Human & experimental toxicology最新文献

Human & experimental toxicology Pub Date : 2025-01-01 DOI: 10.1177/09603271241310364

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Conflicts of interest in the International Agency for Research on Cancer process of identifying carcinogenic hazards to humans.

Human & experimental toxicology Pub Date : 2025-01-01 DOI: 10.1177/09603271241269020

Susan A Elmore, Colin Berry, Brad Bolon, Gary A Boorman, Alys E Bradley, Samuel M Cohen, James E Klaunig, Felix M Kluxen, Robert R Maronpot, Abraham Nyska, Tracey L Papenfuss, Jerold E Rehg, David B Resnik, Ivonne McM Rietjens, Thomas J Rosol, Andrew W Suttie, Trenton R Schoeb, Christian Strupp, Bob Thoolen, Klaus Weber

{"title":"Conflicts of interest in the International Agency for Research on Cancer process of identifying carcinogenic hazards to humans.","authors":"Susan A Elmore, Colin Berry, Brad Bolon, Gary A Boorman, Alys E Bradley, Samuel M Cohen, James E Klaunig, Felix M Kluxen, Robert R Maronpot, Abraham Nyska, Tracey L Papenfuss, Jerold E Rehg, David B Resnik, Ivonne McM Rietjens, Thomas J Rosol, Andrew W Suttie, Trenton R Schoeb, Christian Strupp, Bob Thoolen, Klaus Weber","doi":"10.1177/09603271241269020","DOIUrl":"https://doi.org/10.1177/09603271241269020","url":null,"abstract":"Managing conflicts of interest (COIs) in scientific decision-making is important for minimizing bias and fostering public trust in science. Proper management of COIs has added significance when scientists are making decisions that impact public policy, such as assessing substances for carcinogenicity. The International Agency for Research on Cancer (IARC) organizes expert working groups to identify putative carcinogens and determine whether or not the hazard is likely to present significant potential harm to humans. While IARC has policies for managing COIs, prior professional experience with the substance being assessed is not defined as a COI. Indeed, IARC working group members are chosen based on subject matter expertise, including prior publication on the substance under review. However, a person's prior experience with a substance poses a significant potential COI by equipping them with strong pre-existing views about the substance's toxicity and carcinogenicity. To minimize the risk of bias in IARC working groups, participants with voting powers should be independent scientific experts with sufficient professional experience to review carcinogenicity data but with no substantial prior experience with the substance under review. A related IARC practice restricting data review by working groups to selected publications is another significant COI. Instead, all accessible data should be available for consideration by working groups in assessing the carcinogenic hazard of substances. Another recommendation to reduce potential bias would be to reinstate the option of \"probably not carcinogenic to humans\".","PeriodicalId":94029,"journal":{"name":"Human & experimental toxicology","volume":"44 ","pages":"9603271241269020"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143070406","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Down-regulation of E2F1 attenuates UVB-induced human lens epithelial cell oxidative stress and pyroptosis through inhibiting NLRP3. 下调E2F1通过抑制NLRP3减弱uvb诱导的人晶状体上皮细胞氧化应激和焦亡。

Human & experimental toxicology Pub Date : 2025-01-01 DOI: 10.1177/09603271241309258

