Microplastics (MPs) are widely found in coastal areas and oceans worldwide. The MPs are environmentally concerning due to their bioavailability and potential impacts on a wide range of marine biota, so assessing their impact on the biota has become an urgent research priority. In the present study, we exposed Crassostrea gigas oysters to irregular MPs of two polymer types (polyethylene (PE) and polyethylene terephthalate (PET)) at concentrations of 10 and 1000 μg L⁻¹ for 21 days. Accumulation of MPs, changes in metabolic enzyme activity, and histological damage were evaluated, and metabolomics analysis was conducted. Results demonstrated that PE and PET MPs were detected in the gills and digestive gland following exposure to both tested concentrations, confirming ingestion of MPs by the organisms. Moreover, both PE and PET MPs inhibited lipid metabolism, while energy metabolism enzyme activities were activated in the oysters. Histopathological damage of exposed oysters was also observed in this study. Integrated biomarker response (IBR) results showed that MPs toxicity increased with increasing MPs concentration, and the toxic effects of PET MPs on oysters was greater than PE MPs. In addition, metabolomics analysis suggested that MPs exposure induced alterations in metabolic profiles in oysters, with changes in energy metabolism and inflammatory responses. This study reports new insights into the consequences of MPs exposure in marine bivalves at environmentally relevant concentrations, providing valuable information for ecological risk assessment of MPs in a realistic conditions.

The environmental dioxin 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is classified as a Group 1 human carcinogen and teratogenic agent. We hypothesize that TCDD-induced oxidative stress may also interfere with mitochondrial ATP-sensitive potassium channels (mitoKATP), which are known to regulate and to be regulated by mitochondrial redox state. We investigated the effects of an acute treatment of male Wistar rats with TCDD (50 μg/kg i.p.) and measured the regulation of cardiac mitoKATP. While the function of cardiac mitochondria was slightly depressed, mitoKATP activity was 52% higher in animals treated with TCDD. The same effects were not observed in liver mitochondria isolated from the same animals. Our data also shows that regulation of mitochondrial ROS production by mitoKATP activity is different in both groups. To our knowledge, this is the first report to show that TCDD increases mitoKATP activity in the heart, which may counteract the increased oxidative stress caused by the dioxin during acute exposure.

Particulate matter with aerodynamic diameter not larger than 2.5 μm (PM₂.₅) escalated the risk of respiratory diseases. Mitochondrial dysfunction may play a pivotal role in PM₂.₅-induced airway injury. However, the potential effect of PM₂.₅ on mitochondrial permeability transition pore (mPTP)-related airway injury is still unknown. This study aimed to investigate the role of mPTP in PM₂.₅-induced mitochondrial dysfunction in airway epithelial cells in vitro. PM₂.₅ significantly reduced cell viability and caused apoptosis in BEAS-2B cells. We also found PM₂.₅ caused cellular and mitochondrial morphological alterations, evidenced by the disappearance of mitochondrial cristae, mitochondrial swelling, and the rupture of the outer mitochondrial membrane. PM₂.₅ induced mPTP opening via upregulation of voltage-dependent anion-selective channel (VDAC), leading to deprivation of mitochondrial membrane potential, increased mitochondrial reactive oxygen species (ROS) generation and intracellular calcium level. PM₂.₅ suppressed mitochondrial respiratory function by reducing basal and maximal respiration, and ATP production. The mPTP targeting compounds cyclosporin A [CsA; a potent inhibitor of cyclophilin D (CypD)] and VBIT-12 (a selective VDAC1 inhibitor) significantly inhibited PM₂.₅-induced mPTP opening and apoptosis, and preserved mitochondrial function by restoring mitochondrial membrane potential, reducing mitochondrial ROS generation and intracellular calcium content, and maintaining mitochondrial respiration function. Our data further demonstrated that PM₂.₅ caused reduction in nuclear expressions of PPARγ and PGC-1α, which were reversed in the presence of CsA. These findings suggest that mPTP might be a potential therapeutic target in the treatment of PM₂.₅-induced airway injury.

