Toxicology Mechanisms and Methods最新文献

{"title":"Investigation of Some Metal Levels in People Using Electronic Cigarettes and IQOS.","authors":"Yunus Yüce, Benay Can Eke","doi":"10.1080/15376516.2025.2506796","DOIUrl":"https://doi.org/10.1080/15376516.2025.2506796","url":null,"abstract":"<p><strong>Objectives: </strong>There has been a sharp increase in the use of e-cigarettes and heated tobacco products (HTPs) in the last decade. Related to the increase in the use, serious public health debates have been caused by the safety and risks of these products. Particularly due to the exposure to a lot of toxic substances, including heavy metals, there has been an increasing concern over their health effects. Heavy metals such as lead, arsenic, mercury, and cadmium are environmental pollutants poising significant health risks. These metals have a disposition to accumulate in a human body in time. Even at lower levels of exposure, they might lead to multiple organ damage and adverse health effects, including neurotoxicity, nephrotoxicity, and being carcinogenicity.This study tests the idea that using electronic cigarettes (e-cigarettes) and IQOS devices raises the levels of metals in urine and that the amount of increase depends on which product is used. The study aims to look at the levels of lead, cadmium, nickel, zinc, and selenium in the urine of cigarette smokers, e-cigarette users, IQOS users, and non-smokers; to check for significant differences in metal levels between these groups (with a significance level set at p < 0.05); to compare the metal levels found with safety limits; and to explore if there's a link between the metal levels in urine and the type of product used (cigarettes, IQOS, or e-cigarettes).</p><p><strong>Method: </strong>This study aimed to compare the trace element, heavy element, and nicotine exposures of individuals who smoke (n = 39), use e-cigarettes (n = 28), use IQOS (n = 20), and do not use tobacco or tobacco products (n = 30) while living in Ankara, Türkiye. In order to evaluate the element levels of the participants, the levels of lead, cadmium, nickel, zinc, and selenium metals in their urine were determined using inductively coupled plasma mass spectrometry (ICP-MS), and nicotine exposures were determined using liquid chromatography-tandem mass spectrometry (LC-MS/MS).</p><p><strong>Results: </strong>The measurement showed that lead levels were higher in IQOS users (8.51 ng/g creatinine) and smokers (3.67 ng/g creatinine) compared to e-cigarette users (1.38 ng/g creatinine), and this difference was statistically significant (p < 0.05). In addition, a statistically significant difference was found between the cotinine level and lead level of the smoking and IQOS groups (p ˂ 0.05). No statistically significant difference was found between the groups in terms of cadmium level (p > 0.008). Nickel level was found to be higher in e-cigarette (3.43 ng/g creatinine) and IQOS (3.85 ng/g creatinine) users than in the smoking group (1 ng/g creatinine). In terms of nickel, a statistically significant difference was found between the e-cigarette and IQOS groups and both the smoking and control groups (p ˂ 0.05). No statistically significant difference was found between the selenium level and both the groups and t","PeriodicalId":23177,"journal":{"name":"Toxicology Mechanisms and Methods","volume":" ","pages":"1-26"},"PeriodicalIF":3.2,"publicationDate":"2025-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144080495","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The possible mechanisms of trans fatty acid effects on digestive disorders based on computational toxicology: a case study of elaidic acid.","authors":"Chenyang Yu, Fule Wang, Xinfang Zhang, Changchuan Bai, Guanhua Lv","doi":"10.1080/15376516.2025.2503873","DOIUrl":"10.1080/15376516.2025.2503873","url":null,"abstract":"<p><p>Trans fatty acids (TFAs) are potential health risk factors generated during food processing, and their mechanisms of association with digestive diseases remain incompletely elucidated. This study focused on elaidic acid (EA), integrating computational toxicology and molecular docking to systematically analyze its molecular mechanisms in regulating functional dyspepsia (FD), gastric cancer (GC), nonalcoholic fatty liver disease (NAFLD), and colorectal cancer (CRC) through multi-target networks. Protein Interaction Networks were constructed by screening EA and disease-intersecting targets, enriching and analyzing key pathways, and validating the binding ability of core targets. Results showed that EA shared 22, 67, 56, and 72 common targets with FD, GC, NAFLD, and CRC, respectively. