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Design and computational analysis of a novel Leptulipin-p28 fusion protein as a multitarget anticancer therapy in breast cancer. 设计和计算分析新型 Leptulipin-p28 融合蛋白作为乳腺癌的多靶点抗癌疗法。
IF 2.2 4区 医学
Toxicology Research Pub Date : 2024-10-13 eCollection Date: 2024-10-01 DOI: 10.1093/toxres/tfae174
Sania Khalid, Hafiz Muhammad Rehman, Yasamin Al-Qassab, Irfan Ahmad, Tehreem Fatima, Mian Muhammad Mubasher, Maria Kalsoom, Tariq Nadeem, Hamid Bashir
{"title":"Design and computational analysis of a novel Leptulipin-p28 fusion protein as a multitarget anticancer therapy in breast cancer.","authors":"Sania Khalid, Hafiz Muhammad Rehman, Yasamin Al-Qassab, Irfan Ahmad, Tehreem Fatima, Mian Muhammad Mubasher, Maria Kalsoom, Tariq Nadeem, Hamid Bashir","doi":"10.1093/toxres/tfae174","DOIUrl":"https://doi.org/10.1093/toxres/tfae174","url":null,"abstract":"<p><p>The search for novel therapeutic agents to treat breast cancer has compelled the development of fusion proteins that synergize the functional benefits of different bioactive peptides. Leptulipin, derived from scorpion venom, exhibits antitumor properties. On the other hand, p28, a peptide from the bacterial protein azurin, enhances cell penetration. The current study investigated the design and computational evaluation of a Leptulipin-p28 fusion protein for breast cancer treatment. The amino acid sequences of Leptulipin and p28 were joined via a rigid linker to maintain structural and functional integrity. Secondary and tertiary structure predictions were performed using online servers of GOR-IV and I-TASSER. Physicochemical properties and solubility were analyzed using ProtParam and Protein-Sol. Validation and quality assessment of the fusion protein were confirmed through Rampage and ERRAT2. Finally, the fusion protein was docked with 2 receptors (VEGFR and Cadherin) and docked complexes were simulated on GROMACS. The Leptulipin-p28 fusion protein exhibited a stable structure exhibiting a high quality score of 92 on ERRAT and Ramachandran plot analysis highlighting 76.3% of residues in the favorable region. Docking studies with VEGFR and Cadherin receptors followed by 100 ns simulations on GROMACS showed stable complex formation. Molecular dynamics simulations confirmed the stability and robust interaction of the fusion protein-receptor complexes over time. The computational analysis indicates that the Leptulipin-p28 fusion protein holds promise as a multitarget therapeutic agent in breast cancer. The current findings warrant further investigation through in vitro and in vivo studies to validate the current outcomes.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"13 5","pages":"tfae174"},"PeriodicalIF":2.2,"publicationDate":"2024-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11471314/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142453737","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}
引用次数: 0
HDAC10 inhibits non-small-cell lung cancer cell ferroptosis through the microRNA-223-5p-SLC7A11 axis. HDAC10通过microRNA-223-5p-SLC7A11轴抑制非小细胞肺癌细胞的铁突变。
IF 2.2 4区 医学
Toxicology Research Pub Date : 2024-10-13 eCollection Date: 2024-10-01 DOI: 10.1093/toxres/tfae164
Zhihua Shi, Tao Jiang, Xusheng Sun, Liangbiao Peng, Bingji Cao, Yi Wang
{"title":"HDAC10 inhibits non-small-cell lung cancer cell ferroptosis through the microRNA-223-5p-SLC7A11 axis.","authors":"Zhihua Shi, Tao Jiang, Xusheng Sun, Liangbiao Peng, Bingji Cao, Yi Wang","doi":"10.1093/toxres/tfae164","DOIUrl":"https://doi.org/10.1093/toxres/tfae164","url":null,"abstract":"<p><strong>Objective: </strong>Non-small-cell lung cancer (NSCLC) is a leading attributor to cancer deaths. High HDAC10 and low microRNA (miR)-223-5p levels have been observed in NSCLC. But their roles remain elusive. This study illustrated their roles in NSCLC cell ferroptosis and the mechanism.