Toxicology ResearchPub Date : 2025-04-29eCollection Date: 2025-04-01DOI: 10.1093/toxres/tfaf061
Dan Fu, Ziyou Li, Huafeng Feng, Fangling Fan, Wang Zhang, Liang He
{"title":"Chaperone mediated autophagy modulates microglia polarization and inflammation via LAMP2A in ischemia induced spinal cord injury.","authors":"Dan Fu, Ziyou Li, Huafeng Feng, Fangling Fan, Wang Zhang, Liang He","doi":"10.1093/toxres/tfaf061","DOIUrl":"https://doi.org/10.1093/toxres/tfaf061","url":null,"abstract":"<p><p>Spinal cord injury (SCI)-induced ischemic delayed paralysis is one of the most serious side effects of aneurysms surgeries. Recent studies prove that the activation of autophagy, including macroautophagy and micro-autophagy pathways, occur during SCI-induced brain neuron damage. However, the role of chaperone mediated autophagy (CMA) during SCI remains to be unveiled. In the present work, rat model of delayed paralysis after aneurysms operation and adenovrius induced LAMP2A knockdown in microglia cells were applied in the present work to investigate the involvement of LAMP2A-mediated CMA in the aneurysm operation related SCI and delayed paralysis. The results showed that LAMP2A was upregulated in the SCI procedure, and contributed to neuron death and pro-inflammation perturbation via inducing iNOS<sup>+</sup> polarization in microgila. We additionally observed that knockdown of LAMP2A resulted in the shift of microglia from iNOS<sup>+</sup> to ARG1<sup>+</sup> phenotype, as well as alleviated neuron damage during SCI. Furthermore, the analysis of BBB score, the result of immunohistological staining, and protein detection confirmed the activation of LAMP2A-mediated CMA activation and its interaction with NF-κB signaling, which leads to neuron death and motor function loss. These results prove that LAMP2A-mediated CMA contributes to the upregulation of pro-inflammatory cytokines and results in cell death in neurons during ischemic delayed paralysis via activating NF-κB signaling. Inhibition of LAMP2A promotes neurons survival during ischemic delayed paralysis.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"14 2","pages":"tfaf061"},"PeriodicalIF":2.2,"publicationDate":"2025-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12038812/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143957392","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}
Toxicology ResearchPub Date : 2025-04-26eCollection Date: 2025-04-01DOI: 10.1093/toxres/tfaf058
Yanqi Li, Wanchao Wang, Yuge Wang, Hongmei Ai
{"title":"FTO-mediated m6A demethylation of KLF4 promotes the proliferation and collagen deposition of keloid fibroblasts.","authors":"Yanqi Li, Wanchao Wang, Yuge Wang, Hongmei Ai","doi":"10.1093/toxres/tfaf058","DOIUrl":"https://doi.org/10.1093/toxres/tfaf058","url":null,"abstract":"<p><p>This study aims to elucidate the molecular mechanism mechanism by which FTO affects fibroblast proliferation and collagen deposition in keloids. Human keloid fibroblasts (KFs) and normal fibroblasts were cultured in vitro. FTO expression was silenced in KFs, and cell viability and proliferation were evaluated via CCK-8 and clone formation assays. FTO, KLF4, and MC1R expressions were quantified via qRT-PCR, while the protein levels of FTO, KLF4, MC1R, Collagen I, and Collagen III were determined by Western blot. The m<sup>6</sup>A RNA methylation status of total RNA was evaluated using the EpiQuik m6A RNA Methylation Quantification Kit. Post-actinomycin D treatment, the stability of KLF4 mRNA and its m<sup>6</sup>A modification level were measured. ChIP and dual-luciferase reporter assays confirmed the binding between KLF4 and MC1R promoter. KFs presented with significantly enhanced proliferation and collagen deposition, correlating with elevated FTO expression. Silence of FTO repressed the proliferation and collagen deposition of KFs, and elevated the m6A levels of total RNA and KLF4 mRNA in KFs, resulting in enhanced KLF4 mRNA stability and expression. KLF4 bound to the MC1R promoter and promoted MC1R expression. In conclusion, FTO represses KLF4 expression by removing m6A modification and further diminishes MC1R expression, thereby facilitating KF proliferation and collagen deposition.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"14 2","pages":"tfaf058"},"PeriodicalIF":2.2,"publicationDate":"2025-04-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12031721/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143957069","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}