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analyses indicated that EA acts through pathways including lipid metabolism dysregulation, inflammatory response, and chemical carcinogenesis-receptor activation. Molecular docking confirmed binding affinities between EA and core targets. The present study suggests that EA may promote the progression of digestive diseases through a multi-target-multi-pathway model, providing a new perspective for the study of the toxicity mechanism of TFA and food safety prevention and control.</p>","PeriodicalId":23177,"journal":{"name":"Toxicology Mechanisms and Methods","volume":" ","pages":"1-12"},"PeriodicalIF":3.2,"publicationDate":"2025-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144049980","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Temperature-dependent neuroprotective effects of acorn flour extract in SH-SY5Y cells against gliotoxin.","authors":"Raquel Penalva-Olcina, Giovanni Caprioli, Gianni Sagratini, Laura Acquaticci, Cristina Juan, Ana Juan-García","doi":"10.1080/15376516.2025.2500544","DOIUrl":"https://doi.org/10.1080/15376516.2025.2500544","url":null,"abstract":"<p><p>Gliotoxin (GTX) is a potent mycotoxin that has been shown to induce neurotoxicity through the generation of oxidative stress and disruption of cellular signaling, leading to neuronal cell damage. The neurotoxic effects of GTX have been implicated in various neurodegenerative conditions, making the search for protective agents crucial. This study investigates the chemoprotective effects of acorn flour extract (ACFE) at different temperatures (20 °C, 60 °C, 80 °C, and 100 °C) on SH-SY5Y cells exposed to GTX using both pretreatment and simultaneous treatment strategies (direct treatment, pretreatment and simultaneous treatment). Cell viability was assessed using the MTT assay after 24 and 48 h of exposure. ACFE exhibited varying cytoprotective effects depending on the temperature and exposure conditions. Pre- treatment with 100 °C significantly increased cell viability by up to 51.6% at low GTX concentrations after 48 h; however, ACFE at 60 °C and 80 °C also demonstrated notable protective effects in pretreatment, suggesting a broader range of effective temperatures. Similarly, simultaneous treatment with ACFE (20 °C and 60 °C) enhanced cell viability by up to 124.7% at specific GTX concentrations. In general, higher extraction temperatures (80 °C and 100 °C) were associated with greater chemoprotective potential. These findings support the potential therapeutic application of ACFE in protecting against oxidative stress and neuronal damage, emphasizing the influence of extraction temperature and treatment timing on its efficacy. Further investigations are needed to explore the underlying molecular mechanisms involved in ACFE's protective effects.</p>","PeriodicalId":23177,"journal":{"name":"Toxicology Mechanisms and Methods","volume":" ","pages":"1-9"},"PeriodicalIF":3.2,"publicationDate":"2025-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144080524","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fucoxanthin Ameliorates PM_2.5-mediated Skin Cell Inflammation and Senescence.","authors":"Pincha Devage Sameera Madushan Fernando, Kyoung Ah Kang, Mei Jing Piao, Herath Mudiyanselage Udari Lakmini Herath, Herath Mudiyanselage Maheshika Madhuwanthi Senavirathna, Eui Tae Kim, Hee-Sun Kim, Sungwook Chae, Musun Park, Jin Won Hyun","doi":"10.1080/15376516.2025.2500545","DOIUrl":"https://doi.org/10.1080/15376516.2025.2500545","url":null,"abstract":"<p><p>Fucoxanthin is a naturally derived carotenoid in marine brown algae that has potential curative benefits for treating diseases such as cancer, diabetes, and obesity. Exposure to particulate matter with a diameter of ≤2.5 µm (PM_2.5) is associated with the occurrence of cardiac disorders, cancer, and senescence. The primary objective of this study was to determine the protective effects of fucoxanthin against PM_2.5-induced dysfunction of human HaCaT keratinocytes. Fucoxanthin decreased PM_2.5-induced production of reactive oxygen species and mitigated lipid peroxidation, DNA damage, and depolarization of the mitochondrial membrane potential_. Fucoxanthin inhibited PM_2.5-mediated activation of nuclear factor κB and Nod-like receptor family protein 3 inflammasome and the release of proinflammatory cytokines such as interleukin (IL)-1, IL-6, and cyclooxygenase-2. Additionally, fucoxanthin decreased dysfunctional cell proliferation and reversed the cell cycle arrest in the G₀/G₁ phase. Docking and network analyses revealed that fucoxanthin interacted with seven major proteins related to inflammation and senescence. Senescence-associated β-galactosidase and matrix metalloproteinases were downregulated by fucoxanthin following exposure to PM_2.5. Conclusively, fucoxanthin attenuates the cellular oxidative stress caused by PM_2.5 and suppresses inflammatory responses and senescence, thereby implying its potential in alleviating PM_2.5-induced skin damage.