Soil around the gold tailing due to the smelting process of wastewater and solid waste can lead to metal (loids) contamination, especially arsenic (As). Soil microorganisms have gradually evolved adaptive mechanisms in the process of long-term adaptation to As contamination. However, comprehensive investigations on As metabolism genes and their host microbial communities in soil profiles with different levels under long-term As contamination are lacking. There are selected three typical soil profiles (0–100 cm) with different metal (loids) contamination levels (L-low, M-moderate and H-high) around tailings in this research. It uses a Metagenomic approach to explore the adaptation mechanisms of arsenic metabolism genes and arsenic metabolism gene host microorganisms in both horizontal and vertical dimensions. The results showed that four categories of As metabolism genes were prevalent in soil profiles at different As contamination, with As reduction genes being the most abundant, followed by As oxidation genes, then respiration genes and methylation genes. The As metabolism genes arsBCR, aioE, arsPH, arrAB increased with the increase of metal (loid) contaminants concentration. Longitudinal arsA, arrA, aioA, arsM and acr3 increased in abundance in deep soil. Actinobacteria, Proteobacteria, Acidobacteria, and Chloroflexi were the dominant phylum of As metabolism gene host microorganisms. Different concentrations of metal (loid) contamination significantly affected the distribution of host As metabolism genes. Random forest prediction identified As as the most critical driver of As metabolism genes and their host microorganisms. Overall, this study provides a reference for a comprehensive investigation of the detoxification mechanisms of As metabolism microorganisms in soil profiles with different As contamination conditions, and is important for the development of As metabolism gene host microbial strains and engineering applications of microbial technologies to manage As contamination.

Heavy metal pollution can decrease the soil microbial biomass and significantly alter microbial community structure. In this study, a long-term field experiment (5 years) and short-term laboratory experiment (40 d) were employed to evaluate the effects of heavy metals (Cd, Cu, Zn), and their combinations at different concentrations, on the soil microbial biomass and the bacterial community. The ranges of heavy metal concentration in the long-term and short-term experiments were similar, with concentration ranges of Cd, Cu and Zn of about 0.3–1.5, 100–500, and 150–300 mg kg⁻¹, respectively. Microbial biomass decreased with increasing soil heavy metal concentrations in both the long-term and short-term experiments. The interaction between soil physicochemical factors (pH, TN, TC) and heavy metals (Cd, Cu, Zn) played a major role in change in the bacterial community in long-term polluted soil. In the laboratory experiment, although each heavy metal had an adverse effect on the microbial biomass and community structure, Cu appeared to have a greater role in the changes compared to Cd and Zn. However, the synergistic effects of the heavy metals were greater than those of the single metals and the synergistic effect between Cu and Cd was greater than that of Cu and Zn.

Considerable human data have shown that the exposure to perfluorooctane sulfonate (PFOS) correlates to the risk of metabolic diseases, however the underlying effects are not clearly elucidated. In this study, we investigated the impacts of PFOS treatment, using in-vivo, ex-vivo and in-vitro approaches, on pancreatic β-cell functions. Mice were oral-gavage with 1 and 5 μg PFOS/g body weight/day for 21 days. The animals showed a significant increase in liver triglycerides, accompanied by a reduction of triglycerides in blood sera and glycogen in livers and muscles. Histological examination of pancreases showed no noticeable changes in the size and number of islets from the control and treatment groups. Immunohistochemistry showed a reduction of staining intensities of insulin and the transcriptional factors (Pdx-1, islet-1) in islets of pancreatic sections from PFOS-treated groups, but no changes in the intensity of Glut2 and glucagon were noted. Transcriptomic study of isolated pancreatic islets treated ex vivo with 1 μM and 10 μM PFOS for 24 h, underlined perturbations of the insulin signaling pathways. Western blot analysis of ex-vivo PFOS-treated islets revealed a significant reduction in the expression levels of the insulin receptor, the IGF1 receptor-β, Pdk1-Akt-mTOR pathways, and Pdx-1. Using the mouse β-cells (Min-6) treated with 1 μM and 10 μM PFOS for 24 h, Western blot analysis consistently showed the PFOS-treatment inhibited Akt-pathway and reduced cellular insulin contents. Moreover, functional studies revealed the inhibitory effects of PFOS on glucose-stimulated insulin-secretion (GSIS) and the rate of ATP production. Our data support the perturbing effects of PFOS on animal metabolism and demonstrate the underlying molecular targets to impair β-cell functions.