Environmental toxicology and pharmacology最新文献

In this study, the acute and sublethal toxicity of SDBS was assessed using Tubifex tubifex. In an acute toxicity bioassay, the 96-hour LC₅₀ value for SDBS was determined to be 13.358 mg/L. The survival probability of the test organism under elevated SDBS concentrations was further assessed using General Unified Threshold models of Survival (GUTS), where the GUTS-Individual Tolerance (IT) model was applied over the GUTS-Stochastic Death (SD) model. T. tubifex was exposed for 14 days to concentrations equivalent to 10 % and 20 % of the 96-hour LC₅₀ value (1.33 mg/L and 2.67 mg/L). Significant alterations were observed in total protein content, antioxidant enzyme activities, and histopathological markers. Specifically, levels of proteins, superoxide dismutase (SOD), and catalase (CAT) decreased, while glutathione S-transferase (GST), glutathione peroxidase (GPx), and malondialdehyde (MDA) increased, indicating oxidative stress. These findings suggest exposure to sublethal levels of SDBS may compromise physiological integrity and antioxidative defense mechanisms in invertebrates.

The indiscriminate use of pesticides to control various pests, including insects and fungi, raises concerns about the potential long-term effects of these toxic substances on pollinators. In this study, we evaluated the effects of larval exposure to the insecticide thiamethoxam and the fungicide pyraclostrobin on the morphology of the midgut and Malpighian tubules in newly emerged Scaptotrigona postica workers. The results revealed that larvae exposed to insecticides, alone and in combination, developed into adult workers with an increased loss of cytoplasmic material in the midgut and Malpighian tubules, suggesting autophagic cell death. The loss of brush border integrity was more pronounced following pesticide treatment, suggesting potential impairment of nutrient digestion and absorption. Cell elimination was observed exclusively in the combination treatment group, indicating a synergistic interaction between the pesticides for this particular effect. These effects result in health impairments in adult bees, potentially compromising pollination services.

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.

We analyzed gene expression in THP-1 cells exposed to metal-based nanomaterials (NMs) [TiO₂ (NM-100), ZnO (NM-110), SiO₂ (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.

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.