Toxicology Research最新文献

{"title":"Clinical observation of liposomal doxorubicin on liver and renal function in patients with breast cancer.","authors":"Mingliang Li, Ling Wang, Jie Du","doi":"10.1093/toxres/tfad072","DOIUrl":"10.1093/toxres/tfad072","url":null,"abstract":"<p><strong>Background: </strong>Doxorubicin has become the first-line antitumor drug clinically, but severely limited by multiple side effects, especially cardiotoxicity. Liposomal doxorubicin therefore replaced traditional doxorubicin for low toxicity and high efficiency. Previous studies have suggested liver and kidney may be the main organs affected by liposomal doxorubicin. Due to insufficient clinical evidence, we set out to analyze the effect of liposomal doxorubicin on liver and renal function in breast cancer patients.</p><p><strong>Materials and methods: </strong>Our retrospective analysis included breast cancer patients aged 30-70 years old who were assigned to two groups based on liposomal doxorubicin intake. We evaluated changes in liver and renal function. Multivariate logistic regression model was used to assess the risk factors of liver function damage.</p><p><strong>Results: </strong>Ultimately, 631 patients for liver function analysis cohort and 611 cases for renal function analysis cohort. Patients receiving liposomal doxorubicin had significantly higher liver function damage rate compared to control group (52.20% vs 9.82%, <i>p</i> < 0.001), but there was no difference in the incidence of renal damage events between the two groups. Multivariate analysis shows total doses divided by body surface area is a significant, independent risk factor for liver function damage (odds ratio 1.005 [1.002-1.018], <i>p</i> < 0.001).</p><p><strong>Conclusion: </strong>Liposomal doxorubicin treatment is associated with higher liver function damage in breast cancer patients, but has no effect on renal function. Together with risk factor analysis, our study underlines the importance to pay attention for patient's age before taking liposomal doxorubicin, alongside liver function after the first and long-term treatments.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"12 5","pages":"807-813"},"PeriodicalIF":2.2,"publicationDate":"2023-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10615824/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71418743","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mitigative potential of rhoifolin against cisplatin prompted testicular toxicity: biochemical, spermatogenic and histological based analysis.","authors":"Faria Saher, Muhammad Umar Ijaz, Ali Hamza, Qurat Ul Ain, Muhammad Faisal Hayat, Tayyaba Afsar, Ali Almajwal, Huma Shafique, Suhail Razak","doi":"10.1093/toxres/tfad073","DOIUrl":"10.1093/toxres/tfad073","url":null,"abstract":"<p><p>Rhoifolin (ROF) is a naturally occurring flavonoid compound with diverse pharmacological and therapeutic benefits. The current investigation was designed to evaluate the curative potential of Rhoifolin (ROF) against Cisplatin (CP) induced testicular damage. Mature male albino rats (n = 48) were randomly distributed into 4 equal groups: control, CP (10 mg/kg), CP + ROF (10 mg/kg + 20 mg/kg) and ROF (20 mg/kg) supplemented group. Following 56 days of the trial, biochemical, inflammatory markers, spermatogenic, steroidogenic, hormonal, apoptotic, anti-apoptotic, and histopathological parameters were evaluated. The exposure to CP markedly (p < 0.05) lowered the activities of anti-oxidant enzymes, glutathione reductase (GSR), catalase (CAT), and glutathione peroxidase (GPx) as well as superoxide dismutase (SOD) in testicular tissues of male albino rats. Besides the levels of reactive oxygen species (ROS) and thiobarbituric acid reactive substances (TBARS) were considerably augmented in CP exposed rats. The administration of CP also increased the level of inflammatory cytokines i.e. IL-6, TNF-α, 1L-1β and NF-κβ as well as COX-2 activity. Additionally, a notable (p < 0.05) upsurge was observed in dead sperms count, abnormality in the tail, midpiece as well as head of sperms along with a notable decline in sperm motility in CP treated rats. Moreover, the expressions of steroidogenic enzymes were also lowered in CP administered group. The levels of