</p>","PeriodicalId":23177,"journal":{"name":"Toxicology Mechanisms and Methods","volume":" ","pages":"1-15"},"PeriodicalIF":3.2,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144062097","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inhalation safety and tolerability of a novel fixed-dose combination of glycopyrronium-vilanterol powder in Wistar rats.","authors":"Shitalkumar D Patel, Laxit K Bhatt, Jitendra H Patel, Piyush Patel, Virendrasinh M Zala, Ritu N Laddha, Rajesh Sundar, Mukul R Jain","doi":"10.1080/15376516.2025.2490953","DOIUrl":"https://doi.org/10.1080/15376516.2025.2490953","url":null,"abstract":"<p><p>Fixed-dose combinations (FDCs) offer therapeutic benefits like enhanced efficacy, reduced adverse effects, and better patient compliance, making them cost-effective. They are particularly effective in managing chronic obstructive pulmonary disease (COPD). Combining a long-acting muscarinic antagonist with a long-acting beta-agonist improves lung function, reduces the need for rescue bronchodilators, alleviates respiratory symptoms, and enhances the overall quality of life in COPD patients. This study evaluated the safety and tolerability of a novel FDC containing vilanterol, a selective β2-adrenoreceptor agonist, and glycopyrronium, an antimuscarinic agent, in Wistar rats. Vilanterol promotes bronchodilation, while glycopyrronium reduces bronchoconstriction. Repeated-dose toxicity testing at three dosage levels (6.25 + 12.5 mcg/kg/day, 12.5 + 25 mcg/kg/day, and 25 + 50 mcg/kg/day) through nose-only exposure showed that the FDC was well-tolerated, with no significant clinical signs of toxicity. Key parameters, including body weight, feed consumption, ophthalmic examination, clinical pathology, and bronchoalveolar lavage fluid analysis, showed no adverse effects. Minimal, non-dose-related microscopic lesions and normal alveolar macrophage responses were observed. The no-observed-adverse-effect level, based on actual concentration and duration of exposure, was established at 25 + 50 mcg/kg/day, indicating the FDC's safety and suitability for further development in COPD management.</p>","PeriodicalId":23177,"journal":{"name":"Toxicology Mechanisms and Methods","volume":" ","pages":"1-12"},"PeriodicalIF":3.2,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143983220","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Studies on the toxic effects of acute mercuric chloride poisoning in mice: primary toxicity evaluation analysis of HgCl₂.","authors":"Chenyu Zhao, Simin Jiang, Fan Jin, Lixiang Gu, Mingming Liang, Ying Zhao, Qin Han","doi":"10.1080/15376516.2025.2500547","DOIUrl":"https://doi.org/10.1080/15376516.2025.2500547","url":null,"abstract":"<p><p>The aim of this study was to explore the acute damage caused by acute mercuric chloride poisoning to mice. The mice model of acute mercury (HgCl₂) poisoning was prepared by gavage and intraperitoneal injection, respectively. The experimental results showed that the LD50 was about 24 mg/kg for gavage and 4 mg/kg for intraperitoneal injection. On the basis of gavage, there were differences in the time required for water maze and righting reflex tests between groups of mice gavaged with different doses of HgCl₂ (<i>p < 0.05</i>); The levels of SOD, MDA, GSH-PX, CRE, BUN, AST and ALT in mice were different from those in the control (Normal saline) group (<i>p < 0.05</i>); The degree of inflammation response under microscope was different in different dose groups after HE staining of liver tissues, and there were differences in the degree of intimal thickening and lumen stenosis in different dose groups after HE staining of kidney tissue; The inductively coupled plasma mass spectrometry (ICP-MS) measured the levels of mercury in mice increased with increasing mercuric chloride concentration, with the accumulation in kidney much higher than that in liver. Based on the results of the study, it was concluded that the damage caused by mercuric chloride to memory, oxidative stress, liver and kidney tissues in mice starts from 4 mg/kg, and the mortality rate of mice reached 100% when the gavage dose was greater than or equal to 32 mg/kg, and the intraperitoneal injection of mercuric chloride produced faster and stronger toxic effects than gavage.