The biochemical responses in muscle, such as the enzymatic activities of acetylcholinesterase, lactate dehydrogenase and isocitrate dehydrogenase, were studied in sole (Solea senegalensis) collected in Huelva estuary (SW Spain), in the vicinity of a petrochemical and mining industry. The sampling sites showed different type and degree of pollution. The results demonstrated significant differences in muscle activities of AChE and IDH in Odiel and Tinto Rivers compared to control fish. LDH activity did not show any difference between sampling sites. Significant correlations were established between some biomarkers and heavy metals: AChE was correlated with Pb, Cd and Cu concentrations in water; IDH activity was correlated with Cd and Cu concentrations in water and As, Pb and Cd concentrations in sediments; LDH activity was correlated with As and Zn concentration in water and Cd concentration in sediment. Only one correlation was established between the biomarkers analysed and the concentrations of PAHs: benzo(b)fluoranthene concentration in sediment and IDH.

Corrosion is an environmental and economic global problem. “Smart” or stimuli-responsive colorimetric nanosensors for maritime coatings have been proposed as an asset to overcome the limitations of the current monitoring techniques by changing color in the presence of triggers associated with the early stages of corrosion. Layered double hydroxides (Zn–Al LDH; Mg–Al LDH) and silica mesoporous nanocapsules (SiNC) were used as precursor nanocarriers of active compounds: hexacyanoferrate ions ([Fe(CN)₆]³⁻) and phenolphthalein (PhPh), respectively. Additionally, the safer-by-design principles were employed to optimize the nanosensors in an eco-friendly perspective (e.g., regular vs. warm-washed SiNC-PhPh; immobilization using different carriers: Zn–Al LDH-[Fe(CN)₆]³⁻ vs. Mg–Al LDH-[Fe(CN)₆]³⁻). Therefore, the present study aims to assess the environmental behavior in saltwater and the toxic effects of the nanosensors, their nanocarriers, and the active compounds on the marine microalgae Tetraselmis chuii and the crustacean Artemia salina. Briefly, tested compounds exhibited no acute toxic effects towards A. salina (NOEC = 100 mg/L), apart from SiNC-PhPh (LC₅₀ = 2.96 mg/L) while tested active compounds and nanosensors caused significant growth inhibition on T. chuii (lowest IC₅₀ = 0.40 mg/L for SiNC-PhPh). The effects of [Fe(CN)₆]³⁻ were similar regardless of the nanocarrier choice. Regarding SiNC-PhPh, its toxicity can be decreased at least twice by simply reinforcing the nanocapsules washing, which contributes to the removal (at least partially) of the surfactants residues. Thus, implementing safe-by-design strategies in the early stages of research proved to be critical, although further progress is still needed towards the development of truly eco-friendly nanosensors.

Inhalation represents the most prevalent route of exposure with Thorium-232 compounds (Th-nitrate/Th-dioxide)/Th-containing dust in real occupational scenario. The present study investigated the mechanism of Th response in normal human alveolar epithelial cells (WI26), exposed to Th-nitrate or colloidal Th-dioxide (1–100 μg/ml, 24–72 h). Assessment in terms of changes in cell morphology, cell proliferation (cell count), plasma membrane integrity (lactate dehydrogenase leakage) and mitochondrial metabolic activity (MTT reduction) showed that Th-dioxide was quantitatively more deleterious than Th-nitrate to WI26 cells. TEM and immunofluorescence analysis suggested that Th-dioxide followed a clathrin/caveolin-mediated endocytosis, however, membrane perforation/non-endocytosis seemed to be the mode of Th internalization in cells exposed to Th-nitrate. Th-estimation by ICP-MS showed significantly higher uptake of Th in cells treated with Th-dioxide than with Th-nitrate at a given concentration. Both Th-dioxide and nitrate were found to increase the level of reactive oxygen species, which seemed to be responsible for lipid peroxidation, alteration in mitochondrial membrane potential and DNA-damage. Amongst HSPs, the protein levels of HSP70 and HSP90 were affected differentially by Th-nitrate/dioxide. Specific inhibitors of ATM (KU55933) or HSP90 (17AAG) were found to increase the Th- cytotoxicity suggesting prosurvival role of these signaling molecules in rescuing the cells from Th-toxicity.

