Human & Experimental Toxicology最新文献

{"title":"Hepatoprotective potential of diosmin against hepatotoxic effect of isoniazid and rifampin in wistar rats.","authors":"Tarique Anwer,&nbsp;Mohammed N Alruwaili,&nbsp;Saeed Alshahrani,&nbsp;Saad S Alqahtani,&nbsp;Abdulmajeed Jali,&nbsp;Rayan A Ahmed,&nbsp;Mohammad Firoz Alam,&nbsp;Sivakumar S Moni","doi":"10.1177/09603271221149199","DOIUrl":"https://doi.org/10.1177/09603271221149199","url":null,"abstract":"<p><strong>Objective: </strong>The treatment of tuberculosis with isoniazid and rifampin is associated with hepatocellular damage. Therefore, the study was designed to evaluate the hepatoprotective potential of diosmin against hepatotoxic effect of isoniazid and rifampin in Wistar rats.</p><p><strong>Methods: </strong>Hepatotoxicity was induced by administering isoniazid and rifampin (100 mg/kg), whereas diosmin was given as treatment control. Markers of liver function (ALT, AST, ALP and bilirubin), inflammatory cytokines (TNFα, IL-6 and IL-1β), apoptosis (caspase-3), oxidative stress parameters (LPO, GSH, CAT and SOD) and histological changes in liver were assessed in normal, hepatotoxic control and treatment groups.</p><p><strong>Results: </strong>The administration of isoniazid and rifampin significantly increased markers of liver dysfunction (ALT, AST, ALP and bilirubin), cytokines (TNFα, IL-6 and IL-1β) and apoptosis (caspase-3). However, daily dosing of diosmin significantly reduced these markers of liver dysfunction, inflammatory cytokines and apoptosis to near normal levels. Additionally, markers of hepatocellular oxidative stress parameters were significantly altered as evident from increased LPO level and decreased endogenous antioxidants such as GSH, SOD and CAT in isoniazid-and rifampin-treated hepatotoxic group. It was observed that diosmin treatment reduced high levels of LPO and demonstrated significant improvement in antioxidant levels. Histological studies of liver also supported our biochemical findings, which are also manifested as diosmin treatment exhibited protection against hepatocellular degeneration and inflammation.</p><p><strong>Conclusion: </strong>Results of the present study demonstrate hepatoprotective potential of diosmin against isoniazid-and rifampin-treated hepatotoxicity. Thus, we conclude that diosmin may be used along with anti-tubercular drugs (isoniazid and rifampin) in tuberculosis patients to overcome their hepatotoxic adverse effect.</p>","PeriodicalId":13181,"journal":{"name":"Human & Experimental Toxicology","volume":"42 ","pages":"9603271221149199"},"PeriodicalIF":2.8,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10480585","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":"MiR-3612 targeting THBS1 suppresses nasopharyngeal carcinoma progression by PI3K/AKT signaling pathway.","authors":"Wei Zhang,&nbsp;Qiu Zhang,&nbsp;Qianbo Cui,&nbsp;Yu Xu","doi":"10.1177/09603271221150248","DOIUrl":"https://doi.org/10.1177/09603271221150248","url":null,"abstract":"<p><strong>Background: </strong>MicroRNA-3612 (miR-3612) is considered a tumor suppressor in different cancers. Nonetheless, its function in nasopharyngeal carcinoma (NPC) has yet to be uncovered.</p><p><strong>Methods: </strong>NPC cells and tissues were tested by means of reverse transcription quantitative polymerase chain reaction (RT-qPCR) analysis and western blotting to quantify the expressions of miR-3612 and Thrombospondin 1 (THBS1). Cell Counting Kit-8 (CCK-8) and scratch experiments were carried out to evaluate the migration and proliferation of NPC cells. NPC cell adhesion was also assessed. The predicted interaction of miR-3612 with THBS1 was verified by means of a luciferase reporter assay. <i>In vivo</i> experiments were also conducted to examine how miR-3612 overexpression affects <i>in vivo</i> tumorigenicity. Lastly, phosphatidylinositol 3-kinase (PI3K)/AKT signaling pathway status was assessed via western blotting.