</p><p><strong>Methods: </strong>HDAC10, miR-223-5p, and solute carrier family 7 member 11 (SLC7A11) levels in cells were determined by RT-qPCR. Iron ion content, reactive oxygen species (ROS), and glutathione (GSH) levels were tested using reagent kits, and levels of SLC7A11 and Acyl-CoA synthesis long chain family (ACSL4) were examined using Western blot. Chromatin immunoprecision was performed to analyze the enrichment of HDAC10 and acetylated lysine 9 of histone H3 (H3K9ac) on the miR-223-5p promoter. The targeted binding of miR-223-5p and SLC7A11 was analyzed by dual-luciferase assay. Joint experiments were designed to identify the role of miR-223-5p/SLC7A11 axis in HDAC10-regulated ferroptosis in NSCLC cells.</p><p><strong>Results: </strong>HDAC10 was highly expressed in NSCLC cells. Silencing HDAC10 significantly reduced GSH and SLC7A11 levels, upregulated iron ion content, ROS levels, and ACSL4 expression, promoting cell ferroptosis. Mechanically, HDAC10 inhibited miR-223-5p expression through H3K9ac deacetylation of the miR-223-5p promoter, thereby targeting SLC7A11. The joint experimental results showed that overexpression of SLC7A11 or downregulation of miR-223-5p alleviated the promoting effect of silencing HDAC10 on ferroptosis in NSCLC cells.</p><p><strong>Conclusion: </strong>HDAC10 inhibits miR-223-5p expression through H3K9ac deacetylation of the miR-223-5p promoter, thereby promoting SLC7A11 expression and inhibiting ferroptosis in NSCLC cells.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"13 5","pages":"tfae164"},"PeriodicalIF":2.2,"publicationDate":"2024-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11471316/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142453740","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}
引用次数: 0
Reproductive safety of STING agonists MSA-2 and manganese-MSA-2. STING 激动剂 MSA-2 和锰-MSA-2 的生殖安全性。
IF 2.2 4区 医学
Toxicology Research Pub Date : 2024-10-13 eCollection Date: 2024-10-01 DOI: 10.1093/toxres/tfae172
Ya Cai, Tian He, Tao Yang, Yating Li, Lirong Yi, Wenqing Li, Peng Zhou
{"title":"Reproductive safety of STING agonists MSA-2 and manganese-MSA-2.","authors":"Ya Cai, Tian He, Tao Yang, Yating Li, Lirong Yi, Wenqing Li, Peng Zhou","doi":"10.1093/toxres/tfae172","DOIUrl":"https://doi.org/10.1093/toxres/tfae172","url":null,"abstract":"<p><strong>Background: </strong>MSA-2, as an oral molecule for activating STING signaling pathway to cure the tumor entering clinical trials. The toxicity of MSA-2 has aroused wide concern, especially the reproductive toxicity can not be ignored.</p><p><strong>Objectives: </strong>We synthesized the STING agonist (MSA-2) and its derivative manganese-MSA-2 (MSA-2-Mn) and investigated the reproductive toxicity.</p><p><strong>Methods: </strong>We evaluated the reproductive effects of MSA-2 and MSA-2-Mn in female mice under the administration alone and on the reproductive system of male mice in the presence or absence of combined radiation.</p><p><strong>Results: </strong>Results suggested that MSA-2 and MSA-2-Mn have negligible reproductive toxicity in healthy adults. Conclusions: This provides new ideas to enhance the efficacy of immunotherapy, as well as favorable evidence for future systemic dosing in patients of reproductive age and clinical trials of immunotherapy.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"13 5","pages":"tfae172"},"PeriodicalIF":2.2,"publicationDate":"2024-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11471313/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142453743","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}
引用次数: 0
Ephedrine attenuates LPS-induced M1 polarization of alveolar macrophages via the PKM2-mediated glycolysis. 麻黄碱可通过 PKM2 介导的糖酵解减轻 LPS 诱导的肺泡巨噬细胞 M1 极化。
IF 2.2 4区 医学
Toxicology Research Pub Date : 2024-10-10 eCollection Date: 2024-10-01 DOI: 10.1093/toxres/tfae166
Yijin Xiang, Zaifeng Jiang, Zhigang Yang, Shaomin Gong, Weiran Niu
