Noor Muhammad Khan, Victoria Scott, Mohammad Ghasemzadeh-Hasankolaei, Vasantha Padmanabhan, Arpita Vyas, Neil P Evans, Michelle Bellingham
{"title":"Sexually dimorphic cardiovascular impacts of prenatal exposure to a real-life environmental chemical mixture in adult offspring.","authors":"Noor Muhammad Khan, Victoria Scott, Mohammad Ghasemzadeh-Hasankolaei, Vasantha Padmanabhan, Arpita Vyas, Neil P Evans, Michelle Bellingham","doi":"10.1016/j.etap.2025.104669","DOIUrl":"https://doi.org/10.1016/j.etap.2025.104669","url":null,"abstract":"<p><p>Cardiovascular disease (CVD) is a leading cause of death that is sexually dimorphic. This study used an ovine model to investigate whether maternal exposure to an environmental chemical (EC) mixture (biosolids) prior to and throughout pregnancy, affected offspring cardiovascular (CV) structure and function in adulthood. CV function of male and female offspring from ewes grazed on either conventionally fertilised (control, C) or biosolids-treated pasture (B) was assessed. Males exhibited higher blood pressure compared to females with no significant effect of EC exposure. Heart rate variability in females suggested reduced autonomic regulation in the B group. EC-exposed males, but not females, showed significantly increased left ventricular dimensions, end-diastolic and systolic volumes, and cardiac output. The findings indicate sexually dimorphic effects of maternal EC mixture exposure on adult CV structure and function. Further studies are are needed to explore the mechanisms and long-term implications of prenatal exposure CV health.</p>","PeriodicalId":93992,"journal":{"name":"Environmental toxicology and pharmacology","volume":" ","pages":"104669"},"PeriodicalIF":0.0,"publicationDate":"2025-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143574833","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}
{"title":"Histopathology and changes in the expression of metallothioneins, heat shock proteins and inducible nitric oxide synthase in Prochilodus costatus from a neotropical river contaminated by heavy metals.","authors":"Alessandro Loureiro Paschoalini, Yves Moreira Ribeiro, Breno Thuller, Camila Leandro Gomes Soares, Elizete Rizzo, Nilo Bazzoli","doi":"10.1016/j.etap.2024.104473","DOIUrl":"10.1016/j.etap.2024.104473","url":null,"abstract":"<p><p>The most recent dam rupture in Brazil released tons of mining tailings into the upper course of the Paraopeba River, affecting this river in an unprecedented way. The present study aimed to evaluate the influence of heavy metals on Prochilodus costatus, an important commercial species in Brazil, four years after the dam colapse. To this end, biomarkers of heavy metals, oxidative stress, and environmental stress were analyzed, and histological analyses of target organs were performed. The results demonstrated critical contamination of fish from the Paraopeba River. Increased expression of Metallothioneins - MTs, Heat Shock Protein - HSP70, and inducible nitric oxide synthase - iNOS, as well as greater rates of histological changes in the liver, spleen, and gonads, were observed in P. costatus. These findings demonstrate that, despite past contamination, the metals present in mining tailings have significantly increased the contamination of the Paraopeba River basin.</p>","PeriodicalId":93992,"journal":{"name":"Environmental toxicology and pharmacology","volume":" ","pages":"104473"},"PeriodicalIF":0.0,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140961300","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}
