Toxicology and Industrial Health最新文献_第3页

Manganese exposure and sleep quality in iron and steel industry workers. 钢铁工业工人的锰暴露与睡眠质量

IF 1.7 4区医学

Toxicology and Industrial Health Pub Date : 2025-03-01 Epub Date: 2024-12-18 DOI: 10.1177/07482337241302885

Somayeh Rahimimoghadam, Reza Pourbabaki, Fatemeh Khorashadizadeh, Arash Mohammadi, Mojtaba Emkani

{"title":"Manganese exposure and sleep quality in iron and steel industry workers.","authors":"Somayeh Rahimimoghadam, Reza Pourbabaki, Fatemeh Khorashadizadeh, Arash Mohammadi, Mojtaba Emkani","doi":"10.1177/07482337241302885","DOIUrl":"10.1177/07482337241302885","url":null,"abstract":"Manganese (Mn) is an essential element crucial for the proper functioning of the human body. However, excessive exposure to manganese can lead to complications, particularly neurotoxicity. Among the health issues associated with exposure to heavy metals, one of the major concerns in the adverse effect on sleep quality. A total of 189 employees from a steel factory were divided into two groups: exposed (149 people) and non-exposed (40 people). Air samples were collected using the NIOSH 7300 method, and blood samples were obtained at the end of each shift. The samples underwent analysis by ICP-OES after preparation using the acid-thermal digestion method. To gather information on sleep quality, the Petersburg Sleep Questionnaire (PSQI) was used. The data collected in this study showed abnormal conditions, leading to the inclusion of medians alongside averages. The participants had an average age of 35 and an average work experience of 6 years. The exposed group had a significantly higher median respiratory exposure to manganese (1.32 mg/m3) compared with the non-exposed group (0.20 mg/m3). The average sleep quality score in the exposed group was significantly worse (score of 7) compared with the non-exposed group (score of 4). In addition, there was a significant relationship between the quality of sleep and the level of manganese in the air, so that the quality of sleep decreases with the increase in the level of manganese in the air (p-value = .005). However, no significant relationship was observed between blood manganese level and air manganese level in the exposed group (p-value = .06).","PeriodicalId":23171,"journal":{"name":"Toxicology and Industrial Health","volume":" ","pages":"140-150"},"PeriodicalIF":1.7,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142847987","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}

引用次数: 0

Relationship of perfluoroalkyl chemicals with chronic obstructive pulmonary disease: A cross-sectional study. 全氟烷基化学物质与慢性阻塞性肺疾病的关系：横断面研究。

IF 1.7 4区医学

Toxicology and Industrial Health Pub Date : 2025-03-01 Epub Date: 2025-01-24 DOI: 10.1177/07482337251315216

Xuefang Li, Zhijun Li, Jian Ye, Wu Ye

{"title":"Relationship of perfluoroalkyl chemicals with chronic obstructive pulmonary disease: A cross-sectional study.","authors":"Xuefang Li, Zhijun Li, Jian Ye, Wu Ye","doi":"10.1177/07482337251315216","DOIUrl":"10.1177/07482337251315216","url":null,"abstract":"Perfluoroalkyl chemicals are one of the most stable substances in industry and have become ubiquitous contaminants owing to their persistence in the environment. This study enrolled 1,953 participants aged ≥40 years old using data from the National Health and Nutrition Examination Survey (NHANES). We selected four perfluoroalkyl chemicals with a detection frequency of more than 80%, including perfluorohexane sulfonic acid (PFHxS), perfluorononanoic acid (PFNA), perfluorooctanoic acid (PFOA), and perfluorooctane sulfonic acid (PFOS). Multivariate logistic regression was performed to determine the relationship of serum perfluoroalkyl chemicals with COPD and airflow limitation. We evaluated the interaction between perfluoroalkyl chemicals and lung function using multivariate linear regression analyses. Our results showed that the prevalence of COPD was not significantly related to serum PFHxS, PFNA, PFOA, and PFOS. Airflow limitation was positively linked with serum PFHxS, PFOA, and PFOS. However, these significant differences were not robust after adjustment of all confounders of interest. Serum PFHxS, PFOA, and PFOS were all positively related to the forced expiratory volume in 1 second (FEV1), forced vital capacity (FVC), and peak expiratory flow (PEF). However, only PFOA remained significantly linked with the FEV1 and FVC after covariate adjustment. These results indicated that there was no significant interaction between exposure to perfluoroalkyl chemicals and the prevalence of COPD. Higher levels of serum PFOA appeared to be related to higher measures of FEV1 and FVC.","PeriodicalId":23171,"journal":{"name":"Toxicology and Industrial Health","volume":" ","pages":"176-185"},"PeriodicalIF":1.7,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143034268","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}