{"title":"Ephedrine attenuates LPS-induced M1 polarization of alveolar macrophages via the PKM2-mediated glycolysis.","authors":"Yijin Xiang, Zaifeng Jiang, Zhigang Yang, Shaomin Gong, Weiran Niu","doi":"10.1093/toxres/tfae166","DOIUrl":"https://doi.org/10.1093/toxres/tfae166","url":null,"abstract":"<p><strong>Background: </strong>Asthma is one of chronic inflammatory lung diseases in world. The important role of macrophage polarization and glycolysis in lung inflammation has attracted considerable attention. Ephedrine (EP) is a compound isolated from Ephedra and plays a regulatory role in inflammatory response, but its role in asthma and mechanism involved are not clear. Therefore, the purpose of this study was to investigate the molecular mechanism and effect of EP on lipopolysaccharide (LPS)-induced alveolar macrophage polarization and glycolysis.</p><p><strong>Methods: </strong>We investigated the expression of Tnf-a, Nos2, Il10, and Arg1 using RT-PCR, as well as PKM2 and LDHA protein expression with Western blot. A CCK-8 assay was performed to determine the viability of the cells. The extracellular acidification rate (ECAR), ATP and lactate level were detected using commercial kits.</p><p><strong>Results: </strong>The results revealed that EP alleviated LPS-induced NR8383 cell glycolysis and M1 polarization. Further studies found that EP enhanced the effect of 2-DG on NR8383 cell glycolysis and M1 polarization. More importantly, PKM2 inhibitor alleviated LPS-induced NR8383 cell glycolysis and M1 polarization. In addition, EP alleviated LPS-induced NR8383 cell glycolysis and M1 polarization by targeting PKM2.</p><p><strong>Conclusion: </strong>It is suggested that EP alleviates LPS-induced glycolysis and M1 polarization in NR8383 cells by regulating PKM2, thereby alleviating lung injury, suggesting the involvment of alveolar macrophage polarization and glycolysis in the role of EP in asthma.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"13 5","pages":"tfae166"},"PeriodicalIF":2.2,"publicationDate":"2024-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11465183/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142453738","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}
引用次数: 0
Cytotoxicity induced by three commercial neonicotinoid insecticide formulations in differentiated human neuroblastoma SH-SY5Y cells. 三种商用新烟碱类杀虫剂制剂在分化的人神经母细胞瘤 SH-SY5Y 细胞中诱导的细胞毒性。
IF 2.2 4区 医学
Toxicology Research Pub Date : 2024-10-10 eCollection Date: 2024-10-01 DOI: 10.1093/toxres/tfae171
Karol Ferreira Honatel, Aline Mocellin Conte, Solange Cristina Garcia, Bruno Dutra Arbo, Marcelo Dutra Arbo
{"title":"Cytotoxicity induced by three commercial neonicotinoid insecticide formulations in differentiated human neuroblastoma SH-SY5Y cells.","authors":"Karol Ferreira Honatel, Aline Mocellin Conte, Solange Cristina Garcia, Bruno Dutra Arbo, Marcelo Dutra Arbo","doi":"10.1093/toxres/tfae171","DOIUrl":"https://doi.org/10.1093/toxres/tfae171","url":null,"abstract":"<p><strong>Background: </strong>Neonicotinoid insecticides are used worldwide for crop protection. They act as agonists at postsynaptic nicotinic acetylcholine receptors (nAChRs), disrupting normal neurotransmission in target insects. Human exposure is high due to the widespread use of neonicotinoids and their residues in food. This study aimed to evaluate the in vitro neurotoxicity of three neonicotinoid commercial formulations Much 600 FS® (imidacloprid 600 g L<sup>-1</sup>), Evidence 700 WG® (imidacloprid 700 g kg<sup>-1</sup>), and Actara 250 WG® (thiamethoxam 250 g kg<sup>-1</sup>) in differentiated human neuroblastoma SH-SY5Y cell line.</p><p><strong>Methods: </strong>Cells were incubated with the pesticides for 96 h, and the cytotoxicity was evaluated through the 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium·bromide (MTT) reduction and neutral red (NR) uptake assays. Toxicological pathways such as reactive oxygen (ROS) and nitrogen species (RNS) production, mitochondrial membrane potential, cell death mode, and the expression of the pro-apoptotic protein Bax were also evaluated.