Toxicology ResearchPub Date : 2025-04-24eCollection Date: 2025-04-01DOI: 10.1093/toxres/tfaf057
Eman E El Nahass, Safaa I Abou Eldahab, Elsayed I Salim
{"title":"Catechin designates individual and co-adjuvant antiproliferative effects with docetaxel in prostate cancer cell models.","authors":"Eman E El Nahass, Safaa I Abou Eldahab, Elsayed I Salim","doi":"10.1093/toxres/tfaf057","DOIUrl":"https://doi.org/10.1093/toxres/tfaf057","url":null,"abstract":"<p><p>The current study examined the potential therapeutic advantages of catechin, either alone or in combination with docetaxel (DTX), against PC-3 prostate cancer cells. Following the MTT assay's determination of the IC<sub>50</sub> concentrations, the cell lines were subjected to 48 h of treatment in the following protocol: untreated PC-3 control cells, docetaxel treatment, catechin (Cat) treatment, and DTX + Cat therapy at a ratio of 1:1. Treatments with DTX and Cat significantly decreased the number of viable cells in PC-3 cells in a dose-dependent manner. Additionally, the combo treatments caused the highest cytotoxicity compared with the other treatments. Also, when DTX and Cat were combined, they caused a significant synergistic effect (CI < 1) (combination index < 1). Furthermore, it was demonstrated that all treatments increased the expression of <i>BAX</i>, <i>Caspase-3</i>, and <i>P21</i> mRNA in PC-3 cells while decreasing that of <i>BCL-2</i> mRNA. The highest proportion of overexpression was observed in the combo therapy. A greater proportion of early and late apoptotic cells were caused by the combined treatment than by > DTX > Cat, according to flow cytometry. DNA damage in PC-3 cells was detected using the comet assay, and values of DNA tail, tail length, and tail moment increased considerably with increasing treatment dose. According to this study, Cat is effective against PC-3 cells when used in conjunction with DTX; by causing apoptosis, it enhances DTX's chemotherapeutic capability in cancerous cells.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"14 2","pages":"tfaf057"},"PeriodicalIF":2.2,"publicationDate":"2025-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12021262/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143951143","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}
Toxicology ResearchPub Date : 2025-04-16eCollection Date: 2025-04-01DOI: 10.1093/toxres/tfaf051
Juan Liu, Wei Xu, Yi Liu, Qi Zhang
{"title":"Reproductive and developmental toxicology of nitrosamines.","authors":"Juan Liu, Wei Xu, Yi Liu, Qi Zhang","doi":"10.1093/toxres/tfaf051","DOIUrl":"https://doi.org/10.1093/toxres/tfaf051","url":null,"abstract":"<p><p>With the development of science and technology and the acceleration of industrialization, environmental pollution is becoming more and more serious, and the global fertility rate is decreasing every year, which makes people pay more attention to reproductive health. Nitrosamines are a kind of easy to contact food pollutants, widely exist in pickled food (10.2-14.8 mg/kg) and contaminated water sources (10-150 ng/L), etc. They have been confirmed to be carcinogenic, but the reproductive and developmental toxic effects of nitrosamines have not been systematically reported. Based on relevant researches, the classification, distribution and metabolism kinetics of nitrosamines were summarized in this review. In addition, nitrosamines can inhibit testosterone synthesis (Leydig cells) and spermatogenesis (spermatogenic cells) in F0 male, and reduce ovary functions in F0 female, finally induce parental reproductive toxic effects. Meanwhile, the effects of parental (including maternal pregnancy, paternal) nitrosamine exposure on offspring development (such as cancer susceptibility) and related research deficiencies were summarized. To sum up, this paper systematically reviewed the reproductive and developmental toxic effects caused by exposure to nitrosamines, enabling people to fully understand the negative effects of nitrosamines on the body, so as to effectively avoid and reduce intake in daily life, and at the same time provide a theoretical and literature basis for guiding the healthy life and maintaining fertility.