引用次数: 0

(E)-1,1,1,2,2,5,5,6,6,6-Decafluoro-3-hexene (HFO-153-10mczz-E). (E) 1, 1, 1、2、2、5、5、6、6、6-Decafluoro-3-hexene(高频振荡器- 153 - 10 - mczz - E)。

IF 1.7 4区医学

Toxicology and Industrial Health Pub Date : 2025-03-01 Epub Date: 2025-01-09 DOI: 10.1177/07482337241290870

{"title":"(E)-1,1,1,2,2,5,5,6,6,6-Decafluoro-3-hexene (HFO-153-10mczz-E).","authors":"","doi":"10.1177/07482337241290870","DOIUrl":"10.1177/07482337241290870","url":null,"abstract":"(E)-1,1,1,2,2,5,5,6,6,6-Decafluoro-3-hexene (HFO-153-10mczz-E) (CASRN 1256353-26-0) is a volatile liquid proposed for use as a new low global-warming potential dielectric fluid in cooling applications. Workplace exposures are expected to be by inhalation exposure. The substance has low acute inhalation toxicity as indicated by a 4-h inhalation LC50 value of approximately 8000 ppm. A suite of in vitro assays was negative for skin and eye irritation as well as for skin sensitization potential. The chemical did not induce cardiac sensitization up to 5000 ppm. Repeated inhalation exposure in rats for 4 or 13 weeks did not produce any effects attributable to the substance at 3000 ppm, the maximum tested concentration. No indications of developmental or reproductive toxicity were observed in studies in rats, also conducted with a maximum concentration of 3000 ppm. There was no indication of genotoxicity in the Ames assay, an assay with human TK cells, chromosome aberration in cultured human lymphocytes, or an in vivo rat micronucleus assay. The critical study for the development of the 8-hour TWA WEEL is the 13-week inhalation toxicity study with a NOAEC of 3000 ppm (32,400) mg/m3). This inhalation NOAEC was adjusted by application of appropriate uncertainty factors to account for interindividual variability, subchronic to chronic exposure extrapolation and other sources of uncertainty. A WEEL value of 200 ppm (2160 mg/m3) is expected to provide an acceptable margin of safety for potential adverse health effects in workers.","PeriodicalId":23171,"journal":{"name":"Toxicology and Industrial Health","volume":" ","pages":"123-130"},"PeriodicalIF":1.7,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142955611","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}

引用次数: 0

Prepubertal phthalate exposure can cause histopathological alterations, DNA methylation and histone acetylation changes in rat brain. 青春期前邻苯二甲酸盐暴露可引起大鼠脑组织病理改变、DNA甲基化和组蛋白乙酰化改变。

IF 1.7 4区医学

Toxicology and Industrial Health Pub Date : 2025-03-01 Epub Date: 2025-01-28 DOI: 10.1177/07482337251315212

Seyda Koc, Ekin Erdogmus, Ozlem Bozdemir, Deniz Ozkan-Vardar, Unzile Yaman, Pınar Erkekoglu, Naciye Dilara Zeybek, Belma Kocer-Gumusel