</p><p><strong>Results: </strong>MiR-3612 was downregulated in NPC cells and tissues, whereas THBS1 expression showed an opposite trend. The MiR-3612 mimic inhibited the NPC cell proliferation, adhesion, and migration and also inactivated the PI3K/AKT signaling pathway. Furthermore, miR-3612 mimic also hampered NPC tumorigenesis <i>in vivo</i>. MiR-3612 targeted THBS1 and downregulated THBS1 expression. THBS1 offset the miR-3612-overexpression-induced repression of the migration, adhesion, and proliferation of NPC cells via the activation of the PI3K/AKT pathway.</p><p><strong>Conclusion: </strong>MiR-3612 retarded NPC cell migration, adhesion, and proliferation by targeting THBS1 and inactivating the PI3K/AKT signaling pathway. This provides a novel therapeutic approach for NPC intervention.</p>","PeriodicalId":13181,"journal":{"name":"Human & Experimental Toxicology","volume":"42 ","pages":"9603271221150248"},"PeriodicalIF":2.8,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9124978","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":"Hyperoside exerts protective effects against anticardiolipin antibody-induced recurrent pregnancy loss <i>in vivo</i> and <i>in vitro</i>.","authors":"Yanli Song,&nbsp;Dongjie He,&nbsp;Shaoqi Shi,&nbsp;Tianwei Cui,&nbsp;Hui Zhang,&nbsp;Xianmin Zhao,&nbsp;Tingting Ni,&nbsp;Huidongzi Xiao,&nbsp;Aiwu Wei","doi":"10.1177/09603271231163476","DOIUrl":"https://doi.org/10.1177/09603271231163476","url":null,"abstract":"<p><strong>Background: </strong>Women with antiphospholipid syndrome (APS) or antiphospholipid antibodies (aPLs) are at high risk for obstetric complications, including recurrent pregnancy loss (RPL). However, effective treatments for RPL are lacking.</p><p><strong>Objective: </strong>This study aimed to reveal the function and underlying mechanism of hyperoside (Hyp) in RPL associated with antiphospholipid antibodies (aCLs).</p><p><strong>Methods: </strong>The pregnant rats (<i>N</i> = 24) were divided randomly into four groups: normal human-IgG (NH-IgG); aCL-pregnancy loss (aCL-PL); aCL-PL + Hyp (40 mg/kg/day); aCL-PL + low molecular weight heparin (LMWH, 525 μg/kg/day). HTR-8 cells were treated with 80 μg/mL aCL to establish the cell models of miscarriage.</p><p><strong>Results: </strong>In pregnant rats, aCL-IgG injection raised the abortion rate of embryos, while Hyp treatment inhibited the effects. Additionally, Hyp inhibited the platelet activation and uteroplacental insufficiency caused by aCL. <i>In vivo</i> and <i>in vitro</i> experiments further suggested that Hyp suppressed aCL-induced inflammation and apoptosis by downregulating NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome-related factors and decreasing apoptotic rates. After aCL administration, Hyp therapy downregulated the expression of purinergic ligand-gated ion channel 7 (P2X7), which is reported to induce cytokine release and apoptosis. Furthermore, we found that the treatment of 3'-O-(4-Benzoyl) benzoyl-ATP (BzATP, an agonist of the P2X7 receptor) reversed the inhibitory effects of Hyp on cell function.</p><p><strong>Conclusions: </strong>Hyp exerts protective effects on aCL-induced pregnancy loss by preventing platelet activation-mediated P2X7/NLRP3 pathway. Therefore, Hyp may provide a feasible pharmaceutical strategy for the treatment of RPL.</p>","PeriodicalId":13181,"journal":{"name":"Human & Experimental Toxicology","volume":"42 ","pages":"9603271231163476"},"PeriodicalIF":2.8,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9644157","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":"Establishment of an animal model of sciatic nerve injury induced by local anesthetics.","authors":"Qi E,&nbsp;Yunlin Wu,&nbsp;Xiaoxia Liang,&nbsp;Meixin Chen,&nbsp;Jiayi Peng,&nbsp;Ziyin Zhou,&nbsp;Xianjie Wen","doi":"10.1177/09603271231173382","DOIUrl":"10.1177/09603271231173382","url":null,"abstract":"<p><p>Peripheral neurotoxicity injury caused by local anesthetics is a common complication of clinical anesthesia. The study of its mechanism is helpful to prevent and treat the neurotoxic injury of local anesthetics. Previous studies on peripheral neurotoxicity injury