Pyrazole derivatives display diverse biological and pharmacological activities. The aim of this study is to investigate the antioxidant properties of a novel pyrazolecarboxamide derivative (4-amino-N-[(4-chlorophenyl)]-3-methyl-1-phenyl-1H-thieno [2, 3-c] pyrazole-5-carboxamide) in African catfish, Clarias gariepinus, exposed to 1 mg/L PbNO₃. Fish were intramuscularly injected with pyrazole-5-carboxamidederivative according to the following groupings: Group 1 (control), Group 2 (1 mg/L lead nitrate), Group 3 (1 mg/L lead nitrate + 5 mg pyrazole derivative/kg body weight), and Group 4 (1 mg/L lead nitrate + 10 mg pyrazole derivative/kg body weight) for two weeks and four weeks. Lead nitrate (1 mg/L) caused significant elevation of serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), creatinine, uric acid, cholesterol, and glucose-6-phosphate dehydrogenase (G6PDH) compared to the control group after two and four weeks of exposure, while serum total lipids, alkaline phosphatase (ALP), and lactate dehydrogenase (LDH) were significantly reduced compared to the control group. Furthermore, levels of antioxidant enzymes superoxide dismutase (SOD) and catalase (CAT) and total antioxidant capacity (TAC) were reduced in group 2 compared to the control group. However, in group 2, hepatic lipid peroxidation (LPO) and DNA fragmentation percentage were significantly increased compared to the control group. Histopathological changes in the liver of lead-exposed groups included marked disturbance of hepatic tissue organization, degeneration of hepatocytes, dilation of blood sinusoids and the central vein as well as necrosis. Injection of pyrazole derivative for two weeks and four weeks reversed alterations in biochemical parameters, antioxidant biomarkers, lipid peroxidation, hepatic DNA damage, and histopathological changes in liver tissue induced by 1 mg/L lead nitrate. This amelioration was higher in response to high-dose pyrazole derivative (10 mg) at the fourth week of exposure, showing concentration-and time-dependency. Overall, the sensitized derivative pyrazolecarboxamide is likely a useful tool to minimize the effects of lead toxicity due to its potent antioxidant activity.

Adverse effect studies of gasoline exhaust are scarce, even though gasoline direct injection (GDI) vehicles can emit a high number of particles.The aim of this study was to conduct an in vitro hazard assessment of different GDI exhausts using two different cell culture models mimicking the human airway. In addition to gasoline particle filters (GPF), the effects of two lubrication oils with low and high ash content were assessed, since it is known that oils are important contributors to exhaust emissions.Complete exhausts from two gasoline driven cars (GDI1 and GDI2) were applied for 6 h (acute exposure) to a multi-cellular human lung model (16HBE14o-cell line, macrophages, and dendritic cells) and a primary human airway model (MucilAir™). GDI1 vehicle was driven unfiltered and filtered with an uncoated and a coated GPF. GDI2 vehicle was driven under four settings with different fuels: normal unleaded gasoline, 2% high and low ash oil in gasoline, and 2% high ash oil in gasoline with a GPF. GDI1 unfiltered was also used for a repeated exposure (3 times 6 h) to assess possible adverse effects.After 6 h exposure, no genes or proteins for oxidative stress or pro-inflammation were upregulated compared to the filtered air control in both cell systems, neither in GDI1 with GPFs nor in GDI2 with the different fuels. However, the repeated exposure led to a significant increase in HMOX1 and TNFa gene expression in the multi-cellular model, showing the responsiveness of the system towards gasoline engine exhaust upon prolonged exposure.The reduction of particles by GPFs is significant and no adverse effects were observed in vitro during a short-term exposure. On the other hand, more data comparing different lubrication oils and their possible adverse effects are needed. Future experiments also should, as shown here, focus on repeated exposures.

One of the fundamentals in the ecotoxicological studies is the need of data comparison, which can be easily reached with the help of a standardized biological model. In this context, any biological model has been still proposed for the biomonitoring and risk evaluation of freshwaters until now. The aim of this review is to illustrate the ecotoxicological studies carried out with the zebra mussel Dreissena polymorpha in order to suggest this bivalve species as possible reference organism for inland waters. In detail, we showed its application in biomonitoring, as well as for the evaluation of adverse effects induced by several pollutants, using both in vitro and in vivo experiments. We discussed the advantages by the use of D. polymorpha for ecotoxicological studies, but also the possible limitations due to its invasive nature.

