract":"<p><p>Titanium dioxide nanoparticles (TiO₂ NPs) are extensively utilized in biomedical and pharmacological sectors; however, they may interact with biological systems causing various risks. Therefore, the present study assessed the role of surface modification by either chitosan (CS) or silica (Si) in mitigating TiO₂ NPs-induced neurotoxicity in rats. A total of twenty adult male rats were randomly distributed into 4 experimental groups (n = 5) as follows: control; uncoated TiO₂ NPs (100 mg/kg bwt); CS/TiO₂ NPs (100 mg/kg bwt), and Si/TiO₂ NPs (100 mg/kg bwt). All rats received daily treatments via oral gavage for a period of 2 months. The uncoated TiO₂ NPs elicited pronounced neurobehavioral disturbances, including cognitive disruption, memory impairment, and heightened anxiety, associated with increased acetylcholinesterase (AChE) activity, malondialdehyde (MDA), and nitric oxide (NO) levels, while reduced antioxidant activity. A pronounced upregulation of caspase-3 with downregulation of Nrf2 and Bdnf genes was also observed alongside strong immunoreactivity of caspase-3, iNOS, and GFAP in many brain areas, indicating neurodegenerative and inflammatory responses. In contrast, the encapsulation of TiO₂ NPs with either CS or Si significantly mitigated the biochemical, molecular, histopathological, and behavioral alterations compared to the uncoated TiO₂ NPs.</p>","PeriodicalId":23174,"journal":{"name":"Toxicology and applied pharmacology","volume":" ","pages":"118024"},"PeriodicalIF":3.6,"publicationDate":"2026-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148866870","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}

{"title":"ΔA146Ply exerts anti-triple-negative breast cancer effects by inducing ferroptosis via regulation of the CYP24A1-mediated calcitriol-vitamin D receptor pathway.","authors":"Ye Yu, Zhengkun Zhang, Dingxue Wang, Xin Bai, Dan He, Xuxu Ji, Zhaoru Yin, Keyi Xu, Ji Liu, Jiaqiong Zou","doi":"10.1016/j.taap.2026.118025","DOIUrl":"10.1016/j.taap.2026.118025","url":null,"abstract":"<p><p>Triple-negative breast cancer (TNBC) is the most aggressive breast cancer subtype, typically associated with poor clinical outcomes. Recently, ferroptosis has emerged as a promising therapeutic target for TNBC. ΔA146Ply, a novel pneumolysin variant, has demonstrated potential as an anti-tumor agent; however, its role in regulating ferroptosis remains unclear. This study investigates whether ΔA146Ply exerts anti-TNBC effects by promoting ferroptosis via the CYP24A1-mediated Calcitriol/vitamin D receptor (VDR) pathway. Our in vitro results reveal that ΔA146Ply inhibits MDA-MB-231 cells by inducing ferroptosis. Mechanistically, we demonstrate that CYP24A1 negatively regulates the Calcitriol-VDR pathway and serves as a critical mediator of ferroptosis. In vivo, ΔA146Ply suppresses TNBC tumor growth by downregulating CYP24A1 and promoting ferroptosis. In conclusion, ΔA146Ply exerts anti-TNBC effects by activating ferroptosis through the regulation of the CYP24A1-mediated Calcitriol-VDR pathway.</p>","PeriodicalId":23174,"journal":{"name":"Toxicology and applied pharmacology","volume":" ","pages":"118025"},"PeriodicalIF":3.6,"publicationDate":"2026-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148860362","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}

{"title":"Anti-colorectal cancer activity of sertraline in mice involves regulation of arachidonic acid metabolism revealed by UPLC-Q Exactive Orbitrap MS-based metabolomics.","authors":"Yihong Shen, Leping He, Chenglong Zheng, Dongmeng Liu, Zongmao He, Yuxia Zou, Guo-Sheng Wu, Chengwei He, Xiaofeng Wang, Ren-Bo Ding, Jiaolin Bao","doi":"10.1016/j.taap.2026.118021","DOIUrl":"https://doi.org/10.1016/j.taap.2026.118021","url":null,"abstract":"<p><p>Sertraline, a widely used antidepressant, has shown emerging anticancer activity, but its metabolic mechanism in colorectal cancer (CRC) remains unclear. In this study, we evaluated the in vivo antitumor effect of sertraline using a CT26 tumor-bearing BALB/c mouse model, and performed UPLC-MS-based untargeted metabolomics to characterize serum metabolic alterations. Our results found that sertraline significantly inhibited tumor growth in BALB/c mice and partially reversed tumor-associated metabolic disturbances. Notably, levels of arachidonic acid (AA), 11,12-epoxyeicosatrienoic acid (11,12-EET), and 12-KETE were markedly elevated in the tumor model group but shifted toward normal levels after sertraline treatment. Pathway analysis identified arachidonic acid metabolism as the most significantly affected pathway, and Western blot confirmed that sertraline downregulated ALOXE3 expression in both tumor tissues and CT26 cells. ROC analysis revealed that a panel of only two metabolites achieved an AUC of 0.845, demonstrating good discriminatory ability between the tumor model and sertraline-treated groups, while expanding to ten metabolites further improved the AUC to 0.975 (95% CI: 0.800-1.000). These findings suggest that sertraline exerts antitumor effects in CRC associated with metabolic remodeling of arachidonic acid metabolism and altered ALOXE3 expression, providing preclinical evidence supporting further investigation of sertraline as a potential drug-repurposing candidate for CRC.</p>","PeriodicalId":23174,"journal":{"name":"Toxicology and applied pharmacology","volume":" ","pages":"118021"},"PeriodicalIF":3.6,"publicationDate":"2026-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148857822","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}