caused by local anesthetics have mainly focused on in vitro cell experiments. Due to the lack of an animal model of peripheral neurotoxicity damage caused by local anesthetics, there are few in vivo experimental studies regarding this topic. Herein, 1% ropivacaine hydrochloride was injected into the sciatic nerve by direct incision and exposure of the sciatic nerve to create a local anesthetic neurotoxic injury model. The results showed that 1% ropivacaine hydrochloride could reduce the lower limb motor score and mechanical paw withdrawal threshold in mice 48 hours after injection. Pathological sections showed that 48 hours after treatment with 1% ropivacaine hydrochloride, the sciatic nerve showed increased axonal edema and degeneration, edema between nerve fiber bundles, increased degeneration of axon and myelin sheath vacuoles, edema of nerve bundle membrane and local degeneration and necrosis, and a large number of inflammatory cells around the nerve adventitia were soaked. The above results show that under open vision, 1% ropivacaine hydrochloride can cause injury to the sciatic nerve after 48 h of treatment, which can simulate the neurotoxic damage of local anesthetics. This animal model provides a research tool for studying the mechanism of neurotoxic injury caused by local anesthetics.</p>","PeriodicalId":13181,"journal":{"name":"Human & Experimental Toxicology","volume":"42 ","pages":"9603271231173382"},"PeriodicalIF":2.8,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9747204","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":"Role of hypoxia inducible factor/vascular endothelial growth factor/endothelial nitric oxide synthase signaling pathway in mediating the cardioprotective effect of dapagliflozin in cyclophosphamide-induced cardiotoxicity.","authors":"Marwa Monier Mahmoud Refaie,&nbsp;Asmaa Ma Bayoumi,&nbsp;Sahar Ahmed Mokhemer,&nbsp;Sayed Shehata,&nbsp;Nahla Mohammed Abd El-Hameed","doi":"10.1177/09603271231193392","DOIUrl":"10.1177/09603271231193392","url":null,"abstract":"<p><strong>Background: </strong>Cyclophosphamide (CP) is a commonly used chemotherapeutic and immunosuppressive alkylating agent. However, cardiac adverse effects of CP interfere with its clinical benefit. Cardio-oncology research is currently an important issue and finding effective cardiopreserving agents is a critical need. For the first time, we aimed to detect if dapagliflozin (DAP) could ameliorate CP-induced cardiac injury and investigated the role of hypoxia inducible factor α (HIF1α)/vascular endothelial growth factor (VEGF)/endothelial nitric oxide synthase (eNOS) pathway.</p><p><strong>Methods: </strong>Forty male Wistar albino rats were included in the current model. Studied groups are: control group; CP-induced cardiotoxicity group; CP group treated with DAP; CP group treated with DAP and administered a nitric oxide synthase inhibitor; nitro-ω-L-arginine (L-NNA) before DAP to explore the role of eNOS.</p><p><strong>Results: </strong>Our data revealed that CP could induce cardiac damage as manifested by significant increases in cardiac enzymes, blood pressure, malondialdehyde (MDA), tumor necrosis factor alpha (TNFα), HIF1α, sodium glucose co-transporter 2 (SGLT2) and cleaved caspase-3 levels with toxic histopathological changes. However, there are significant decreases in reduced glutathione (GSH), total antioxidant capacity (TAC), VEGF, and eNOS. On the opposite side, co-administration of DAP showed marked improvement of CP-induced cardiac damage that may be due to its ability to inhibit SGLT2, antioxidant, anti-inflammatory and anti-apoptotic properties. Results showed decreasing the cardioprotective effect of DAP on administration of L-NNA, reflecting the critical effect of eNOS in mediating such protection.</p><p><strong>Conclusion: </strong>DAP could reduce CP cardiotoxicity based upon its ability to modulate SGLT2 and HIF1α/VEGF/eNOS signaling pathway.