follicle stimulating hormone (FSH) and plasma testosterone as well as luteinizing hormone (LH) were decreased in CP treated group. Moreover, the expression of Bax as well as Caspase-3 (apoptotic markers) were increased. On the other hand, Bcl-2 expression (anti-apoptotic marker) was reduced. Furthermore, the histopathological analysis showed that CP considerably (p < 0.05) damaged the testicular tissues. However, the administration of ROF significantly reduced the damaging effects of CP in testicular tissues. The results of our study suggested that ROF can potentially alleviate CP-induced testicular damages due to its androgenic, anti-oxidant and anti-inflammatory as well as anti-apoptotic nature.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"12 5","pages":"814-823"},"PeriodicalIF":2.2,"publicationDate":"2023-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10615821/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71418657","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"2-Chloro-3,7,8-tribromodibenzofuran as a new environmental pollutant inducing atypical ultrasonic vocalization in infant mice.","authors":"Eiki Kimura,&nbsp;Go Suzuki,&nbsp;Naoto Uramaru,&nbsp;Masaki Kakeyama,&nbsp;Fumihiko Maekawa","doi":"10.1093/toxres/tfad069","DOIUrl":"https://doi.org/10.1093/toxres/tfad069","url":null,"abstract":"<p><p>Epidemiological and experimental studies indicate that maternal exposure to environmental pollutants impairs the cognitive and motor functions of offspring in humans and laboratory animals. Infant ultrasonic vocalizations (USVs), the communicative behavior of pups toward caregivers, are impaired in rodent models of neurodevelopmental disorders, suggesting a useful method to evaluate the developmental neurotoxicity of environmental pollutants. Therefore, we investigated USVs emitted by mouse pups of dams exposed to 2-chloro-3,7,8-tribromodibenzofuran (TeXDF) and 1,2,3,7,8-pentabromodibenzofuran (PeBDF), which are detected in the actual environment. The USV duration and number in the pups born to dams administered with TeXDF 40 μg/kg body weight (b.w.), but not 8 μg/kg b.w., on gestational day (GD) 12.5, were significantly lower than those in the corresponding pups on postnatal days 3-9. Conversely, there was no statistical change in the USVs emitted by the pups of dams administered with PeBDF 35 or 175 μg/kg b.w. on GD 12.5. To examine whether maternal exposure leads to behavioral impairments in adulthood, we analyzed exploratory behaviors in a novel environment using IntelliCage, a fully automated testing apparatus for group-housed mice. Neither TeXDF nor PeBDF exposure induced significant differences in offspring exploration. Considered together, our findings revealed that TeXDF induces atypical USV emission in infant mice, suggesting the importance of further studies on the risk assessment of mixed brominated/chlorinated dibenzo-<i>p</i>-dioxins and dibenzofurans.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"12 5","pages":"999-1004"},"PeriodicalIF":2.1,"publicationDate":"2023-08-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10615804/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71418739","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The synthetic cannabinoid 5F-MDMB-PICA enhances the metabolic activity and angiogenesis in human brain microvascular endothelial cells by upregulation of VEGF, ANG-1, and ANG-2.","authors":"Laith Naser Al-Eitan, Saif Zuhair Alahmad, Mohd Fahmi Munib ElMotasem, Mansour Abdullah Alghamdi","doi":"10.1093/toxres/tfad068","DOIUrl":"10.1093/toxres/tfad068","url":null,"abstract":"<p><p>Brain angiogenesis, the formation of new blood vessels from existing brain vasculature, has been previously associated with neural plasticity and addictive behaviors related to substances. Synthetic cannabinoids (SCs) have become increasingly popular due to their ability to mimic the effects of cannabis, offering high potency and easy accessibility. In the current study, we reveal that the SC 5F-MDMB-PICA, the most common SC in the United States in 2019, increases cell metabolic activity and promotes angiogenesis in human brain microvascular endothelial cells (HBMECs). First, we performed an MTT assay to evaluate the effects of 5F-MDMB-PICA