Thais R R Alves, Matheus F Trivellato, Tainá A L Freitas, Aline Y Kato, Cássia R A Gomes, Yara M M Ferraz, Jéssica A Serafim, David De Jong, Evandro P Prado, Eduardo F Vicente, Ricardo O Orsi, Gener T Pereira, Camila A Miranda, Fábio E Mingatto, Daniel Nicodemo
{"title":"Pollen contaminated with a triple-action fungicide induced oxidative stress and reduced longevity though with less impact on lifespan in honey bees from well fed colonies.","authors":"Thais R R Alves, Matheus F Trivellato, Tainá A L Freitas, Aline Y Kato, Cássia R A Gomes, Yara M M Ferraz, Jéssica A Serafim, David De Jong, Evandro P Prado, Eduardo F Vicente, Ricardo O Orsi, Gener T Pereira, Camila A Miranda, Fábio E Mingatto, Daniel Nicodemo","doi":"10.1016/j.etap.2024.104587","DOIUrl":"10.1016/j.etap.2024.104587","url":null,"abstract":"<p><p>Experiments were conducted to determine the effects of a triple-action fungicide on bees and whether improved nutrition can ameliorate eventual negative impacts. In cage tests, newly-emerged bees from well fed and from nutritionally-restricted honey bee colonies were fed for five days with pollen from sunflowers that had been sprayed or not with a commercial fungicide containing bixafen, prothioconazole and trifloxystrobin. Bees from well-fed colonies were significantly larger and consumed more uncontaminated pollen. They also exhibited increased glutathione peroxidase activity and higher concentrations of pyridine nucleotides, both of which are involved in antioxidase defense. However, pollen contaminated with fungicide led to an increase in lipoperoxidation, regardless of nutritional status. Bee longevity was reduced by both fungicide contamination of the pollen diet and poor nutritional condition. The fungicide adversely affected bees fed with contaminated pollen, though nutritional supplementation of the bee colonies that reared the bees partially compensated for these effects.</p>","PeriodicalId":93992,"journal":{"name":"Environmental toxicology and pharmacology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-11-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142591063","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":null,"pages":null},"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":null,"pages":null},"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":null,"pages":null},"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":null,"pages":null},"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}