Toxicology Research最新文献

{"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}

{"title":"The synthetic dye malachite green found in food induces cytotoxicity and genotoxicity in four different mammalian cell lines from distinct tissuesw.","authors":"Andryo O de Almada Vilhena,&nbsp;Karina M M Lima,&nbsp;Luana F C de Azevedo,&nbsp;Jorge D Rissino,&nbsp;Augusto C P de Souza,&nbsp;Cleusa Y Nagamachi,&nbsp;Julio C Pieczarka","doi":"10.1093/toxres/tfad059","DOIUrl":"https://doi.org/10.1093/toxres/tfad059","url":null,"abstract":"<p><p>Malachite green (MG) is a synthetic dye that uses ranges from its application as a tissue dye to that as an antiparasitic in aquaculture. Several studies have reported the presence of this compound in food dyes and in the meat of fish raised in captivity for human consumption, suggesting risks both for the end user and for as those who handle these products because of MG toxic properties described in the literature. Here we evaluated the cytotoxic and genotoxic profiles of MG in four different cell lines (ACP02, L929, MNP01, and MRC-5). Two of these cell lines are stomach cells (normal and cancer lineages) and the potential ingestion of MG makes this a relevant cell type. Cells were treated with MG at concentrations ranging from 0.1 μM to 100 μM, and tested by MTT assay, a differential apoptosis/necrosis assay (EB/OA), the micronucleus test (MN), and the comet assay. MG exhibits dose-dependent cytotoxicity toward all of the tested cell types; higher concentrations of MG cause cell necrosis, while lower concentrations induce apoptosis. MG has a genotoxic profile increasing the rates of micronuclei, nucleoplasmic bridges, nuclear buds, and DNA fragmentation; L929 and MRC-5 showed more sensibility than ACP02 and MNP01.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"12 4","pages":"693-701"},"PeriodicalIF":2.1,"publicationDate":"2023-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10470350/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10506067","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":"Metformin and Aspirin: Anticancer effects on A549 and PC3 cancer cells and the mechanisms of action.","authors":"Farzaneh Motafeghi, Romina Shahsavari, Parham Mortazavi, Aysan Babaei, Pouria SamadiMojaveri, Omid Abed Khojasteh, Mohammad Shokrzadeh","doi":"10.1093/toxres/tfad060","DOIUrl":"10.1093/toxres/tfad060","url":null,"abstract":"<p><p>Metformin exerts its anticancer effect through two mechanisms, directly affecting the tumor and indirectly reducing systemic insulin levels. The anticancer effects of aspirin occur by inhibiting Cyclooxygenase (COX)-2. COX-2 is absent in many cell types under normal conditions and increases under pathological conditions such as cancer. This study aims to investigate the effect of metformin and aspirin and their combination of them on A549 and PC3 cell lines. Metformin and aspirin were investigated separately and in combination on two cancer cell lines, A549 and PC3. The examined groups include the negative control of untreated cells and the positive control of cisplatin and drugs at concentrations of 15, 10, and 20 μg/ mL to investigate the mechanism of oxidative stress factors (reactive oxygen species, lipid peroxidation, Glutathione (GSH)) and apoptosis (lactate dehydrogenase). The results showed that aspirin, metformin, and their combination could affect cancer cell growth by damaging mitochondria, releasing reactive oxygen species, and activating the oxidative stress pathway. Also, these two drugs show the activation of the apoptotic pathway in cancer cells by increasing the lactate dehydrogenase factor and releasing it from the cells. By disrupting the balance of oxidants and antioxidants in the cell, metformin and aspirin cause an increase in the level of reactive oxygen species and a decrease in the level of glutathione reserves, followed by an increase in the level of lipid peroxidation and a decrease in cell viability. Unlike common chemotherapy drugs, these drugs have no known severe side effects; Therefore, in the not-so-distant future, these drugs can also be used as anticancer drugs.