Fang Wang, Fan Yang, Guiqi Yang, Qi Zhou, Hongbin Lv

{"title":"Down-regulation of E2F1 attenuates UVB-induced human lens epithelial cell oxidative stress and pyroptosis through inhibiting NLRP3.","authors":"Fang Wang, Fan Yang, Guiqi Yang, Qi Zhou, Hongbin Lv","doi":"10.1177/09603271241309258","DOIUrl":"https://doi.org/10.1177/09603271241309258","url":null,"abstract":"Background: It is well-known that ultraviolet B (UVB) causes cataracts by inducing pyroptosis and the production of reactive oxygen species (ROS) in human lens epithelial cells (HLECs). The transcription factor E2F1 (E2F1) serves as a positive regulator of disrupted pathways involved in histone modification and cell cycle regulation. However, its function in UVB-treated HLECs remains unknown.Purpose: This study aims to investigate the function of E2F1 in UVB-treated HLECs, with a particular focus on its interaction with NLRP3 and its impact on oxidative stress and pyroptosis. Research Design: HLECs were irradiated with UVB, and cell damage was assessed using CCK-8, ROS, and pyroptosis detection. The interaction between E2F1 and NLRP3 was confirmed using Chromatin immunoprecipitation (ChIP)-qPCR and dual-luciferase reporter assays.Study Sample: The study was conducted using UVB-treated HLECs.Data collection and/or analysis: Collected data were statistically analyzed using one-way analysis of variance (ANOVA).Results: Our results show that HLECs were much more susceptible to oxidative stress, pyroptosis, and E2F1 in response to UVB-irradiation, but that E2F1 down-regulation effectively counteracted these effects. E2F1 was then suggested as a potential NLRP3 transcription factor by bioinformatics studies. At the same time, luciferase and CHIP assays showed that E2F1 could bind to the NLRP3 promoter and enhance NLRP3 transcription. In addition, the protective effects of si-E2F1 against oxidative stress and pyroptosis in HLECs are counteracted by overexpressing NLRP3.Conclusions: All of the above provided the possibility to demonstrate that E2F1 plays a crucial role in regulating oxidative stress and pyroptosis in UVB-induced HLECs through inhibiting NLRP3, and it promotes oxidative stress-induced pyroptosis by suppressing NLRP3 expression.","PeriodicalId":94029,"journal":{"name":"Human & experimental toxicology","volume":"44 ","pages":"9603271241309258"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142934227","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Ginsenoside Re suppresses high glucose-induced apoptosis of placental trophoblasts through endoplasmic reticulum stress-related CHOP/GADD153. 人参皂苷Re通过内质网应激相关的CHOP/GADD153抑制高糖诱导的胎盘滋养细胞凋亡。

Human & experimental toxicology Pub Date : 2025-01-01 DOI: 10.1177/09603271241307835

Guihong Zeng, Weiyang Zou, Changdi Liu, Yulan Chen, Tingmei Wen

{"title":"Ginsenoside Re suppresses high glucose-induced apoptosis of placental trophoblasts through endoplasmic reticulum stress-related CHOP/GADD153.","authors":"Guihong Zeng, Weiyang Zou, Changdi Liu, Yulan Chen, Tingmei Wen","doi":"10.1177/09603271241307835","DOIUrl":"https://doi.org/10.1177/09603271241307835","url":null,"abstract":"Background: Gestational diabetes mellitus (GDM) is a metabolic disorder that arises during pregnancy and heightens the risk of placental dysplasia. Ginsenoside Re (Re) may stabilize insulin and glucagon to regulate glucose levels, which may improve diabetes-associated diseases. Purpose: This study aims to investigate the mechanism of Re in high glucose (HG)-induced apoptosis of trophoblasts through endoplasmic reticulum stress (ERS)-related protein CHOP/GADD153. Research Design: Human trophoblast cells HTR-8/SVneo were treated with HG to simulate the HG environment in vitro, while normal glucose (NG) was used as the control. Study Sample: NG (5 mM) or HG (25 mM)-cultured HTR-8/SVneo cells were treated with 10, 20 or 40 μM Re. HG-cultured cells were treated with 5 mM ERS inducer 2-Deoxy-D-glucose (2-DG) and transfected with oe- CHO. Data Collection and/or Analysis: Cell viability and apoptosis were detected by CCK-8 and flow cytometry; LDH release, superoxide dismutase (SOD), malonaldehyde (MDA) and glutathione (GSH) levels were detected using kits; the apoptosisrelated proteins and ERS-related proteins were assessed by western blot. Results: Re (10, 20 or 40 μM) had no significant effect on NG-treated HTR-8/SVneo cell viability. Re (20 or 40 μM) could enhance the viability of HG-treated trophoblasts. Re (40 μM) inhibited apoptosis of HGtreated trophoblasts, ERS and alleviated oxidative stress evidenced by suppressed phosphorylation of PERK, IRE1α, reduced protein expression of ATF6, CHOP/GADD153, and inhibited MDA accumulation, GSH and SOD loss. ERS activation or CHOP/GADD153 overexpression reversed Re's inhibition on HG-induced apoptosis of trophoblasts. Conclusions: Re repressed HG-induced placental trophoblast apoptosis by mediating ERS-related protein CHOP/GADD153.","PeriodicalId":94029,"journal":{"name":"Human & experimental toxicology","volume":"44 ","pages":"9603271241307835"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142967656","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

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Thanks to Reviewers.