</p><p><strong>Results: </strong>EC<sub>50</sub> values of 266.4, 4,175, and 653.2 mg L<sup>-1</sup> were found for Much®, Evidence® and Actara®, respectively. Significant increases in ROS and RNS generation were observed for all pesticides, while mitochondrial membrane potential and Bax protein expression showed no significant changes. Analysis of cell death mode revealed an increase in early apoptotic cells.</p><p><strong>Conclusion: </strong>Therefore, neonicotinoid insecticides are potentially neurotoxic, reinforcing concerns about human exposure to these commercial formulations.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"13 5","pages":"tfae171"},"PeriodicalIF":2.2,"publicationDate":"2024-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11464667/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142453736","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}
引用次数: 0
Repeated radon exposure induced ATM kinase-mediated DNA damage response and protective autophagy in mice and human bronchial epithelial cells. 反复氡照射诱导小鼠和人类支气管上皮细胞发生 ATM 激酶介导的 DNA 损伤反应和保护性自噬。
IF 2.2 4区 医学
Toxicology Research Pub Date : 2024-10-07 eCollection Date: 2024-10-01 DOI: 10.1093/toxres/tfae165
Xiaoyu Chen, Shan Shan, Aiqing Wang, Cheng Tu, Jianmei Wan, Chengjiao Hong, Xiaohan Li, Xueying Wang, Jieyun Yin, Jian Tong, Hailin Tian, Lili Xin
{"title":"Repeated radon exposure induced ATM kinase-mediated DNA damage response and protective autophagy in mice and human bronchial epithelial cells.","authors":"Xiaoyu Chen, Shan Shan, Aiqing Wang, Cheng Tu, Jianmei Wan, Chengjiao Hong, Xiaohan Li, Xueying Wang, Jieyun Yin, Jian Tong, Hailin Tian, Lili Xin","doi":"10.1093/toxres/tfae165","DOIUrl":"https://doi.org/10.1093/toxres/tfae165","url":null,"abstract":"<p><strong>Objective: </strong>Radon ( <sup><b>222</b></sup> Rn) is a naturally occurring radioactive gas that has been closely linked with the development of lung cancer. In this study, we investigated the radon-induced DNA strand breaks, a critical event in lung carcinogenesis, and the corresponding DNA damage response (DDR) in mice and human bronchial epithelial (BEAS-2B) cells.</p><p><strong>Methods: </strong>Biomarkers of DNA double-strand breaks (DSBs), DNA repair response to DSBs, ataxia-telangiectasia mutated (ATM) kinase, autophagy, and a cell apoptosis signaling pathway as well as cell-cycle arrest and the rate of apoptosis were determined in mouse lung and BEAS-2B cells after radon exposure.</p><p><strong>Results: </strong>Repeated radon exposure induced DSBs indicated by the increasing expressions of γ-Histone 2AX (H2AX) protein and <i>H2AX</i> gene in a time and dose-dependent manner. Additionally, a panel of ATM-dependent repair cascades [i.e. non-homologous DNA end joining (NHEJ), cell-cycle arrest and the p38 mitogen activated protein kinase (p38MAPK)/Bax apoptosis signaling pathway] as well as the autophagy process were activated. Inhibition of autophagy by 3-methyladenine pre-treatment partially reversed the expression of NHEJ-related genes induced by radon exposure in BEAS-2B cells.</p><p><strong>Conclusions: </strong>The findings demonstrated that long-term exposure to radon gas induced DNA lesions in the form of DSBs and a series of ATM-dependent DDR pathways. Activation of the ATM-mediated autophagy may provide a protective and pro-survival effect on radon-induced DSBs.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"13 5","pages":"tfae165"},"PeriodicalIF":2.2,"publicationDate":"2024-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11457374/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142386487","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}
引用次数: 0
Proteomic analysis of toxic effects of short-term cadmium exposure on goat livers. 短期镉暴露对山羊肝脏毒性效应的蛋白质组分析
IF 2.2 4区 医学
Toxicology Research Pub Date : 2024-10-07 eCollection Date: 2024-10-01 DOI: 10.1093/toxres/tfae162
