Perfluorooctane sulfonate (PFOS) and perfluorooctanoic acid (PFOA) are persistent environmental pollutants, raising concerns due to their widespread presence and disruptive biological effects. These compounds are highly stable, allowing them to bioaccumulate in the environment and living organisms, potentially impacting critical physiological functions such as hormonal balance, immune response, and increasing cancer risk. Despite regulatory restrictions, their pervasive nature necessitates further research into their potential effects on cellular and neuronal function. This study first evaluated the cytotoxic effects of PFOS and PFOA on S1 neuroblastoma cells; a dose-dependent reduction in cell viability was revealed for PFOS, while PFOA exhibited minimal toxicity until millimolar concentrations. We further investigated their potential to modulate GABAergic neurotransmission using patch-clamp electrophysiology. Both PFOS and PFOA caused a significant but reversible reduction in GABA receptor-mediated currents following one-minute pre-treatment. These findings suggest that PFOS and PFOA can interfere with both cellular viability and GABAergic signaling, providing critical insights into their functional impacts and highlighting the need for further investigation into the long-term consequences of PFAS exposure on nervous system health.

Per- and polyfluoroalkyl substances (PFAS) are a class of persistent organic pollutants that pose a growing threat to environmental and human health. Soil acts as a long-term reservoir for PFAS, potentially impacting soil biodiversity and ecosystem function. Earthworms, as keystone species in soil ecosystems, are particularly vulnerable to PFAS exposure. In this study, we investigated the sublethal effects of three short-chain (C4–C6) next-generation perfluoropropylene oxide acids (PFPOAs) on the earthworm Eisenia fetida, using a legacy perfluoroalkyl carboxylic acid (PFCA), perfluorooctanoic acid (PFOA), as a reference. We assessed a suite of biochemical endpoints, including markers for oxidative stress (catalase and superoxide dismutase activity), immunity (phenol oxidase activity), neurotoxicity (acetylcholinesterase activity), and behavioural endpoints (escape test). Results indicate that all tested PFAS, even at sub-micromolar concentrations, elicited significant effects across multiple physiological domains. Interestingly, HFPO-DA demonstrated the most substantial impact across all endpoints tested, indicating broad and significant biochemical and neurotoxic effects. Our findings underscore the potential risks of both legacy and emerging PFAS to soil ecosystems, emphasising the need for further research to understand the long-term consequences of PFAS contamination.

Silver is back in vogue today as this metal is used in the form of nanomaterials in numerous commercial products. We have developed in-gel electrophoretic techniques to measure the activity of the antioxidant enzymes catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPX), and used the same techniques in combination with HSP70 Western blot analysis to evaluate the effects of nanomolar amounts of silver nitrate and 5 nm alkane-coated silver nanoparticles in tissues of the marine bivalve Mytilus galloprovincialis (Lam.) exposed for 28 days in mesocosms. Our results showed a negligible effect for nanosilver exposure and dose-dependent effects for the nitrate form.

Per- and polyfluoroalkyl substances (PFAS) persist in soils, yet their effects on invertebrate immunity remain poorly understood. We compared a legacy congener, perfluorooctanoic acid (PFOA), with three short-chain ether acids GenX (C6), MOBA (C5), and MOPrA (C4) using a 72 h OECD-207 filter-paper assay in the earthworm Eisenia fetida. Endpoints spanned cellular and humoral defenses: amoebocyte morphometry, oxidative burst (ROS production), phenol oxidase (PO) activity, and the transcription of the lectin CCF-1 and the pore-forming protein lysenin. MOBA and MOPrA caused enlargement of amoebocytes, whereas PFOA and GenX had no morphometric impact. Oxidative burst fell significantly for all congeners. PO inhibition followed the same potency order (MOPrA > GenX > MOBA ≫ PFOA), with near-complete loss at 229 µM MOPrA. Gene expression assays for CCF-1 and lysenin showed shifts in relative fold change for each PFAS congener. The combined biomarker panel—amoebocyte size, ROS, CAT, PO, CCF-1, and lysenin—offers a concise framework for assessing terrestrial PFAS risk and guiding remediation monitoring.

Gravity is a primary physical force that has a profound influence on the stability of the cell cytoskeleton. In our research, we investigated the influence of microgravity on altering the cytoskeletal pathways of glioblastoma cells. The highly infiltrative behavior of glioblastoma is supported by cytoskeletal dynamics and surface proteins that allow glioblastoma cells to avoid stable connections with the tissue environment and other cells. Glioblastoma cell line C6 was exposed to a microgravity environment for 24, 48, and 72 h by 3D-RPM, a laboratory instrument recognized to reproduce the effect of microgravity in cell cultures. The immunofluorescence for GFAP, vinculin, and Connexin-43 was investigated as signals related to cytoskeleton dynamics. The polymerization of GFAP and the expression of focal contact structured by vinculin were found to be altered, especially after 48 and 72 h of microgravity. Connexin-43, involved in several intracellular pathways that critically promote cell motility and invasion of glioma cells, was found to be largely reduced following microgravity exposure. In conclusion, microgravity, by reducing the expression of Connexin-43, alters the architecture of specific cytoskeletal elements such as GFAP and increases the focal contact, which can induce a reduction in glioma cell mobility, thereby inhibiting their aggressive metastatic behavior.