{"title":"RAB17 downregulation elicits antitumor impacts in prostate cancer by triggering ferroptotic cell death through the regulation of TfR1-mediated iron overload.","authors":"Dongli Ruan, Wanghui Su, Yang Zhang, Xiulong Ma","doi":"10.1016/j.taap.2026.118023","DOIUrl":"10.1016/j.taap.2026.118023","url":null,"abstract":"<p><p>Increasing evidence suggests that Ras-related protein RAB17 plays a crucial role in tumor progression. Our preliminary data demonstrated that RAB17 is overexpressed in prostate cancer; however, its specific function in this malignancy is still poorly understood. This study sought to systematically clarify the functional role of RAB17 in prostate cancer, delineate its underlying molecular mechanisms, and evaluates its therapeutic potential. Analysis of clinical samples revealed that elevated RAB17 levels correlate with poorer overall survival in prostate cancer patients. Gene knockdown experiments demonstrated that silencing RAB17 exhibited notable tumor-suppressive effects in prostate cancer cells. Further investigations revealed that RAB17 knockdown increased intracellular iron concentrations and elevated lipid peroxidation levels, thereby triggering ferroptosis. Inhibiting ferroptosis significantly rescued the cancer-inhibiting impact elicited by RAB17 depletion. Notably, RAB17 was identified to interact with the iron uptake receptor transferrin receptor 1 (TfR1), promoting its degradation. Consequently, RAB17 knockdown increased TfR1 protein levels, enhancing iron influx and leading to iron overload and ferroptosis. Silencing TfR1 in RAB17 knockdown cells significantly reversed the tumor-suppressive and ferroptosis-inducing effects. In vivo experiments demonstrated that targeting RAB17 significantly delayed xenograft tumor growth associated with the induction of ferroptotic changes in tumor tissues. In conclusion, RAB17 is overexpressed in prostate cancer and exerts a tumor-promoting function. Silencing RAB17 induces ferroptosis through TfR1-mediated iron overload, thereby exerting tumor-suppressive effects. The RAB17-TfR1-ferroptosis axis may represent a pivotal modulator of prostate cancer and a promising candidate for targeted therapeutic intervention.</p>","PeriodicalId":23174,"journal":{"name":"Toxicology and applied pharmacology","volume":" ","pages":"118023"},"PeriodicalIF":3.6,"publicationDate":"2026-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148841344","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}

{"title":"Irisin restores testicular metabolic homeostasis and spermatogenesis against chronic unpredictable stress in rats: An integrated ¹H NMR metabolomics and molecular study.","authors":"Itishree Dubey, Gurvinder Singh, Dinesh Kumar, Sapana Kushwaha","doi":"10.1016/j.taap.2026.118019","DOIUrl":"10.1016/j.taap.2026.118019","url":null,"abstract":"<p><p>Chronic unpredictable stress (CUS) is a significant contributor to male reproductive dysfunction; however, no effective clinical therapies are available, highlighting the need to explore novel preclinical interventions with translational potential. CUS disrupts testicular metabolic homeostasis, however the metabolic mechanisms underlying spermatogenic dysfunction remain poorly understood. Irisin is an exerkine with recognized metabolic functions and may counteract stress-induced testicular injury. In the present study, we investigated whether Irisin restores stress-induced metabolic remodeling in the testis using ¹H NMR-based metabolomics together with molecular and histological analyses. The study demonstrated for the first time that Irisin (100 ng/kg/day, s.c., for 4 weeks) exerts protective effects in a CUS-induced adult male rat model. CUS elevated corticosterone, anxiety-like behaviour, decreased sperm count, viability, chromatin integrity, and circulating Irisin, luteinizing hormone, testosterone, and follicle-stimulating hormone, which were restored by Irisin. Irisin also restored testicular histoarchitecture, increased the Johnsen score and seminiferous tubule diameter, thereby improving spermatogenesis impaired by CUS. At the molecular level, Irisin suppressed NF-κB signaling, enhanced Nrf2/HO-1 antioxidant defense, and restored blood-testis barrier (BTB) integrity and ectoplasmic specialization (ES) proteins disrupted by CUS. Further, metabolomic profiling identified significant alterations in lactate, pyruvate, citrate, succinate, glutamate, betaine, glycerol, and choline, reflecting impaired glycolysis, tricarboxylic acid cycle activity, antioxidant metabolism, and membrane homeostasis in the testis. Pathway analysis further identified disruptions in alanine, aspartate, and glutamate; glycine, serine, and threonine; phenylalanine; and taurine and hypotaurine metabolism. Collectively, Irisin preserved testicular function by restoring metabolic homeostasis, redox balance, and BTB integrity under chronic stress.</p>","PeriodicalId":23174,"journal":{"name":"Toxicology and applied pharmacology","volume":" ","pages":"118019"},"PeriodicalIF":3.6,"publicationDate":"2026-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148832445","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}

{"title":"Erratum to \"Untargeted serum lipidomics reveals lipid metabolic disturbances and identifies candidate lipid biomarkers in acute diquat poisoning\" [Toxicology and Applied Pharmacology 516 (2026) 117995].","authors":"Xinxin Huang, Xunan Kan, Lei Xiao, Chuanguang Han, Ge Li, Quan Xia, Qianli Zou, Qinhai Ma, Shuai Song","doi":"10.1016/j.taap.2026.118020","DOIUrl":"10.1016/j.taap.2026.118020","url":null,"abstract":"","PeriodicalId":23174,"journal":{"name":"Toxicology and applied pharmacology","volume":" ","pages":"118020"},"PeriodicalIF":3.6,"publicationDate":"2026-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148832438","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}