Guangyang Liu, Xiaoyun Shen, Yuanfeng Li
{"title":"Proteomic analysis of toxic effects of short-term cadmium exposure on goat livers.","authors":"Guangyang Liu, Xiaoyun Shen, Yuanfeng Li","doi":"10.1093/toxres/tfae162","DOIUrl":"https://doi.org/10.1093/toxres/tfae162","url":null,"abstract":"<p><p>Food safety is closely related to environmental pollution. It is worth noting that the long-term accumulation of Cd, a toxic heavy metal, in animals may pose a threat to human health through food chain. Previous studies have found that Cd exposure may cause liver metabolic disorders of black goats, but the mechanism of its impact on liver proteome of goats has not been widely studied. Therefore, in this study, ten male goats (Nubian black goat × native black goat) were exposed to Cd via drinking water containing CdCl2 (20 mg Cd·kg - 1·BW) for 30 days (five male goats per group). Blood physiology and liver antioxidant indices in black goats were determined and differentially expressed proteins (DEPs) in the livers of Cd-exposed goats were profiled by using TMT-labelled proteomics. It was found that plasma Hb and RBC levels as well as PCV values were decreased, liver SOD, GSH-Px, T-AOC and CAT levels were decreased, and MDA level was increased in Cd-treated goats, and 630 DEPs (up 326, down 304) in the livers of Cd-treated goats. Proteomics analysis revealed that Cd exposure affected glutathione metabolism and drug metabolism-cytochrome P450. We identified GP×2, GSTM3, and TBXAS1 as potential protein markers of early Cd toxicity in goats. This study provided theoretical basis for early diagnosis of Cd poisoning in goats.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"13 5","pages":"tfae162"},"PeriodicalIF":2.2,"publicationDate":"2024-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11457375/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142386486","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}
引用次数: 0
Serum glucose/potassium ratio as an indicator of early and delayed outcomes of acute carbon monoxide poisoning. 血清葡萄糖/钾比率作为急性一氧化碳中毒早期和延迟预后的指标。
IF 2.2 4区 医学
Toxicology Research Pub Date : 2024-10-07 eCollection Date: 2024-10-01 DOI: 10.1093/toxres/tfae168
Alshaimma Mahmoud Elmansy, Dalia Mustafa Hannora, Heba K Khalifa
{"title":"Serum glucose/potassium ratio as an indicator of early and delayed outcomes of acute carbon monoxide poisoning.","authors":"Alshaimma Mahmoud Elmansy, Dalia Mustafa Hannora, Heba K Khalifa","doi":"10.1093/toxres/tfae168","DOIUrl":"https://doi.org/10.1093/toxres/tfae168","url":null,"abstract":"<p><strong>Background: </strong>Carbon monoxide (CO) poisoning is a major health problem associated with a high rate of severe morbidity and mortality.</p><p><strong>Aims: </strong>This study aimed to evaluate the validity of the serum glucose/potassium (Glu/K) ratio as a quick predictor of both early and delayed unfavorable outcomes following acute CO poisoning.</p><p><strong>Patients and methods: </strong>This prospective cohort study included 136 patients with acute CO poisoning admitted at Tanta Poison Control Center, Egypt, between January 2023 and June 2024. The serum Glu/K ratio was calculated for all patients. The primary outcome was a prediction of mortality. Secondary outcomes were the prediction of delayed neurological sequelae (DNS) within six months after CO exposure, the need for mechanical ventilation, and the need for hyperbaric oxygen. A receiver operating curve analysis was applied to test the performance of the Glu/K ratio in predicting acute CO poisoning outcomes.</p><p><strong>Results: </strong>The mortality rate was 12.5% of patients with acute CO poisoning. Meanwhile, 14.7% of patients developed DNS. Furthermore, mechanical ventilation was required in 16.9% of patients. An elevated Glu/K ratio was significantly associated with the severity of acute CO poisoning. At a cut-off value of >31.62, the Glu/K ratio demonstrated an AUC of 0.649 for predicting mortality. The Glu/K ratio was employed to predict DNS at a cut-off value of 33.10, with a sensitivity of 60.0%, a specificity of 82.76%, and an AUC of 0.692.