</p>","PeriodicalId":23177,"journal":{"name":"Toxicology Mechanisms and Methods","volume":" ","pages":"1-13"},"PeriodicalIF":3.2,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144038465","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neodymium nitrate promotes the apoptosis of mouse liver cells via Bcl2l1/Caspase 3 pathway.","authors":"Jing Leng, Ning Wang, Xiu-Li Chang, Xiao-Peng Zhang, Jing Xu, Zheng-Li Yang, Ke-Lei Qian, Zhi-Qing Zheng, Gong-Hua Tao, Xu-Dong Jia, Ping Xiao, Xin-Yu Hong","doi":"10.1080/15376516.2025.2501253","DOIUrl":"https://doi.org/10.1080/15376516.2025.2501253","url":null,"abstract":"<p><strong>Background: </strong>Neodymium, as a strategic rare earth element (REE), has demonstrated bioaccumulative potential and can permeate human systems through inhalation of airborne particulates, ingestion of contaminated food/water, and dermal absorption from soil matrices, ultimately eliciting multi-organ toxicological manifestations. However, the hepatotoxicological profile of neodymium species and their pathophysiological mechanisms remain inadequately characterized. Neodymium nitrate (Nd(NO₃)₃), the predominant water-soluble neodymium species, exhibits marked bioavailability with particular hepatic tropism.</p><p><strong>Objective: </strong>This study aims to investigate the effects of neodymium nitrate on apoptosis of mouse liver cells and its underlying molecular mechanisms.</p><p><strong>Results: </strong>Mouse liver cell line AML12 was treated with gradient concentrations of neodymium nitrate. The results showed that neodymium nitrate inhibited liver cell proliferation, induced apoptosis, and exhibited a dose-dependent relationship. Western blotting and quantitative real-time PCR (qRT-PCR) revealed that neodymium nitrate suppressed Bcl2l1 transcription and activated the proteolysis of Caspase 3. To further explore the molecular mechanism, Bcl2l1 protein was overexpressed in mouse liver cells. The findings indicated that overexpression of Bcl2l1 rescued neodymium nitrate-induced apoptotic phenotypes and attenuated Caspase 3 cleavage.</p><p><strong>Conclusion: </strong>The present data suggest that neodymium nitrate induces apoptosis of mouse liver cells through the Bcl2l1/Caspase 3 pathway. However, further studies are called for to substantiate this view, as the findings may provide critical mechanistic evidence for revising the toxicological risk assessment frameworks of rare earth elements.</p>","PeriodicalId":23177,"journal":{"name":"Toxicology Mechanisms and Methods","volume":" ","pages":"1-36"},"PeriodicalIF":3.2,"publicationDate":"2025-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144000390","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Diacerein counteracts amiodarone‑induced hepatotoxicity in rats via targeting TLR4/NF-kB/NLRP3 pathways.","authors":"Passant E Moustafa, Hadir Farouk, Marwa S Khattab, Salma A El-Marasy","doi":"10.1080/15376516.2025.2499024","DOIUrl":"https://doi.org/10.1080/15376516.2025.2499024","url":null,"abstract":"<p><p>This study investigates the protective effects of diacerein (DCN) against amiodarone (AMIO)-induced hepatotoxicity in a rat model. AMIO administration resulted in significant elevations of liver enzymes, ALT and AST, indicating hepatocellular membrane disruption and oxidative stress, as demonstrated by elevated levels of malondialdehyde (MDA) and decreased glutathione (GSH). Additionally, pro-inflammatory cytokines including TNF-α and IL-1β were expressed more when AMIO triggered the Toll-like receptor 4/nuclear factor kappa B/inflammasome 3 (TLR4/NF-κB/NLRP3) inflammatory pathway, along with elevated caspase-1 (CASP1) levels, which promoted apoptosis. In contrast, oral administration of DCN for two weeks effectively mitigated these effects by reducing liver enzyme levels and improving histopathological alterations. DCN also demonstrated anti-oxidant properties by decreasing MDA levels and increasing nuclear factor erythroid 2-related factor 2 (Nrf2) and GSH content. Furthermore, DCN downregulated the hepatic content of TLR4, NF-κB p65, NLRP3, CASP1, and pro-inflammatory cytokines, thereby inhibiting the activation of the inflammatory cascade. Moreover, DCN reduced protein expression of caspase 3. Those findings suggest that DCN exerts its hepatoprotective effects through its anti-oxidant activity, modulation of TLR4/NF-κB/NLRP3 inflammatory pathways, and reduction of apoptosis. These results provide new insights into potential therapeutic strategies for managing AMIO-induced hepatotoxicity, warranting further investigation into the underlying molecular mechanisms of DCN's protective effects.