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"14 2","pages":"tfaf051"},"PeriodicalIF":2.2,"publicationDate":"2025-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12001771/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143952313","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":"Ellagic acid alleviates PM<sub>2.5</sub>-induced senescence of lung epithelial cells by mediating autophagy.","authors":"Yuqi Tong, Yanping Lu, Yaqi Li, Jiaquan Ding, Chenxi Yan, Zhihui Deng, Jiekang Chen, Zhaohui Zhang","doi":"10.1093/toxres/tfaf055","DOIUrl":"https://doi.org/10.1093/toxres/tfaf055","url":null,"abstract":"<p><p>Fine particulate matter (PM<sub>2.5</sub>) exposure is significantly linked to lung epithelial cell senescence, and autophagy dysfunction being a key contributor to the aging process. Although the anti-aging properties of ellagic acid (EA) are well-documented, its specific protective effect on PM<sub>2.5</sub>-induced lung epithelial cell senescence still needs to be studied in depth. To investigate the impacts of PM<sub>2.5</sub> on autophagy and senescence in lung epithelial cells, 16HBE and A549 cells were exposed to PM<sub>2.5</sub> suspension. Additionally, to explore the potential intervention effect of EA, cells were pretreated with EA before exposure to PM<sub>2.5</sub> suspension. Cell morphology, proliferation, senescence-related markers, senescence-associated secretory phenotype (SASP), and autophagy-related markers were then assessed. Our results showed that the proliferation of 16HBE and A549 cells were inhibited and autophagy dysfunction and senescence were induced under PM<sub>2.5</sub> exposure. However, pretreatment with EA can significantly improve the obstruction of autophagy flux caused by PM<sub>2.5</sub>, thereby effectively alleviating cell senescence. This study reveals the mechanism by which PM<sub>2.5</sub> induces senescence in lung epithelial cells and confirms the protective role of ellagic acid in this process.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"14 2","pages":"tfaf055"},"PeriodicalIF":2.2,"publicationDate":"2025-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12001767/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143953554","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}
Toxicology ResearchPub Date : 2025-04-14eCollection Date: 2025-04-01DOI: 10.1093/toxres/tfaf052
Rajesh Pamanji, Gisha Sivan
{"title":"Toxic endpoints or ubiquitous expression?","authors":"Rajesh Pamanji, Gisha Sivan","doi":"10.1093/toxres/tfaf052","DOIUrl":"https://doi.org/10.1093/toxres/tfaf052","url":null,"abstract":"<p><p>This opinion article questions the underlying causes of malformations observed in early developmental stages of zebrafish exposed to a range of chemicals. The research focuses on determining whether these developmental abnormalities arise due to the inherent sensitivity of zebrafish to chemical exposure or if they are related to the ubiquitous expression of certain genes within the zebrafish genome. By analysing different studies on zebrafish embryos to various chemical agents and analysing the resulting malformations, the study aims to differentiate between the effects of chemical sensitivity and the role of gene expression in developmental disruptions. Findings from this investigation will contribute to a deeper understanding of the mechanisms driving developmental toxicity in zebrafish, with implications for broader environmental and genetic research.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"14 2","pages":"tfaf052"},"PeriodicalIF":2.2,"publicationDate":"2025-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11994994/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143951960","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}
Toxicology ResearchPub Date : 2025-04-14eCollection Date: 2025-04-01DOI: 10.1093/toxres/tfaf053
Chul-Hong Kim, Geun-Seup Shin, Sehwan Park, Ji-Young Kim, Mi-Jin An, Hyun-Min Lee, Ah-Ra Jo, Yuna Park, Tae Kyung Hong, Jinho Kim, Yujeong Hwangbo, Jung-Woong Kim