Human & experimental toxicology Pub Date : 2025-01-01 DOI: 10.1177/09603271251315241

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Nomogram for predicting mechanical ventilation need among acutely intoxicated patients with impaired consciousness: Correspondence. 预测意识障碍的急性中毒患者机械通气需求的提名图：通讯。

Human & experimental toxicology Pub Date : 2024-01-01 DOI: 10.1177/09603271241285992

Hineptch Daungsupawong, Viroj Wiwanitkit

引用次数: 0

Performance assessment of new Poisoning Mortality Score and PGI score for predicting mortality in patients with acute aluminum phosphide poisoning. 预测急性磷化铝中毒患者死亡率的新中毒死亡率评分和 PGI 评分的性能评估。

Human & experimental toxicology Pub Date : 2024-01-01 DOI: 10.1177/09603271241302208

Ghada N El-Sarnagawy, Amira A Abdelnoor, Mona M Ghonem

{"title":"Performance assessment of new Poisoning Mortality Score and PGI score for predicting mortality in patients with acute aluminum phosphide poisoning.","authors":"Ghada N El-Sarnagawy, Amira A Abdelnoor, Mona M Ghonem","doi":"10.1177/09603271241302208","DOIUrl":"https://doi.org/10.1177/09603271241302208","url":null,"abstract":"Background: Until now, no definite standardized method has been used to promptly assess the severity and outcome of acute aluminum phosphide (ALP) poisoning. The current study aimed to evaluate the performance of the new Poisoning Mortality Score (PMS) and PGI score for predicting mortality in acute ALP-poisoned patients, highlighting the accuracy of new PMS components.Patients and methods: A 2-year cross-sectional study was conducted on ALP-poisoned patients admitted to Tanta University Poison Control Centre from April 2021 to March 2023. Socio-demographics, poisoning data, and initial vital signs were recorded. Additionally, new PMS and PGI scores were calculated on admission. Patients were categorized according to the mortality outcome into survivors and nonsurvivors.Results: Out of 160 included ALP poisoned patients, mortality was recorded in 112 (70%) patients. The nonsurvivors had significantly higher median PGI and new PMS values than survivors. New PMS, vital signs component of new PMS, and PGI conveyed good discriminatory power for predicting mortality (AUC = 0.883, 0.873, and 0.817, respectively). Although the new PMS outperformed PGI in all predictive metrics, no significant difference in AUCs was observed between the new PMS and its vital signs component.Conclusion: The new PMS vital signs component is closely aligned with the new PMS. Thus, it can be used as a valid, comprehensive, and practical tool to substitute the whole score calculation for rapid ALP-poisoned patient assessment to enhance emergency clinical decision-making.","PeriodicalId":94029,"journal":{"name":"Human & experimental toxicology","volume":"43 ","pages":"9603271241302208"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142678159","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Outbreaks of mushroom poisoning associated with acute kidney injury. 与急性肾损伤相关的蘑菇中毒爆发。

Human & experimental toxicology Pub Date : 2024-01-01 DOI: 10.1177/09603271241304368

Zelal Adibelli, Hayrunisa Bas Sermenli, Ziynet Alphan Uc

{"title":"Outbreaks of mushroom poisoning associated with acute kidney injury.","authors":"Zelal Adibelli, Hayrunisa Bas Sermenli, Ziynet Alphan Uc","doi":"10.1177/09603271241304368","DOIUrl":"https://doi.org/10.1177/09603271241304368","url":null,"abstract":"Introduction: The outbreak of acute kidney injury (AKI) due to mushroom poisoning is not a frequently encountered medical challenge. Herein, we present 13 mushroom poisoning cases associated with AKI related to Amanita Proxima (A. Proxima) causing poisoning reported in a short time period in Turkey.Methods: A total of 13 patients with AKI due to mushroom poisoning admitted to Usak Research and Training Hospital between November and December 2020 were included. Under morphological and microscopical investigations of mushroom specimens (from three patients), the species of the mushrooms were identified.Results: The median age of 13 patients presenting with AKI due to mushroom poisoning was 55 (ranging between 19 and 72 years), and 60.4% were males. Nausea and vomiting were the first symptoms in most patients and appeared at a mean time of 12.8 ± 7.6 h after ingesting mushrooms. Mean serum creatinine on admission was 7.2 ± 3.8 mg/dL. Kidney replacement therapy (KRT) was administered to all patients, and mortality occurred in two due to sepsis and heart failure (HF). Species of the mushroom specimens obtained from three patients were identified as A. Proxima, a rarely encountered type of mushroom. A. Proxima has a considerable similarity to a common and edible species specific to the Mediterranean Basin, known as A. Ovoidea.Discussion: Based on our findings, we emphasize the consideration of nephrotoxic mushrooms of the genus Amanita in the evaluation of mushroom poisoning cases, as well as the efforts needed to increase public awareness regarding the risk of fatal outcomes of consuming wild mushrooms.","PeriodicalId":94029,"journal":{"name":"Human & experimental toxicology","volume":"43 ","pages":"9603271241304368"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142718084","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Persistent diazinon induced neurotoxicity: The effect on inhibitory avoidance memory performance, amyloid precursor proteins, and TNF-α levels in the prefrontal cortex of rats. 持续性二嗪农诱导的神经毒性：对大鼠前额叶皮层抑制性回避记忆能力、淀粉样前体蛋白和 TNF-α 水平的影响