{"title":"Prepubertal phthalate exposure can cause histopathological alterations, DNA methylation and histone acetylation changes in rat brain.","authors":"Seyda Koc, Ekin Erdogmus, Ozlem Bozdemir, Deniz Ozkan-Vardar, Unzile Yaman, Pınar Erkekoglu, Naciye Dilara Zeybek, Belma Kocer-Gumusel","doi":"10.1177/07482337251315212","DOIUrl":"10.1177/07482337251315212","url":null,"abstract":"Di-2-(ethylhexyl)phthalate (DEHP) is a phthalate derivative used extensively in a wide range of materials, such as medical devices, toys, cosmetics, and personal care products. Many mechanisms, including epigenetics, may be involved in the effects of phthalates on brain development. In this study, Sprague-Dawley male rats were obtained 21-23 days after their birth (post-weaning) and were exposed to DEHP during the prepubertal period with low-dose DEHP (DEHP-L, 30 mg/kg/day) and high-dose DEHP (DEHP-H, 60 mg/kg/day, 37 days) until the end of adolescence (PND 60). The rats in the study groups were sacrificed during adulthood, and histopathological changes, epigenetic changes, and oxidative stress parameters were evaluated in brain tissues. Histopathological findings indicating the presence of deterioration in brain tissue morphology were obtained, more prominently in the DEHP-H group. Examining the hippocampus under the light microscope, pyramidal neuron loss was detected only in CA1 of the DEHP-L group, while in DEHP-H rats, pyramidal neuron losses were detected in the CA1, CA2, and CA3 regions. No significant change was observed in brain lipid peroxidation levels with DEHP compared to control. Significant increases in total glutathione (GSH) in both dose groups were considered to be an adaptive response to DEHP-induced oxidative stress. The decrease in DNA methylation in the brain, although not statistically significant, and the increase in histone modification showed that exposure to DEHP may cause epigenetic changes in the brain and these epigenetic changes may also take place as one of the mechanisms underlying the damage observed in the brain. The results suggest that DEHP exposure during early development may have a significant effect on brain development.","PeriodicalId":23171,"journal":{"name":"Toxicology and Industrial Health","volume":" ","pages":"163-175"},"PeriodicalIF":1.7,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143053773","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}

引用次数: 0

Case series and clinical analysis of acute hydrogen sulfide poisoning: Experience from 10 cases at a hospital in Zhoushan. 舟山某医院急性硫化氢中毒10例病例分析及临床分析

IF 1.7 4区医学

Toxicology and Industrial Health Pub Date : 2025-03-01 Epub Date: 2024-12-20 DOI: 10.1177/07482337241308388

Yuechuan Shen, Guangfen Zhao, Jingkai Lin, Junyan Wang, Bin Luo, Jingye Liu, Yini Zhang, Junhua Huang

{"title":"Case series and clinical analysis of acute hydrogen sulfide poisoning: Experience from 10 cases at a hospital in Zhoushan.","authors":"Yuechuan Shen, Guangfen Zhao, Jingkai Lin, Junyan Wang, Bin Luo, Jingye Liu, Yini Zhang, Junhua Huang","doi":"10.1177/07482337241308388","DOIUrl":"10.1177/07482337241308388","url":null,"abstract":"This study investigated the etiology, clinical features, and management of acute hydrogen sulfide (H2S) poisoning in Zhoushan. A retrospective analysis was conducted on 10 patients admitted to our hospital between August and September 2023 due to two incidents of acute H2S poisoning. The first incident involved fishermen working in a fishing cabin (6 patients), while the second involved sanitation workers during sewer maintenance (4 patients). Among the patients, 4 had severe poisoning, 3 had moderate poisoning, and 3 had mild poisoning. Corneal chemical injuries were observed in 4 severe patients, and chest CT scans showed bilateral infiltrative changes in 7 patients. Elevated lactate concentrations, and low oxygenation indices were noted in all severe patients. Severe cases received intensive care, including tracheal intubation, mechanical ventilation, corticosteroids, methylene blue, ulinastatin, and hyperbaric oxygen therapy. Patients with mild to moderate symptoms received supportive treatments, including oxygen therapy and hyperbaric oxygen therapy. With the exception of one fatality, all other patients were discharged after successful treatment. Fishing boat cabins and decomposed sewage channels in island areas are common sites for acute H2S poisoning. Rapid identification of H2S poisoning and evaluation are crucial. Early airway management is essential for severe cases to prevent vital organ hypoxia.","PeriodicalId":23171,"journal":{"name":"Toxicology and Industrial Health","volume":" ","pages":"151-162"},"PeriodicalIF":1.7,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142865506","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}

引用次数: 0

Activation of Ferroptosis and NF-κB/NLRP3/MAPK Pathways in Methylmercury-Induced Hepatotoxicity. 甲基汞诱导的肝毒性中铁下垂和NF-κB/NLRP3/MAPK通路的激活

IF 1.7 4区医学

Toxicology and Industrial Health Pub Date : 2025-03-01 Epub Date: 2024-12-13 DOI: 10.1177/07482337241307067