{"title":"Benzo(a)pyrene triggers cytotoxicity by disrupting cell cycle dynamics and activating Caspase-3-mediated apoptosis in multiple human cell lines.","authors":"Chul-Hong Kim, Geun-Seup Shin, Sehwan Park, Ji-Young Kim, Mi-Jin An, Hyun-Min Lee, Ah-Ra Jo, Yuna Park, Tae Kyung Hong, Jinho Kim, Yujeong Hwangbo, Jung-Woong Kim","doi":"10.1093/toxres/tfaf053","DOIUrl":"https://doi.org/10.1093/toxres/tfaf053","url":null,"abstract":"<p><p>Benzo(a)pyrene (B(a)P), a polycyclic aromatic hydrocarbon (PAH), is a known endocrine disruptor linked to various environmentally induced diseases. While recent studies have explored its role in short- and long-term disease development, there is limited research on B(a)P's cytotoxic effects across different cell types. This study aims to evaluate the cytotoxicity of B(a)P exposure in several human cell lines under controlled conditions. We employed flow cytometry (FACS) for quantitative cytotoxicity analysis at the single-cell level. Our findings revealed that B(a)P exhibited minimal cytotoxicity in lung and liver cells, but potent toxicity in breast cells. Notably, B(a)P-induced cytotoxicity in breast cells was associated with increased cleaved caspase-3 expression, leading to cell death. This process was further linked to cell cycle arrest, as indicated by altered cyclin B1 expression in a B(a)P-dependent manner, resulting in reduced cell viability. In summary, these results suggest that breast cells are particularly sensitive to B(a)P-induced cytotoxicity, which is driven by apoptosis and cell cycle disruption.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"14 2","pages":"tfaf053"},"PeriodicalIF":2.2,"publicationDate":"2025-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11994996/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143951380","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}
Toxicology ResearchPub Date : 2025-04-07eCollection Date: 2025-04-01DOI: 10.1093/toxres/tfaf049
Baridoo Donatus Dooka, Chinna N Orish, Anthonet N Ezejiofor, Theresa C Umeji, Kpobari W Nkpaa, Ifeoma Okereke, Ana Cirovic, Aleksandar Cirovic, Orish E Orisakwe
{"title":"Rice bran extract ameliorate heavy metal mixture induced hippocampal toxicity via inhibiting oxido-inflammatory damages and modulating Hmox-1/BDNF/Occludin/Aβ40/Aβ42 in rats.","authors":"Baridoo Donatus Dooka, Chinna N Orish, Anthonet N Ezejiofor, Theresa C Umeji, Kpobari W Nkpaa, Ifeoma Okereke, Ana Cirovic, Aleksandar Cirovic, Orish E Orisakwe","doi":"10.1093/toxres/tfaf049","DOIUrl":"10.1093/toxres/tfaf049","url":null,"abstract":"<p><p>The hippocampus executes the integration of memory and spatial learning information. This study evaluated the effect of rice bran extract (RBE) on heavy metal mixture (MM) induced hippocampal toxicity and its underlying mechanism in albino rats. Thirty five rats were exposed to MM alone at Pb 20 mg/kg, Al 35 mg/kg, and Mn 0.564 mg/kg body weight or co-exposed with RBE at 125, 250 and 500 mg/kg body weight, 125 RBE mg/kg b.wt only, and 500 RBE mg/kg b.wt only 5 days a wk for 13 wk (90 days). Subsequently, oxidative stress, inflammation (cyclooxygenase-2) and caspase-3, amyloid precursor proteins (Aβ40 and Aβ42), HMOX-1, occludin and BDNF and transcription factor Nrf-2 in the hippocampus were investigated. MM treatment resulted in significantly higher escape latency time than both the control and MM plus RBE group. MM exposure induced increased oxidative stress, inflammation resulting in enhanced hippocampal apoptosis. MM significantly increased bioaccumulation of Pb, Al, and Pb; increased caspase-3, Nrf-2, Aβ40 and Aβ42 and significantly decreased occludin, BDNF, HMOX-1 when compared with the control. All these effects were reversed by RBE. Collectively, RBE ameliorated MM - induced oxidative stress, neuro-inflammation and hippocampal apoptosis via attenuation of oxidative damages of cellular constituents, neuronal inflammation and subsequent down regulation of amyloid precursor proteins Aβ40, Aβ42 and up regulation of occludin, BDNF, HMOX-1 protein expression via Nrf-2 dependent pathways to abrogate hippocampal toxicity associated with spatial learning and memory deficits.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"14 2","pages":"tfaf049"},"PeriodicalIF":2.2,"publicationDate":"2025-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11975361/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143810405","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}
Toxicology ResearchPub Date : 2025-04-04eCollection Date: 2025-04-01DOI: 10.1093/toxres/tfaf046
Dilek Akyil, Edanur Yeniyol