treatment at various concentrations (0.0001 μM, 0.001 μM, 0.01 μM, 0.1 μM, and 1 μM) on HBMECs metabolic activity. The results demonstrated higher concentrations of the SC improved cell metabolic activity. Furthermore, 5F-MDMB-PICA treatment enhanced tube formation and migration of HBMECs in a dosage-dependent manner. Additionally, the mRNA, secreted protein, and intracellular protein levels of vascular endothelial growth factor, angiopoietin-1, and angiopoietin-2, which are involved in the regulation of angiogenesis, as well as the protein levels of cannabinoid receptor type-1, were all increased following treatment with 5F-MDMB-PICA. Notably, the phosphorylation levels at Serine 9 residue of glycogen synthase kinase-3β were also increased in the 5F-MDMB-PICA treated HBMECs. Collectively, our findings demonstrate that 5F-MDMB-PICA can enhance angiogenesis in HBMECs, suggesting the significant role of angiogenesis in the response to SCs. Manipulating this interaction may pave the way for innovative treatments targeting SC addiction and angiogenesis-related conditions.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"12 5","pages":"796-806"},"PeriodicalIF":2.2,"publicationDate":"2023-08-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10615825/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71418679","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hexaconazole exposure disrupt acetylcholinesterase, leading to mental illness.","authors":"Abuzer Ali, Sayed Aliul Hasan Abdi, Amena Ali, Wasim Ahmad","doi":"10.1093/toxres/tfad067","DOIUrl":"10.1093/toxres/tfad067","url":null,"abstract":"<p><p>Hexaconazole is widely used in agricultural work, and it has been observed that it has potential to disrupt endocrine function and it has also capacity of bioaccumulation. In this study, we examined how the hexaconazole disrupts the usual balance of acetylcholinesterase. It has been already reported that heavy pesticide exposures may be a reason for several mental illnesses because these pesticides may disrupt normal balance of acetylcholinesterase. In this paper, we have done a complete molecular and dynamics analysis to understand the behavior of hexaconazole with acetylcholinesterase so that its toxicological aspect may be explored. Our findings revealed that hexaconazole has potency to interact with acetylcholinesterase in a stable manner. The binding energy of hexaconazole was found to be -7.95 kcal/mol. However, chlorpyrifos, known inhibitors of acetylcholinesterase, has binding energy of -7.17 kcal/mol. With respect to stability analysis, hexaconazole has similar stability like chlorpyrifos. Root-mean-square deviation, root-mean-square fluctuation, radius of gyration, hydrogen bonding, and solvent accessible surface area were similar to chlorpyrifos. In addition, density functional theory computations analysis reveals that hexaconazole is energetically stable like chlorpyrifos, which is necessary for establishing a stable ligand-protein complex. The result of this complete molecular analysis reveals that hexaconazole may disrupt the acetylcholinesterase balance, which leads to mental illness.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"12 5","pages":"775-782"},"PeriodicalIF":2.2,"publicationDate":"2023-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10615806/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71418753","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Anti-inflammatory and antioxidative effects of elderberry diet in the rat model of seizure: a behavioral and histological investigation on the hippocampus.","authors":"Amir-Hossein Bayat, Neda Eskandari, Mojtaba Sani, Farid Fotouhi, Zahra Shenasandeh, Sara Saeidikhoo, Razieh Rohani, Mohammadamin Sabbagh Alvani, Mohammadreza Mafi Balani, Mahdi Eskandarian Boroujeni, Mohammad-Amin Abdollahifar, Faezeh Tajari, Abbas Aliaghaei, Meysam Hassani Moghaddam","doi":"10.1093/toxres/tfad070","DOIUrl":"10.1093/toxres/tfad070","url":null,"abstract":"<p><p>The present study was designed to evaluate whether elderberry (EB) effectively reduces inflammation and oxidative stress in hippocampal cells to modify seizure damage. Seizure was induced in rats by the injection of pentylenetetrazol (PTZ). In the Seizure + EB group, EB powder