Yueqing Xie, Hongsen Yu, Yingrong Ye, Jingjing Wang, Zhengtao Yang, Ershun Zhou

{"title":"Activation of Ferroptosis and NF-κB/NLRP3/MAPK Pathways in Methylmercury-Induced Hepatotoxicity.","authors":"Yueqing Xie, Hongsen Yu, Yingrong Ye, Jingjing Wang, Zhengtao Yang, Ershun Zhou","doi":"10.1177/07482337241307067","DOIUrl":"10.1177/07482337241307067","url":null,"abstract":"Methylmercury (MeHg) is a potent hepatotoxin with a complex mechanism of inducing liver injury. Ferroptosis, an iron-dependent form of non-apoptotic cell death, is implicated in various toxicological responses, but its role in MeHg-induced liver damage remains under investigation. In this study, we established an acute liver injury (ALI) model in mice via gavage of MeHg (0, 40, 80, 160 μmol/kg). Histopathological analysis revealed dose-dependent liver damage, corroborated by elevated serum biochemical markers, confirming MeHg-induced hepatotoxicity. MeHg exposure raised MDA levels, inhibited SOD and GSH activity, and downregulated CAT expression. Increased iron accumulation and elevated transferrin receptor expression were observed, alongside decreased GPX4 and SLC7A11 levels, indicating ferroptosis involvement. Additionally, inflammation in MeHg-exposed livers was markedly intensified, as evidenced by increased MPO activity, upregulation of pro-inflammatory cytokines, and activation of the NF-κB/NLRP3 signaling pathway. The Keap1/NRF2/HO-1 oxidative stress response pathway was significantly activated, and p38/ERK1/2 MAPK signaling was notably increased. These findings suggested that MeHg induced acute liver injury through the interplay of ferroptosis, oxidative stress, inflammation, and MAPK signaling pathways, providing a scientific basis for future exploration of the mechanisms underlying MeHg-induced hepatotoxicity and potential therapeutic strategies.","PeriodicalId":23171,"journal":{"name":"Toxicology and Industrial Health","volume":" ","pages":"131-139"},"PeriodicalIF":1.7,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142822567","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}

引用次数: 0

Perfluorooctane sulfonate causes HK-2 cell injury through ferroptosis and endoplasmic reticulum stress pathways. 全氟辛烷磺酸通过铁突变和内质网应激途径导致 HK-2 细胞损伤

IF 1.7 4区医学

Toxicology and Industrial Health Pub Date : 2025-02-01 Epub Date: 2024-11-19 DOI: 10.1177/07482337241300722

Shuqi Yan, Haoyan Ma, Yuwan Ren, Pingwei Wang, Dongge Liu, Na Ding, Yanping Liu, Qianqian Chen, Shuping Ren, Yan Mou

{"title":"Perfluorooctane sulfonate causes HK-2 cell injury through ferroptosis and endoplasmic reticulum stress pathways.","authors":"Shuqi Yan, Haoyan Ma, Yuwan Ren, Pingwei Wang, Dongge Liu, Na Ding, Yanping Liu, Qianqian Chen, Shuping Ren, Yan Mou","doi":"10.1177/07482337241300722","DOIUrl":"10.1177/07482337241300722","url":null,"abstract":"Perfluorooctane sulfonate (PFOS) is a synthetic persistent organic compound that is widely used in industrial products. Studies have shown that PFOS can accumulate in environment and pose a threat to human health. As the kidney is the main excretory organ for PFOS, it is important to study PFOS damage to the kidney to investigate its toxicity. Human proximal tubular epithelial cells (HK-2) were treated with 200 μM PFOS or 1 μM Fer-1. Cell viability, the levels of MDA, GSH, intracellular iron ion, and GPX-4 were determined. The expression of KIM-1 and endoplasmic reticulum stress (ERS) related proteins were determined. The expression levels of KIM-1, a marker of renal tubular injury, and ERS-related proteins, GRP78, ATF6, IRE1, and PERK, were significantly increased in HK-2 cells exposed to PFOS. The levels of MDA and intracellular total iron ion also were significantly increased in HK-2 cells exposed to PFOS and the levels of GSH and GPX-4 were significantly decreased. PFOS can damage HK-2 cells through ferroptosis and endoplasmic reticulum stress, which provides a theoretical foundation for exploring the toxicity of PFOS to the kidney.","PeriodicalId":23171,"journal":{"name":"Toxicology and Industrial Health","volume":" ","pages":"73-82"},"PeriodicalIF":1.7,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142668049","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}