</p><p><strong>Highlights: </strong>Metformin and aspirin, commonly used drugs for diabetes and inflammation, inhibit the growth of cancer cell lines, A549 and PC3.Metformin and aspirin, either separately or in combination, can potentially impede cancer cell growth by disrupting mitochondrial function, inducing the release of reactive oxygen species (ROS), and activating oxidative stress pathways.Furthermore, these drugs can trigger apoptosis, a programmed cell death mechanism, in cancer cells by increasing lactate dehydrogenase (LDH) levels and facilitating its release from the cells.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"12 4","pages":"702-708"},"PeriodicalIF":2.2,"publicationDate":"2023-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10470367/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10151911","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":"Protective impacts of <i>Withania somnifera</i> leaf extract from Taif area against <i>diclofenac</i> induced hepato-renal toxicity: role of antioxidants, inflammation, apoptosis, and anti-oxidative stress biomarkers.","authors":"Mohamed Mohamed Soliman, Ahmed M Elshehawei, Saed Althobaiti, Samy M Sayed","doi":"10.1093/toxres/tfad058","DOIUrl":"10.1093/toxres/tfad058","url":null,"abstract":"<p><p>Current study examined the boosting impacts of <i>Withania somnifera</i> leaf extract from Taif area (high-altitude area) against hepatic and renal toxicity induced by diclofenac in experimental rats. Withania is highly grown on Taif area as environmental herb with multiple functions. Diclofenac is non-steroidal medication used for treatment of pain but over dose has severe side effects. Thirty-two adult Wistar rats of male type were subdivided into 4 groups. The control rats (group 1) received saline. Second group received diclofenac (50 mg/kg BW intraperitoneally) at days 4 and 5. Third group received <i>W. somnifera</i> leaf extract (250 mg /kg body weight) for 6 days. The fourth protective group, received <i>W. somnifera</i> leaf extract plus diclofenac for 6 days as shown in groups 2 and 3. Diclofenac significantly increased serum AST, ALT, and decreased albumin and total proteins levels. It also increased serum concentrations of uric acid and creatinine. In addition, it increased lipid peroxidation, and decreased reduced glutathione and superoxide dismutase levels. Diclofenac increased inflammatory cytokines secretion and up-regulated hepatic oxidative stress genes (HO-1; hemoxygenase-1 and Nrf2nuclear factor erythroid 2-related factor 2 (Nrf2) and renal inflammatory transcriptional markers (TGF-β1; transforming growth factor-beta1 and COX-2; cycloxygenas-2). In parallel, hepatic caspase-3 expression was up-regulated as an apoptotic marker, while Bcl2; (B-cell lymphoma 2) mRNA expression was down regulated as anti-apoptotic marker. <i>W. somnifera</i> pre-administration in the protective group ameliorated the altered parameters induced by diclofenac. In conclusion, <i>W. somnifera</i> leaf extract has the potential to antagonize side effects of diclofenac by regulating the pathways of oxidative stress, inflammation, and apoptosis/antiapoptosis.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"12 4","pages":"685-692"},"PeriodicalIF":2.2,"publicationDate":"2023-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10470349/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10143892","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":"Study on the mechanism of PM2.5 affecting Th1/Th2 immune imbalance through the notch signaling pathway in asthmatic mice.","authors":"Ji-Rong Wu, Zheng He, Hai-Rong Bao, Xiao-Li Zeng, Xiao-Ju Liu","doi":"10.1093/toxres/tfad044","DOIUrl":"10.1093/toxres/tfad044","url":null,"abstract":"<p><p>Some research has shown that PM2.5 causes Th1/Th2 immune imbalance and aggravates asthma. However, the exact mechanism of PM2.5 causing aggravation of asthma remains unclear. The purpose of this study was to investigate whether exposure to PM2.5 exacerbates Th1/Th2 immune imbalance through the Notch signaling pathway. Eight-week-old SPF female BALF/c mice were sensitized by ovalbumin to establish an asthma mouse model. PM2.5 exposure was carried out by aerosol inhalation of PM2.5 (510 μg/m³) after each provocation. The lung function of mice was measured and Splenic T lymphocyte subsets were detected. Notch signaling pathway was tested. The levels of interferon (IFN)-γ and interleukin (IL)-4 in serum and bronchoalveolar lavage fluid were determined. The results showed that the expression of the mRNA and protein of