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.

Currently, urbanization is associated with an increase in air pollutants that contribute to invasive pathogen infections by altering the host's innate immunity and antimicrobial resistance capability. Streptococcus pyogenes, also known as Group A Streptococcus (GAS), is a gram-positive opportunistic pathogen that causes a wide range of diseases, especially in children and immunosuppressed individuals. Diesel exhaust particle (DEP), a significant constituent of particulate matter (PM), are considered a prominent risk factor for respiratory illness and circulatory diseases worldwide. Several clinical and epidemiological studies have identified a close association between PM and the prevalence of viral and bacterial infections. This study investigated the role of DEP exposure in increasing pulmonary and blood bacterial counts and mortality during GAS M1 strain infection in mice. Thus, we characterized the upregulation of reactive oxygen species production and disruption of tight junctions in the A549 lung epithelial cell line due to DEP exposure, leading to the upregulation of GAS adhesion and invasion. Furthermore, DEP exposure altered the leukocyte components of infiltrated cells in bronchoalveolar lavage fluid, as determined by Diff-Quik staining. The results highlighted the DEP-related macrophage dysfunction, neutrophil impairment, and imbalance in pro-inflammatory cytokine production via the toll-like receptor 4/mitogen-activated protein kinase signaling axis. Notably, the tolerance of the GAS biofilms toward potent antibiotics and bacterial resistance against environmental stresses was also significantly enhanced by DEP. This study aimed to provide a better understanding of the physiological and molecular interactions between exposure to invasive air pollutants and susceptibility to invasive GAS infections.

As drug abuse has become increasingly serious, carbamazepine (CBZ) is discharged into the aquatic environment with municipal sewage, causing potential harm to aquatic organisms. Here, we utilized zebrafish, an aquatic vertebrate model, to comprehensively evaluate the hepatotoxicity of CBZ. The larvae were exposed to 0.07, 0.13, and 0.26 mmol/L CBZ from 72 hpf to 144 hpf, and the adults were exposed to 0.025, 0.05, and 0.1 mmol/L CBZ for 28 days. The substantial changes were observed in the size and histopathology of livers, indicating that CBZ induced severe hepatoxicity in the larvae and adults. Oil red O staining demonstrated CBZ exposure caused severe lipid accumulation in the livers of both larvae and adults. Furthermore, CBZ exposure facilitated hepatocyte apoptosis through TUNEL staining, which was caused by rising ROS content. Subsequently, down-regulation of genes related to the Wnt pathway in exposure groups indicated that CBZ inhibited the development of liver via the Wnt/β-catenin signaling pathway. In conclusion, CBZ induced severe hepatotoxicity by promoting lipid accumulation, generating excessive ROS production, and inhibiting the Wnt/β-catenin signaling pathway in zebrafish. The results reveal the occurrence of CBZ-induced hepatotoxicity in zebrafish and clarify its mechanism of action, which potentially illustrate environmental concerns associated with CBZ exposure.

Although the abiotic and biotic transformation/degradation (T/D) processes of tetrabromobisphenol A (TBBPA) have been widely investigated in model experiments, few reviews have focused on these processes along with their metabolites or degradation products. In this paper, we summarize the current knowledge on the T/D of TBBPA and its derivatives, including abiotic and biotic T/D strategies/conditions, mechanisms, metabolites and environmental occurrences. Various treatments, such as pyrolysis, photolysis, chemical reactions and biotransformation, have been employed to study the metabolic mechanism of TBBPA and its derivatives and to remediate associated contaminated environments. To date, more than 100 degradation products and metabolites have been identified, dominated by less brominated compounds such as bisphenol A, 2,6-dibromo-4-isopropylphenol, 2,6-dibromo-4-hydroxyl-phenol, 2,6-dibromophenol, isopropylene-2,6-dibromophenol, 4-(2-hydroxyisopropyl)-2,6-dibromophenol, etc. It can be concluded that the T/D of TBBPA mainly takes place through debromination and β-scission. In some environmental media and human and animal tissues, brominated metabolites, glucoside and sulfate derivatives are also important T/D products. Here, the T/D products of TBBPA and its derivatives have been most comprehensively presented from the literature in recent 20 years. This review will enhance the understanding of the environmental behaviors of TBBPA-associated brominated flame retardants along with their ecological and health risks.