引用次数: 0

Wnt5a promotes Kupffer cell activation in trichloroethylene-induced immune liver injury. 在三氯乙烯诱导的免疫性肝损伤中，Wnt5a促进了Kupffer细胞的活化。

IF 1.7 4区医学

Toxicology and Industrial Health Pub Date : 2025-02-01 Epub Date: 2024-11-26 DOI: 10.1177/07482337241300953

Lei Gao, Ya-Ni Ding, Peng-Cheng Zhou, Luo-Lun Dong, Xin-Yu Peng, Yi-Ru Tang, Qi-Xing Zhu, Jia-Xiang Zhang

{"title":"Wnt5a promotes Kupffer cell activation in trichloroethylene-induced immune liver injury.","authors":"Lei Gao, Ya-Ni Ding, Peng-Cheng Zhou, Luo-Lun Dong, Xin-Yu Peng, Yi-Ru Tang, Qi-Xing Zhu, Jia-Xiang Zhang","doi":"10.1177/07482337241300953","DOIUrl":"10.1177/07482337241300953","url":null,"abstract":"Trichloroethylene (TCE) is a volatile, colorless liquid that is widely used as a chlorinated organic vehicle in industrial production and processing industries. Many workers exposed to trichloroethylene may develop trichloroethylene hypersensitivity syndrome (THS). However, the underlying mechanism of THS is still unclear, especially liver injury. The present study aimed to investigate whether Wnt5a/c-Jun N-terminal kinase (JNK) is involved in and regulates liver injury caused by TCE exposure and to provide new directions for the prevention and treatment in clinical settings of liver injury caused by TCE exposure. We used 6- to 8-week-old SPF-grade BALB/c female mice to establish a TCE sensitization model and explored the mechanism through inhibitor intervention. We found that the expression of Wnt5a/JNK was significantly elevated in the liver of TCE sensitization-positive mice. Inhibitors of Wnt Production 2 (IWP-2) are known antagonists of the Wnt pathway. TCE-sensitization mice treated with IWP-2 showed downregulated Wnt5a/JNK expression, reduced Kupffer cell activation, and decreased liver injury. At the same time, we found that phosphorylated JNK in TCE-sensitization mouse livers and extracted Kupffer cells showed a significant downward trend after inhibition of Wnt5a function. We also found that a specific JNK inhibitor, SP600125, decreased the secretion of cytokines and chemokines and decreased Kupffer cell activation. We demonstrated that Wnt5a/JNK was involved in the regulation of liver injury in TCE-sensitization mice and that it exacerbated liver injury by activating Kupffer cells and releasing chemokines. We therefore hypothesized that Kupffer cell activation was affected by JNK, which reduced chemokine and cytokine secretion and attenuated liver injury in TCE-sensitization mice.","PeriodicalId":23171,"journal":{"name":"Toxicology and Industrial Health","volume":" ","pages":"83-96"},"PeriodicalIF":1.7,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142717161","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}

引用次数: 0

Metabolomics reveals that phosphatidylethanolamine can alleviate the toxicity of silica nanoparticles in human lung A549 cells. 代谢组学研究表明，磷脂酰乙醇胺可减轻二氧化硅纳米颗粒对人肺A549细胞的毒性。

IF 1.7 4区医学

Toxicology and Industrial Health Pub Date : 2025-02-01 Epub Date: 2024-11-29 DOI: 10.1177/07482337241304166