was added to the rats' routine diet for eight consecutive weeks. The study included several behavioral tests, immunohistopathology, Voronoi tessellation (to estimate the spatial distribution of cells in the hippocampus), and Sholl analysis. The results in the Seizure + EB group showed an improvement in the behavioral aspects of the study, a reduction in astrogliosis, astrocyte process length, number of branches, and intersections distal to the soma in the hippocampus of rats compared to controls. Further analysis showed that EB diet increased nuclear factor-like 2 expression and decreased caspase-3 expression in the hippocampus in the Seizure + EB group. In addition, EB protected hippocampal pyramidal neurons from PTZ toxicity and improved the spatial distribution of hippocampal neurons in the pyramidal layer and dentate gyrus. The results of the present study suggest that EB can be considered a potent modifier of astrocyte reactivation and inflammatory responses.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"12 5","pages":"783-795"},"PeriodicalIF":2.2,"publicationDate":"2023-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10615822/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71418741","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of mitochondrial disruption and oxidative stress in plasticizer phthalate-induced cytotoxicity to human bone osteoblasts.","authors":"Ekramy Mahmoud Elmorsy, Ayat Al-Ghafari, Huda Al Doghaither","doi":"10.1093/toxres/tfad065","DOIUrl":"10.1093/toxres/tfad065","url":null,"abstract":"<p><p>Phthalates are frequently utilized in a wide range of products such as plasticizers with reported negative effects on bones. The current study evaluated the effect of butyl cyclohexyl phthalate on the human osteoblasts via different assays. MTT and lactate dehydrogenase assays were used to examine the in-vitro cytotoxic effect of butyl cyclohexyl phthalate on human bone osteoblasts <i>in</i> concentrations 0.1, 1, 10, and 100 μM for 12 to 72 h postexposures. Incubation of osteoblasts with butyl cyclohexyl phthalate significantly reduced cell viability based on its concentrations and durations of exposure. In parallel, osteoblast secretion of procollagen type 1, osteocalcin, as well as alkaline phosphatase was significantly decreased by butyl cyclohexyl phthalate in concentrations (1 or 2 μM). Butyl cyclohexyl phthalate decreased ATP synthesis and mitochondrial complexes I and III activities, with increased lactate production, all of which were detrimental to cellular bioenergetics. The cellular redox defense systems were significantly depleted by increased lipid peroxidation, elevated reactive oxygen species, decreased catalase and superoxide dismutase enzymes activities, and decreased intracellular reduced glutathione (GSH). Redox stress was also induced. Interestingly, preincubating osteoblasts with reduced GSH before exposing them to butyl cyclohexyl phthalate significantly lowered the cytotoxicity of the butyl cyclohexyl phthalate, suggesting that antioxidants may play a helpful protective effect.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"12 5","pages":"765-774"},"PeriodicalIF":2.2,"publicationDate":"2023-08-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10615828/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71418661","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Scorpion venom heat-resistant peptide alleviates mitochondrial dynamics imbalance induced by PM_2.5 exposure by downregulating the PGC-1α/SIRT3 signaling pathway.","authors":"Lanyi Huang, Jingbin Xu, Kaiqian Duan, Tuya Bao, Yu Cheng, Haimin Zhang, Yong Zhang, Yingwei Lin, Fasheng Li","doi":"10.1093/toxres/tfad064","DOIUrl":"10.1093/toxres/tfad064","url":null,"abstract":"<p><strong>Background: </strong>Epidemiological inquiry reveals that neuroinflammation and mitochondrial dysfunction caused by PM_2.5 exposure are associated with Alzheimer's disease. Nevertheless, the molecular mechanisms of mitochondrial dynamics and neuroinflammation induced by PM_2.5 exposure remain elusive. In this study, our objective was to explore the impact of PM_2.5 on mitochondrial dynamics and neuroinflammation, while also examining the reparative potential of scorpion venom heat-resistant synthetic peptide (SVHRSP).