</p><p><strong>Conclusions: </strong>Early Glu/K ratio may be an effective, reliable, and convenient laboratory predictor of mortality, DNS, and the need for mechanical ventilation in patients with acute CO poisoning.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"13 5","pages":"tfae168"},"PeriodicalIF":2.2,"publicationDate":"2024-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11457236/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142386488","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}
引用次数: 0
"Exploring therapeutic potential and toxicological profiles of Cuscuta species: insights from pharmacological studies and an anti-cholinergic toxicity report." "探索菟丝子的治疗潜力和毒理学特征:药理学研究的启示和抗胆碱能毒性报告"。
IF 2.2 4区 医学
Toxicology Research Pub Date : 2024-10-03 eCollection Date: 2024-10-01 DOI: 10.1093/toxres/tfae160
Saurabh Dilip Bhandare
{"title":"\"Exploring therapeutic potential and toxicological profiles of <i>Cuscuta</i> species: insights from pharmacological studies and an anti-cholinergic toxicity report.\"","authors":"Saurabh Dilip Bhandare","doi":"10.1093/toxres/tfae160","DOIUrl":"10.1093/toxres/tfae160","url":null,"abstract":"<p><p>This study examines the therapeutic potential and toxicological profiles of <i>Cuscuta</i> species based on recent pharmacological investigations: \"a therapeutic potential vs. toxicological risks of <i>Cuscuta</i> species: a pharmacological-toxicology dilemma.\" The study encompasses diverse research areas, including the mitigation of Bisphenol A (BPA)-induced ovarian damage using <i>Cuscuta chinensis</i> flavonoids (CCFs), acute and sub-acute toxicity assessments of <i>Cuscuta chinensis Lam.</i> water extract (CLW), and observations on <i>Cuscuta campestris</i> toxicity in horses. In addition, this scientific study discusses the interplant communication dynamics between soybean and the parasitic dodder (<i>Cuscuta australis</i>) under nutrient deficiency conditions. Key significant findings highlight the efficacy of CCFs in alleviating BPA-induced ovarian damage, the safety profile of CLW within specified doses, and clinical manifestations of <i>C. campestris</i> toxicity in horses. Moreover, insights into interplant communication mechanisms emphasise the significance of protein-mediated interactions in nutrient-deficient environments. The report illustrates the potential toxicity of Dodder in humans, and further research findings into its chemical composition and toxicological profiles reveal great data on its phytotoxicity. Greater awareness and understanding of the risks associated with consuming Dodder and other similar plant species are crucial for preventing plant intoxication and have been a significant major focus of the present toxicology study of <i>Cuscuta</i> species. Hence, by addressing these objectives, the scientific study aims to balance the therapeutic benefits of Cuscuta species with their potential toxicological risks, contributing to a more nuanced understanding of their role in pharmacology and toxicology. This dual focus is crucial for guiding future research and informing safe usage practices.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"13 5","pages":"tfae160"},"PeriodicalIF":2.2,"publicationDate":"2024-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11447373/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142379551","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}
引用次数: 0
Impacts of gentamycin toxicity: nephroprotective role of guarana through different signaling pathways. 庆大霉素毒性的影响:瓜拉纳纳通过不同信号通路发挥肾保护作用
IF 2.2 4区 医学
Toxicology Research Pub Date : 2024-10-03 eCollection Date: 2024-10-01 DOI: 10.1093/toxres/tfae167
Adel Qlayel Alkhedaide
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