Notch1 and Hes1 in the asthma group were significantly higher than those in healthy controls. The levels of IL-4 were also remarkably high; while the levels of IFN-γ were remarkably low in serum and BALF, the Th1% and Th1/Th2 ratios were significantly lower, and Th2% was significantly higher in the asthma group than in the healthy controls. PM2.5 promoted further activation of the Notch signaling pathway and aggravated Th1/Th2 immune imbalance in asthmatic mice. γ-secretase inhibitor can partially inhibit the activation of the Notch signaling pathway and alleviate aggravation of immune imbalance. In conclusion, the asthmatic mice had a Th1/Th2 immune imbalance and an overactivated Notch signaling pathway. PM2.5 further aggravated Th1/Th2 immune imbalance by activating the Notch signaling pathway.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"12 4","pages":"675-684"},"PeriodicalIF":2.2,"publicationDate":"2023-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10470343/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10525133","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":"HM-chromanone alleviates hyperglycemia and inflammation in mice with endotoxin-induced insulin resistance.","authors":"Ha J Lim, Jae E Park, Ji S Han","doi":"10.1093/toxres/tfad057","DOIUrl":"10.1093/toxres/tfad057","url":null,"abstract":"<p><p>This study was designed to investigate whether (E)-5-hydroxy-7-methoxy-3-(2'-hydroxybenzyl)-4-chromanone alleviates inflammation and hyperglycemia in mice with endotoxin-induced insulin resistance. (E)-5-hydroxy-7-methoxy-3-(2'-hydroxybenzyl)-4-chromanone (10, 30, and 50 mg/kg bodyweight) was orally pre-administered to C57BL/6 J mice. An hour later, lipopolysaccharides (20 mg/kg bodyweight) was administered intraperitoneally to induce endotoxins. Blood samples were collected from the tail vein of the mice every 0, 30, and 90 min. The results indicated that (E)-5-hydroxy-7-methoxy-3-(2'-hydroxybenzyl)-4-chromanone effectively regulated blood glucose levels in mice with endotoxin-induced insulin resistance. Furthermore, (E)-5-hydroxy-7-methoxy-3-(2'-hydroxybenzyl)-4-chromanone significantly reduced the phosphorylation of mammalian target of rapamycin, ribosomal protein S6 kinase 1, and protein kinase C θ. Additionally, (E)-5-hydroxy-7-methoxy-3-(2'-hydroxybenzyl)-4-chromanone suppressed the phosphorylation of c-Jun-NH2-terminal kinase and IkB kinase β, thereby decreasing the phosphorylation of inhibitor of nuclear factor kappa-B α and activating the nuclear factor-κB and activator protein-1 in the liver. Therefore, the expression of tumor necrosis factor-α, interleukin-6, and interleukin-1β was significantly reduced by suppressing the nuclear factor-κB and activator protein 1 activity. Suppression of mammalian target of rapamycin, S6 kinase 1, protein kinase C θ, c-Jun-NH2-terminal kinase, and IkB kinase β also ameliorated insulin resistance by reducing the phosphorylation of insulin receptor substrate-1 serine 307, thereby decreasing hyperglycemia. These findings suggest that (E)-5-hydroxy-7-methoxy-3-(2'-hydroxybenzyl)-4-chromanone can alleviate hyperglycemia and inflammation in mice with endotoxin-induced insulin resistance.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"12 4","pages":"665-674"},"PeriodicalIF":2.2,"publicationDate":"2023-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10470335/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10525134","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":"Zerumbone attenuates the excessive proliferation of keratinocytes in psoriasis mice through regulating NLRP3/NF-κB pathway.","authors":"Jin Lin, Yimiao Fang, Yi Cao, Lili Ma, Maocan Tao, Xiao Wang, Yuanyuan Li, Lijun Qing","doi":"10.1093/toxres/tfad056","DOIUrl":"10.1093/toxres/tfad056","url":null,"abstract":"<p><p>Psoriasis is a common chronic disease, and existing treatment regimens often exhibit certain toxicities and side effects. Zerumbone (Zer) may possess therapeutic effect, and the objective of this study is to investigate the effect of Zer on psoriasis. A mouse model of psoriasis was established using imiquimod cream, and the role of Zer on the pathological alterations in psoriatic mouse skin was evaluated by psoriasis area and severity index (PASI) score; the effect of Zer on keratinocyte proliferation was evaluated via hematoxylin