</p>","PeriodicalId":13181,"journal":{"name":"Human & Experimental Toxicology","volume":"42 ","pages":"9603271231193392"},"PeriodicalIF":2.8,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9920243","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":"Hydroxychloroquine ameliorates dasatinib-induced liver injury via decrease in hepatic lymphocytes infiltration.","authors":"Khalid Alhazzani,&nbsp;Salah Q Alrewily,&nbsp;Khaldoon Aljerian,&nbsp;Khaled Alhosaini,&nbsp;Mohammad M Algahtani,&nbsp;Mohammed Fhad Almutery,&nbsp;Abdullah S Alhamed,&nbsp;Ahmed Nadeem,&nbsp;Moureq R Alotaibi,&nbsp;Ahmed Z Alanazi","doi":"10.1177/09603271231188492","DOIUrl":"https://doi.org/10.1177/09603271231188492","url":null,"abstract":"<p><p>Dasatinib is an effective treatment for chronic myeloid leukemia. However, cases of idiosyncratic hepatotoxicity were reported. This study was conducted to investigate the chemopreventive effects of hydroxychloroquine against dasatinib-induced hepatotoxicity. Balb/c mice were randomly assigned into four groups; vehicle control (5% DMSO, i.p., <i>n</i> = 6), dasatinib (50 mg/kg; i.p., <i>n</i> = 6), hydroxychloroquine (10 mg/kg, i.p., <i>n</i> = 6), and hydroxychloroquine + dasatinib (10 mg/kg + 50 mg/kg; i.p., <i>n</i> = 6). Treatments were given once every 2 days for 14 days. Serum and histopathological assessments of liver architecture and fibrosis were performed using H&E, Masson's trichrome, and reticulin staining. The infiltration of lymphocytes was assessed using immunohistochemistry. The gene expression of antioxidant enzymes (CAT, SOD-2, GPX-1) was assessed using real-time quantitative PCR. Dasatinib showed a significant increase in liver injury biomarkers (AST and ALT) with higher lymphocytes infiltration (as indicated by CD3⁺, CD4⁺, CD8⁺, and CD20⁺ immunohistochemistry). Hepatic tissue of Dasatinib group exhibited significant downregulation in the gene expression of antioxidant enzymes (CAT, SOD-2, and GPX-1) compared to the control group. However, the combination of hydroxychloroquine with dasatinib showed a slight increase in AST and ALT. Also, hydroxychloroquine + dasatinib treated mice showed a significant reduction in lymphocytes infiltration as compared to dasatinib. The results showed that dasatinib induces an immune response leading to an increase in lymphocytes infiltration which promotes hepatocyte destruction and persistent liver injury. The results also suggest that hydroxychloroquine ameliorates dasatinib-induced hepatotoxicity via reduction in hepatic infiltration of T and B immune cells.</p>","PeriodicalId":13181,"journal":{"name":"Human & Experimental Toxicology","volume":"42 ","pages":"9603271231188492"},"PeriodicalIF":2.8,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9803481","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":"Circular RNA 0000157 depletion protects human bronchial epithelioid cells from cigarette smoke extract-induced human bronchial epithelioid cell injury through the microRNA-149-5p/bromodomain containing 4 pathway.","authors":"B Song,&nbsp;S Wu,&nbsp;L Ye,&nbsp;Z Jing,&nbsp;J Cao","doi":"10.1177/09603271231167581","DOIUrl":"10.1177/09603271231167581","url":null,"abstract":"<p><strong>Background: </strong>Circular RNA (circRNA) has been reported to regulate respiratory diseases. In the study, we aimed to elucidate the role of circ_0000157 in smoke-related chronic obstructive pulmonary disease (COPD) and the inner mechanism.</p><p><strong>Methods: </strong>COPD-like cell injury was induced by treating human bronchial epithelioid cells (16HBE) with cigarette smoke extract (CSE). The expression of circ_0000157, miR-149-5p, bromodomain containing 4 (BRD4), BCL2-associated x protein (Bax) and B-cell lymphoma-2 (Bcl-2) was analyzed by quantitative real-time polymerase chain reaction (qRT-PCR) or Western blotting. Enzyme-linked immunosorbent assay was performed to detect interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) levels. Malondialdehyde (MDA) production was detected by a lipid peroxidation MDA assay kit. Superoxide dismutase (SOD) activity was analyzed by a SOD activity assay kit.