</p><p><strong>Methods: </strong>Western blot and quantitative reverse transcription polymerase chain reaction (RT-qPCR) were employed to ascertain the protein and gene levels of IL-1β, IL-6, and TNF-α in BV2 cells. The concentration of IL-6 in the supernatant of the BV2 cell culture was measured by enzyme-linked immunosorbent assay. For the assessment of mitochondrial homeostasis, western blot, RT-qPCR, and cellular immunohistochemistry methods were utilized to investigate the protein and gene levels of DRP1 and MFN-2 in HT22 cells. In the context of signal pathway analyses, western blot, RT-qPCR, and immunofluorescence techniques were employed to detect the protein and gene expressions of PGC-1α and SIRT3 in HT22 cells, respectively. Following the transfection with siPGC-1αRNA, downstream proteins of PGC-1α/SIRT3 pathway in HT22 cells were investigated by Western blot and RT-qPCR.</p><p><strong>Results: </strong>The experimental findings demonstrated that exposure to PM_2.5 exacerbated neuroinflammation, resulting in elevated levels of IL-1β, IL-6, and TNF-α. Furthermore, it perturbed mitochondrial dynamics, as evidenced by increased DRP1 expression and decreased MFN-2 expression. Additionally, dysfunction was observed in the PGC-1α/SIRT3 signal pathway. However, intervention with SVHRSP ameliorated the cellular damage induced by PM_2.5 exposure.</p><p><strong>Conclusions: </strong>SVHRSP alleviated neuroinflammation and mitochondrial dynamics imbalance induced by PM_2.5 exposure by downregulating the PGC-1α/SIRT3 signaling pathway.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"12 5","pages":"756-764"},"PeriodicalIF":2.2,"publicationDate":"2023-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10615811/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71418674","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comparison of nickel oxide nano and microparticles toxicity in rat liver: molecular, biochemical, and histopathological study.","authors":"Caglar Adiguzel,&nbsp;Hatice Karaboduk,&nbsp;Fatma Gokce Apaydin,&nbsp;Suna Kalender,&nbsp;Yusuf Kalender","doi":"10.1093/toxres/tfad062","DOIUrl":"https://doi.org/10.1093/toxres/tfad062","url":null,"abstract":"<p><p>The unique properties of nickel oxide nanoparticles distinguish it from classical nickel compounds, increasing its use in agriculture, industry, and many industrial areas. The aim of this study is to investigate the possible toxicity of nickel oxide and nickel oxide nanoparticles in the liver. For this purpose, Wistar rats were given nickel oxide and nickel oxide nanoparticles orally, intraperitoneally, and intravenously for 21 days. Liver organ weight, biochemical and hematological parameters, oxidative stress (malondialdehyde, catalase, superoxide dismutase, glutathione peroxidase, and glutathione S transferase), acetylcholinesterase activities, inflammation levels, apoptotic markers, and histopathological changes were evaluated comparatively. When the data obtained were examined in general, it was observed that nickel oxide nanoparticles caused more hepatotoxicity in liver tissue than nickel oxide in terms of oxidative stress parameters, apoptotic markers, inflammation indicators, and other parameters examined. The results suggest that toxicity induced by both nickel oxide and nickel oxide nanoparticles plays an important role in hepatocyte apoptosis.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"12 5","pages":"741-750"},"PeriodicalIF":2.1,"publicationDate":"2023-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10615818/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71418746","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to: Acetylcysteine in paracetamol poisoning: a perspective of 45 years of use.","authors":"","doi":"10.1093/toxres/tfad045","DOIUrl":"https://doi.org/10.1093/toxres/tfad045","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.1039/c9tx00002j.].</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"12 4","pages":"709"},"PeriodicalIF":2.1,"publicationDate":"2023-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10470351/pdf/tfad045.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10519425","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}