{"title":"Green synthesized zinc oxide nanoparticle with <i>Mentha pulegium</i> L. extracts in A549 cell line, characterization, biological activities, Genotoxicity in comet test and SMART assay in <i>Drosophila melanogaster</i>.","authors":"Dilek Akyil, Edanur Yeniyol","doi":"10.1093/toxres/tfaf046","DOIUrl":"10.1093/toxres/tfaf046","url":null,"abstract":"<p><p>In this study, zinc oxide nanoparticles (ZnO NPs) were obtained by green synthesis method using extracts prepared from <i>Mentha pulegium</i> L. species in order to investigate the cytotoxic, genotoxic and antimicrobial activities of nanoparticles. For the characterization of these nanoparticles, UV-Vis spectrophotometer, FT-IR, XRD and SEM analysis methods were used. For cell culture studies were carried out to determine the cytotoxic and genotoxic activities of ZnO NPs obtained by green synthesis with A549 cell line, which is a lung cancer cell. In the genotoxicity results determined by the Comet method, the highest DNA damage was seen at a concentration of 3.75 mg/mL. The genotoxic activity of different concentrations (0.1, 1, 5, 10 mM) of ZNO NPs were evaluated with SMART assay on <i>Drosophila melanogaster</i>. According to results ZNO NPs applications were found to be similar to the control group in all doses. On the other hand, in order to determine the antimicrobial activity, <i>Escherichia coli</i> (ATTC 25922), <i>Staphylococcus aureus</i> (ATTC 29213), <i>Candida albicans</i> (ATTC 90028), <i>Klebsiella pneumoniae</i> (ATTC 700603) and <i>Salmonella enteritidis</i> (ATTC 13076) microorganisms were cultured and disc diffusion test method was applied. In the disc diffusion test, dose application was made in the range of 15.6-500 mg/mL concentrations and it was observed that inhibition zone was formed at all concentrations.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"14 2","pages":"tfaf046"},"PeriodicalIF":2.2,"publicationDate":"2025-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11969665/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143794082","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}
Toxicology ResearchPub Date : 2025-04-04eCollection Date: 2025-04-01DOI: 10.1093/toxres/tfaf050
Aisha E ElMehy, Ghada N El-Sarnagawy, Basma Adel
{"title":"Predictive models assessing the impact of intensive care unit admission on the outcomes of acutely poisoned patients.","authors":"Aisha E ElMehy, Ghada N El-Sarnagawy, Basma Adel","doi":"10.1093/toxres/tfaf050","DOIUrl":"10.1093/toxres/tfaf050","url":null,"abstract":"<p><p>Although intensive care unit (ICU) admission is the cornerstone in management of critically acute poisoned patients, the decision of ICU admission is often challenging, especially with limited resources. Hence, our study aimed to assess predictive models of the impact of ICU admission on outcomes of patients with acute poisoning. This retrospective cohort study recruited records of acutely poisoned patients admitted to Tanta University Poison Control Center between 2021 and 2023. Patient demographic and toxicological data, as well as initial clinical and laboratory profiles, were retrieved. Afterward, patients were categorized according to mortality and complicated outcomes. Out of 221 acutely poisoned patients admitted to the ICU, the incidences of mortality and complications in survivors were 54.3% and 57.4%, respectively. Aluminum phosphide (ALP) was the most common cause of poisoning (59%), with a significant association with mortality and predominance in cardiac complications. However, respiratory and neurological complications were evident among illicit substances, cholinesterase inhibitors, and neuropsychiatric drugs. The model anticipating morality included time from presentation to ICU admission, mean arterial pressure (MAP), oxygen saturation, pH, and ALP poisoning. Furthermore, the complication predictive model comprised time from exposure to poison center presentation, time from presentation to ICU admission, and MAP. Both models exhibited good to excellent discrimination performance and consistent calibration. Accordingly, prompt admission of all ALP-poisoned patients to ICU with a highly standardized level of care may alleviate their deleterious outcomes. However, drug categories with reversible courses should be adequately treated with frequent respiratory and hemodynamic monitoring in less-equipped ICUs.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"14 2","pages":"tfaf050"},"PeriodicalIF":2.2,"publicationDate":"2025-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11969671/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143794118","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}