and eosin staining, Zen image analysis, and immunofluorescence; Immunohistochemistry and enzyme-linked immunoassay were used to evaluate the effect of Zer on tissue inflammatory responses, while malondialdehyde (MDA) and glutathione (GSH) levels were measured to elucidate the role of Zer in modulating oxidative stress; the signaling pathway regulated by Zer was evaluated by western blotting. The results demonstrated that Zer could alleviate the pathological manifestations of psoriasis, reduce PASI score, reduce skin pathological damage and epidermal hyperplasia, diminish the number of CD8⁺ T cells and cytokine expression levels, decrease the level of MDA and GSH and increase the expression of Nrf and HO-1. Zer was found to regulate the NLRP3/nuclear factor-kappa B (NF-κB) signaling pathway. In conclusion, Zer ameliorated the symptoms of psoriasis in mice, suppressed the keratinocyte hyperproliferation, and mitigates inflammation and oxidative stress in psoriatic skin tissue by regulating the NLRP3/NF-κB pathway.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"12 4","pages":"658-664"},"PeriodicalIF":2.2,"publicationDate":"2023-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10470342/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10151910","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":"HM-chromanone isolated from <i>Portulaca oleracea</i> L. alleviates insulin resistance and inhibits gluconeogenesis by regulating palmitate-induced activation of ROS/JNK in HepG2 cells.","authors":"Jae Eun Park, Ji Sook Han","doi":"10.1093/toxres/tfad055","DOIUrl":"10.1093/toxres/tfad055","url":null,"abstract":"<p><p>Oxidative stress is a major cause of hepatic insulin resistance. This study investigated whether <i>(E</i>)-5-hydroxy-7-methoxy-3-(2-hydroxybenzyl)-4-chromanone (HM-chromanone), a homoisoflavonoid compound isolated from <i>Portulaca oleracea</i> L., alleviates insulin resistance and inhibits gluconeogenesis by reducing palmitate (PA)-induced reactive oxygen species (ROS)/c-Jun NH2-terminal kinase (JNK) activation in HepG2 cells. PA treatment (0.5 mM) for 16 h resulted in the highest production of ROS and induced insulin resistance in HepG2 cells. HM-chromanone, like N-acetyl-1-cysteine, significantly decreased PA-induced ROS production in the cells. HM-chromanone also significantly inhibited PA-induced JNK activation, showing a significant reduction in tumor necrosis factor and interleukin expression levels. Thus, HM-chromanone decreased the phosphorylation of Ser307 in insulin receptor substrate 1, while increasing phosphorylation of serine-threonine kinase (AKT), thereby restoring the insulin signaling pathway impaired by PA. HM-chromanone also significantly increased the phosphorylation of forkhead box protein O, thereby inhibiting the expression of gluconeogenic enzymes and reducing glucose production in PA-treated HepG2 cells. HM-chromanone also increased glycogen synthesis by phosphorylating glycogen synthase kinase-3β. Therefore, HM-chromanone may alleviate insulin resistance and inhibit gluconeogenesis by regulating PA-induced ROS/JNK activation in HepG2 cells.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"12 4","pages":"648-657"},"PeriodicalIF":2.2,"publicationDate":"2023-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10470364/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10525138","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":"Astragaloside IV protects LO2 cells from oxidative damage caused by radiation-induced bystander effect through Akt/Nrf2 pathway.","authors":"Danting Wan, Zihao Zhu, Jie Zhou, Zhengzheng Deng, Pengyuan Lei, Qi Liu, Xiaoya Sun, Bo Huang","doi":"10.1093/toxres/tfad048","DOIUrl":"10.1093/toxres/tfad048","url":null,"abstract":"<p><strong>Background: </strong>The protective effects of astragaloside IV (ASIV) on various diseases are well known, but its potential impact on radiation-induced bystander effect (RIBE) has remained unclear.</p><p><strong>Objective: </strong>This study aimed to explore the protective mechanism of ASIV against oxidative damage caused by RIBE in LO2 cells.</p><p><strong>Methods: </strong>To construct the RIBE model, the conditioned medium from HepG2 cells irradiated with radiation was transferred to nonirradiated LO2 cells. LY294002, a commonly used phosphatidylinositol 3-kinase/Akt pathway inhibitor, was added to LO2 cells 1 h before exposing HepG2 cells to radiation. LO2 cells were then collected for analyses after RIBE exposure.