</p>","PeriodicalId":23177,"journal":{"name":"Toxicology Mechanisms and Methods","volume":" ","pages":"1-13"},"PeriodicalIF":3.2,"publicationDate":"2025-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144038482","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of Micro- and Nanoplastic Exposure on Macrophages: A Review of Molecular and Cellular Mechanisms.","authors":"Parisa Ahmadi, David Doyle, Negin Mojarad, Soroush Taherkhani, Atousa Janzadeh, Maryam Honardoost, Mitra Gholami","doi":"10.1080/15376516.2025.2500546","DOIUrl":"https://doi.org/10.1080/15376516.2025.2500546","url":null,"abstract":"<p><p>Micro- and nanoplastics (MNPs), pervasive environmental pollutants, contaminate water, soil, air, and the food chain and ultimately accumulate in living organisms. Macrophages are the main immune cells that gather around MNPs and engulf them through the process of phagocytosis. This internalization triggers M1 polarization and the secretion of inflammatory cytokines, including IL-1, IL-18, IL-12, TNF-α, and IFN-γ. Furthermore, MNPs damage mitochondria and lysosomes, causing overactivation of iNOS and excessive production of ROS. This results in cellular stress and induce apoptosis, necroptosis, and, in some cases, metosis in macrophages. The internalization of MNPs also increases the expression of receptors, involving CD36, SR-A, LOX-1, and the macrophage receptor with a collagenous structure (MARCO) while decreasing ABCA-1 and ABCG-1. MNPs in adipose tissue macrophages trigger proinflammatory cytokine secretion, causing adipogenesis, lipid accumulation, insulin resistance, and the secretion of inflammatory cytokines in adipocytes. Various factors influence the rate of MNP internalization by macrophages, including size, charge, and concentration, which affect internalization through passive diffusion. Receptor-mediated phagocytosis of MNPs occurs directly via receptors like T-cell immunoglobulin and mucin domain containing 4 (TIM-4) and MARCO. The attachment of biomolecules, including proteins, antibodies, opsonins, or microbes to MNPs (forming corona structures) promotes indirect receptor-mediated endocytosis, as macrophages possess receptors like TLRs and FcγRIII. MNPs also cause gut dysbiosis, a risk factor for proinflammatory microenvironment and M1 polarization. Here, we review the mechanisms and consequences of MNP macrophage exposure, which is linked to autoimmunity, inflammation, and cardiometabolic syndrome manifestations, including atherosclerosis and obesity, highlighting the immunotoxicity of MNPs.</p>","PeriodicalId":23177,"journal":{"name":"Toxicology Mechanisms and Methods","volume":" ","pages":"1-40"},"PeriodicalIF":3.2,"publicationDate":"2025-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144050161","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Development of a gradual hypoxia chamber for assessing copper toxicity on air-breathing behavior in <i>Lymnaea stagnalis</i>.","authors":"Lauren Zink, Chris M Wood","doi":"10.1080/15376516.2024.2449417","DOIUrl":"https://doi.org/10.1080/15376516.2024.2449417","url":null,"abstract":"<p><p>Behavioral endpoints are of increasing interest in toxicology because of their sensitivity, but require clear guidance for experimental design. This study describes the design of a hypoxia chamber for use with pond snails, <i>Lymnaea stagnalis</i>. Studies assessing the switch from water- to air-breathing in hypoxic conditions have previously utilized methods that neglect intricacies of animal behavior such as handling stress and acclimation. The chamber provides a linear decline in dissolved oxygen, against which surfacing behavior for air-breathing can be precisely measured. The maximum biomass of snails suitable for use in the hypoxia chamber, such that the nitrogen-driven deoxygenation curve is not altered by the snails' own metabolism, was established to be greater than 10 adult snails. The capacity of most analysis softwares is below accurately tracking 10 individuals at once, indicating this is likely not a limitation. The size of snails determined the amount of time each episode of aerial respiration was, with smaller snails spending more time air-breathing. A proof-of-principle experiment using acute copper exposure (0 - 60 µg/L) yielded a concentration-response curve, with greater copper concentrations inhibiting air-breathing. The chamber described in the present study provides an improved framework for assessing hypoxic response and is presented in a manner allowing for further modification to meet unique research needs.</p>","PeriodicalId":23177,"journal":{"name":"Toxicology Mechanisms and Methods","volume":"35 4","pages":"422-429"},"PeriodicalIF":3.2,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144028415","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}