</p><p><strong>Results: </strong>Circ_0000157 and BRD4 expression were upregulated, while miR-149-5p expression was downregulated in the blood of smokers with COPD and CSE-induced 16HBE cells compared with control groups. CSE treatment inhibited 16HBE cell proliferation and induced cell apoptosis, inflammation, and oxidative stress; however, these effects were remitted when circ_0000157 expression was decreased. In addition, circ_0000157 acted as a miR-149-5p sponge and regulated CSE-caused 16HBE cell damage by targeting miR-149-5p. The overexpression of BRD4, a target gene of miR-149-5p, attenuated the inhibitory effects of miR-149-5p introduction on CSE-induced cell damage. Further, circ_0000157 modulated BRD4 expression by associating with miR-149-5p in CSE-treated 16HBE cells.</p><p><strong>Conclusion: </strong>Circ_0000157 knockdown ameliorated CSE-caused 16HBE cell damage by targeting the miR-149-5p/BRD4 pathway, providing a potential therapeutic strategy for clinic intervention in COPD.</p>","PeriodicalId":13181,"journal":{"name":"Human & Experimental Toxicology","volume":"42 ","pages":"9603271231167581"},"PeriodicalIF":2.8,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9981269","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":"Genistein attenuates renal ischemia-reperfusion injury via ADORA2A pathway.","authors":"H Y He,&nbsp;H Z Shan,&nbsp;S Q Li,&nbsp;R G Diao","doi":"10.1177/09603271231164913","DOIUrl":"https://doi.org/10.1177/09603271231164913","url":null,"abstract":"<p><strong>Background: </strong>Studies have shown oxidative stress and apoptosis are the main pathogenic mechanisms of renal ischemia/reperfusion (IR) injury (IRI). Genistein, a polyphenolic non-steroidal compound, has been extensively explored in oxidative stress, inflammation and apoptosis. Our research aims to reveal the potential role of genistein on renal IRI and its potential molecular mechanism both in vivo and in vitro.</p><p><strong>Methods: </strong>In vivo experiments, mice were pretreated with or without genistein. Renal pathological changes and function, cell proliferation, oxidative stress and apoptosis were measured. In vitro experiments, overexpression of ADORA2A and knockout of ADORA2A cells were constructed. Cells proliferation, oxidative stress and apoptosis were analyzed.</p><p><strong>Results: </strong>Our results in vivo showed that the renal damage induced by IR was ameliorated by genistein pretreatment. Moreover, ADORA2A was activated by genistein, along with inhibition of oxidative stress and apoptosis. The results in vitro showed that genistein pretreatment and ADORA2A overexpression reversed the increase of apoptosis and oxidative stress in NRK-52E cells induced by H/R, while the knockdown of ADORA2A partially weakened this reversal from genistein treatment.</p><p><strong>Conclusions: </strong>Our results demonstrated that genistein have a protective effect against renal IRI by inhibiting oxidative stress and apoptosis via activating ADORA2A, presenting its potential use for the treatment of renal IRI.</p>","PeriodicalId":13181,"journal":{"name":"Human & Experimental Toxicology","volume":"42 ","pages":"9603271231164913"},"PeriodicalIF":2.8,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9143034","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":"Retraction Notice.","authors":"","doi":"10.1177/09603271231192798","DOIUrl":"10.1177/09603271231192798","url":null,"abstract":"","PeriodicalId":13181,"journal":{"name":"Human & Experimental Toxicology","volume":"42 ","pages":"9603271231192798"},"PeriodicalIF":2.8,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10129962","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":"Retraction Notice.","authors":"","doi":"10.1177/09603271231192802","DOIUrl":"10.1177/09603271231192802","url":null,"abstract":"","PeriodicalId":13181,"journal":{"name":"Human & Experimental Toxicology","volume":"42 ","pages":"9603271231192802"},"PeriodicalIF":2.8,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10139168","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}