{"title":"Gene expression profiles and protein-protein interaction networks in THP-1 cells exposed to metal-based nanomaterials.","authors":"Šíma Michal, Líbalová Helena, Závodná Táňa, Vrbová Kristýna, Kléma Jiří, Rössner Pavel","doi":"10.1016/j.etap.2024.104469","DOIUrl":"https://doi.org/10.1016/j.etap.2024.104469","url":null,"abstract":"<p><p>We analyzed gene expression in THP-1 cells exposed to metal-based nanomaterials (NMs) [TiO<sub>2</sub> (NM-100), ZnO (NM-110), SiO<sub>2</sub> (NM-200), Ag (NM-300 K)]. A functional enrichment analysis of the significant differentially expressed genes (DEGs) identified the key modulated biological processes and pathways. DEGs were used to construct protein-protein interaction networks. NM-110 and NM-300 K induced changes in the expression of genes involved in oxidative and genotoxic stress, immune response, alterations of cell cycle, detoxification of metal ions and regulation of redox-sensitive pathways. Both NMs shared a number of highly connected protein nodes (hubs) including CXCL8, ATF3, HMOX1, and IL1B. NM-200 induced limited transcriptional changes, mostly related to the immune response; however, several hubs (CXCL8, ATF3) were identical with NM-110 and NM-300 K. No effects of NM-100 were observed. Overall, soluble nanomaterials NM-110 and NM-300 K exerted a wide variety of toxic effects, while insoluble NM-200 induced immunotoxicity; NM-100 caused no detectable changes on the gene expression level.</p>","PeriodicalId":93992,"journal":{"name":"Environmental toxicology and pharmacology","volume":" ","pages":"104469"},"PeriodicalIF":0.0,"publicationDate":"2024-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140961297","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}
{"title":"Chlorpyrifos-induced suppression of the antioxidative defense system leads to cytotoxicity and genotoxicity in macrophages.","authors":"Yin-Che Lu, Chen-Yu Chiang, Shih-Pin Chen, Yu-Wei Hsu, Wen-Ying Chen, Chun-Jung Chen, Yu-Hsiang Kuan, Sheng-Wen Wu","doi":"10.1016/j.etap.2024.104468","DOIUrl":"https://doi.org/10.1016/j.etap.2024.104468","url":null,"abstract":"<p><p>Chlorpyrifos, widely used for pest control, is known to have various harmful effects, although its toxic effects in macrophages and the mechanisms underlying its toxicity remain unclear. The present study investigated the toxic effects of chlorypyrifos in a macrophage cell line. Here, we found that chlorpyrifos induced cytotoxicity and genotoxicity in RAW264.7 macrophages. Moreover, chlorpyrifos induced intracellular ROS production, subsequently leading to lipid peroxidation. Chlorpyrifos reduced the activation of antioxidative enzymes including superoxide dismutase, catalase, and glutathione peroxidase. Chlorpyrifos upregulated HO-1 expression and activated the Keap1-Nrf2 pathway, as indicated by enhanced Nrf2 phosphorylation and Keap1 degradation. Chlorpyrifos exerted effects on the following in a dose-dependent manner: cytotoxicity, genotoxicity, lipid peroxidation, intracellular ROS production, antioxidative enzyme activity reduction, HO-1 expression, Nrf2 phosphorylation, and Keap1 degradation. Notably, N-acetyl-L-cysteine successfully inhibited chlorpyrifos-induced intracellular ROS generation, cytotoxicity, and genotoxicity. Thus, chlorpyrifos may induce cytotoxicity and genotoxicity by promoting intracellular ROS production and suppressing the antioxidative defense system activation in macrophages.</p>","PeriodicalId":93992,"journal":{"name":"Environmental toxicology and pharmacology","volume":" ","pages":"104468"},"PeriodicalIF":0.0,"publicationDate":"2024-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140961294","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}
Jin Chen, Mingxuan Zhang, Stanley Aniagu, Yan Jiang, Tao Chen
{"title":"PM2.5 induces cardiac defects via AHR-SIRT1-PGC-1α mediated mitochondrial damage","authors":"Jin Chen, Mingxuan Zhang, Stanley Aniagu, Yan Jiang, Tao Chen","doi":"10.1016/j.etap.2024.104393","DOIUrl":"https://doi.org/10.1016/j.etap.2024.104393","url":null,"abstract":"","PeriodicalId":93992,"journal":{"name":"Environmental toxicology and pharmacology","volume":"2013 4","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139879273","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}