</p><p><strong>Results: </strong>The study found that ASIV significantly improved cell proliferation and promoted the recovery of mitochondrial membrane potential while reducing the rate of apoptosis. Western blot analyses demonstrated that ASIV upregulated B-cell lymphoma 2 and downregulated B-cell lymphoma 2-related X protein and cleaved-caspase 3. Measurement of reactive oxygen species, superoxide dismutase, glutathione peroxidase, and malondialdehyde levels showed that ASIV effectively restored the oxidative stress state induced by RIBE. Additionally, immunofluorescence and western blots analyses confirmed that ASIV enhanced the translocation of Nrf2 to the nucleus and activated downstream nicotinamide adenine dinucleotide phosphate: quinine oxidoreductase 1 and heme oxygenase 1. Importantly, Akt pathway inhibitor repressed ASIV-induced activation of Nrf2 and its protective effect against RIBE.</p><p><strong>Conclusion: </strong>This study demonstrates that ASIV protects LO2 cells against oxidative damage caused by RIBE through activation of the Akt/Nrf2 pathway.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"12 4","pages":"635-647"},"PeriodicalIF":2.2,"publicationDate":"2023-07-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10470369/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10151906","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":"Clinical and demographic features with outcome predictors of adult patients with acute intoxication admitted to a medical intensive care unit in the Mediterranean part of Croatia.","authors":"Vedran Kovacic, Lukas Kvartuc, Marijana Mikacic, Ivan Jerkovic, Tanja Ilic Begovic, Marina Maras, Jurica Nazlic","doi":"10.1093/toxres/tfad054","DOIUrl":"10.1093/toxres/tfad054","url":null,"abstract":"<p><strong>Background: </strong>The objective of the study was to assess the demographics, clinical parameters, and outcome of acute intoxications among adult patients admitted to a medical intensive care unit in southern Croatia.</p><p><strong>Materials and methods: </strong>An observational retrospective study was conducted over a 1-year period. The subjects were patients admitted to the intensive care unit for acute poisoning.</p><p><strong>Results: </strong>In all, 81 subjects (32.1% females) aged 43.16 ± 14.77 years were admitted to the intensive care unit because of poisoning (14.97% of the total annual intensive care unit admissions). Psychiatric disorders were previously established in 76.5% participants, and 69.1% of all acute intoxications were classified as suicidal. Non-suicidal subjects differed from suicidal subjects in age (37.36 ± 9.71 vs. 45.75 ± 15.93 years; <i>P</i> = 0.009), in pCO2 (6.38 ± 1.78 vs. 5.50 ± 1.26 kPa; <i>P</i> = 0.020), in length-of-stay in intensive care unit (median 1.00, interquartile range 1.00 vs. median 2.00, interquartile range 2.00 days; <i>P</i> = 0.022), and in length-of-stay in hospital (median 2.00, interquartile range 2.00 vs. median 10.50, interquartile range 15.25 days; <i>P</i> < 0.001). Three (3.7%) patients died. Pharmaceutical psychoactive drug intoxications were the most common poisoning cases; of these, diazepam was the most frequent (16.8%), followed by ethanol (9.0%) and alprazolam (7.8%). Benzodiazepines/hypnotics were the most common group (28.7%), followed by antipsychotics (13.2%). Intoxications with more than 1 poison accounted for the largest number of cases (67.9%). The number of toxins was significantly correlated with length-of-stay in the hospital (rho = -0.265; <i>P</i> = 0.008), systolic blood pressure (rho = -0.318; <i>P</i> = 0.002), and diastolic blood pressure (rho = -0.262; <i>P</i> = 0.009). The electrocardiogram was considered abnormal in 50.62% of the cases.</p><p><strong>Conclusion: </strong>Acute intoxicants were most commonly caused by psychiatric pharmaceutical drugs. Multidrug exposure was a typical pattern of acute intoxication.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"12 4","pages":"626-634"},"PeriodicalIF":2.2,"publicationDate":"2023-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10470373/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10150396","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}