Shuang Chen, Chengzhi Liu, Yifan Yang, Jiangliang Chu, Beilei Yuan, Zhe Wang

{"title":"Metabolomics reveals that phosphatidylethanolamine can alleviate the toxicity of silica nanoparticles in human lung A549 cells.","authors":"Shuang Chen, Chengzhi Liu, Yifan Yang, Jiangliang Chu, Beilei Yuan, Zhe Wang","doi":"10.1177/07482337241304166","DOIUrl":"10.1177/07482337241304166","url":null,"abstract":"Silica nanoparticles (SiNPs) are widely utilized in occupational settings where they can cause lung damage through inhalation. The objective of this research was to explore the metabolic markers of SiNPs-induced toxicity on A549 cells by metabolomics and provide a foundation for studying nanoparticle-induced lung toxicity. Metabolomics analysis was employed to analyze the metabolites of SiNPs-treated A549 cells. LASSO regression was applied for selection, and protective measure experiments were conducted to validate the efficacy of selected potential toxicity mitigators. After SiNPs treatment, 23 differential metabolites were identified, including lipids, nucleotides, and organic oxidants. Pathway analysis revealed involvement in various biological processes. LASSO regression further identified six metabolites significantly associated with SiNPs toxicity. Notably, phosphatidylethanolamine (PE (14:1(9Z)/14:0)) showed enrichment in six significant metabolic pathways and with an AUC of 1 in the ROC curve. Protective measure experiments verified its protective effect on A549 cells and demonstrated its considerable inhibition of SiNPs-induced cytotoxicity. This study elucidated SiNPs-induced cytotoxicity on A549 cells and identified PE as a potential toxicity mitigator. These findings contribute to understanding the mechanisms of nanoparticle-induced lung toxicity and inform occupational health preventive strategies.","PeriodicalId":23171,"journal":{"name":"Toxicology and Industrial Health","volume":" ","pages":"97-107"},"PeriodicalIF":1.7,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142755636","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}

引用次数: 0

Transcriptome analysis reveals the molecular mechanisms of neonicotinoid acetamiprid in Leydig cells. 转录组分析揭示了新烟碱啶虫脒在睾丸细胞中的分子机制。

IF 1.7 4区医学

Toxicology and Industrial Health Pub Date : 2025-02-01 Epub Date: 2024-11-11 DOI: 10.1177/07482337241300215

Xun Liu, Ce Wang, Yue Ma, Linxiang Fu, Wanji Luo, Changjie Xu, Ying Tian, Mingyue Ma, Yaping Mao

{"title":"Transcriptome analysis reveals the molecular mechanisms of neonicotinoid acetamiprid in Leydig cells.","authors":"Xun Liu, Ce Wang, Yue Ma, Linxiang Fu, Wanji Luo, Changjie Xu, Ying Tian, Mingyue Ma, Yaping Mao","doi":"10.1177/07482337241300215","DOIUrl":"10.1177/07482337241300215","url":null,"abstract":"At present, the reproductive toxicology of neonicotinoids has received greater attention, however, its potential mechanisms are still not fully understood. Acetamiprid (ACE) is a new-generation neonicotinoid and has become a ubiquitous contaminant in the environment. This study aimed to investigate the toxic effects of ACE in TM3 Leydig cells based on transcriptome analysis. The viability and apoptosis of TM3 cells exposed to different concentrations of ACE were assessed by CCK8 and flow cytometry, respectively. After ACE exposure, transcriptome analysis was performed to screen differential expression genes (DEGs), followed by qPCR verification. Results showed that ACE exposure resulted in a time- and dose-dependent decrease in the viability of TM3 cells (p < .05). ACE also exerted a dose-dependent pro-apoptotic effect on TM3 cells. Results of RNA-seq showed that 1477 DEGs were obtained, of which 539 DEGs were up-regulated and 938 DEGs were down-regulated. GO and KEGG analyses of DEGs showed that DNA replication and cell cycle might be the key mechanisms for the cytotoxicity of ACE. qPCR results demonstrated that Mdm2, Cdkn1a (p21) and Gadd45 were significantly increased, and Pcna, Ccna2 (CycA), Ccnb1 (CycB), Ccne1 (CycE), and Cdk1 were significantly decreased, indicating that ACE exposure might promote G1/S and G2/M cell cycle arrest. Additionally, FoxO, p53, and HIF-1 signaling pathways and ferroptosis might play important roles in ACE-induced reproductive toxicity. Collectively, this study provides new perspectives into the mechanism of ACE-induced reproductive toxicity and lays a theoretical foundation for the in-depth study of non-target toxicity mechanisms of neonicotinoid insecticides.","PeriodicalId":23171,"journal":{"name":"Toxicology and Industrial Health","volume":" ","pages":"61-72"},"PeriodicalIF":1.7,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142628737","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}

引用次数: 0