Human & experimental toxicology Pub Date : 2024-01-01 DOI: 10.1177/09603271241235408

Salva Afshari, Mehdi Sarailoo, Vahid Asghariazar, Elham Safarzadeh, Masoomeh Dadkhah

{"title":"Persistent diazinon induced neurotoxicity: The effect on inhibitory avoidance memory performance, amyloid precursor proteins, and TNF-α levels in the prefrontal cortex of rats.","authors":"Salva Afshari, Mehdi Sarailoo, Vahid Asghariazar, Elham Safarzadeh, Masoomeh Dadkhah","doi":"10.1177/09603271241235408","DOIUrl":"10.1177/09603271241235408","url":null,"abstract":"Introduction: Organophosphate pesticides (Ops) like diazinon (DZN) have well-known neurotoxic effects and low-level chronic exposure has been linked to detrimental neurobehavioral impairments and memory deficits. However, it's not entirely clear how DZN-induced biological changes, particularly in the prefrontal cortex (PFC) contribute to these effects. The purpose of this study is to investigate the impact of DZN exposure on inhibitory avoidance (IA) memory function, amyloid precursor expression (APP), and proinflammatory tumor necrosis factor-α (TNF-α) levels in the rat cortex.Materials and methods: Rats were divided into 4 groups and recived 2 mg/kg DZN for 5-days or 12-weeks and two control groups recived the same volume of vehicle. IA memory was assesed using the shuttle box apparatus. Rats were sacrificed and the prefrontal cortex PFC were removed. Real-time PCR and Western blotting were used to messure TNF-α, and amyloid protein precursors gene expression and protein levels.Results: Our findings indicated that DZN caused body weight loss and a notable decline in performance on the IA memory. Additionally, 5-days exposure increased APP and APLP2 protein levels in the PFC, while 12-weeks exposure decreased these levels. Furthermore, expression of APP and APLP2 gens were decreased in PFC. TNF-α levels increased as a result of 5-days exposure to DZN, but these levels dropped to normal after 12-weeks administration, and this observation was significant.Conclusion: Taken together, exposure to low doses of DZN leads to disturbances in IA memory performance and also alternations in amyloid beta precursors that can be related to increased risk of Alzheimer's disease.","PeriodicalId":94029,"journal":{"name":"Human & experimental toxicology","volume":"43 ","pages":"9603271241235408"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140112517","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

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Unveiling thioacetamide-induced toxicity: Multi-organ damage and omitted bone toxicity. 揭示硫代乙酰胺诱导的毒性：多器官损伤和遗漏的骨毒性。

Human & experimental toxicology Pub Date : 2024-01-01 DOI: 10.1177/09603271241241807

Haodong Zhang, Jian Xu

{"title":"Unveiling thioacetamide-induced toxicity: Multi-organ damage and omitted bone toxicity.","authors":"Haodong Zhang, Jian Xu","doi":"10.1177/09603271241241807","DOIUrl":"10.1177/09603271241241807","url":null,"abstract":"Thioacetamide (TAA), a widely employed hepatotoxic substance, has gained significant traction in the induction of liver failure disease models. Upon administration of TAA to experimental animals, the production of potent oxidative derivatives ensues, culminating in the activation of oxidative stress and subsequent infliction of severe damage upon multiple organs via dissemination through the bloodstream. This review summarized the various organ damages and corresponding mechanistic explanations observed in previous studies using TAA in toxicological animal experiments. The principal pathological consequences arising from TAA exposure encompass oxidative stress, inflammation, lipid peroxidation, fibrosis, apoptosis induction, DNA damage, and osteoclast formation. Recent in vivo and in vitro studies on TAA bone toxicity have confirmed that long-term high-dose use of TAA not only induces liver damage in experimental animals but also accompanies bone damage, which was neglected for a long time. By using TAA to model diseases in experimental animals and controlling TAA dosage, duration of use, and animal exposure environment, we can induce various organ injury models. It should be noted that TAA-induced injuries have a time-dependent effect. Finally, in our daily lives, especially for researchers, we should take precautions to minimize TAA exposure and reduce the probability of related organ injuries.","PeriodicalId":94029,"journal":{"name":"Human & experimental toxicology","volume":"43 ","pages":"9603271241241807"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140295674","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0