In recent years, the cardiovascular toxicity of urban fine particulate matter (PM₂.₅) has sparked significant alarm. Mitochondria produce 90% of ATP and make up 30% of the volume of cardiomyocytes. Thus knowledge of myocardial mitochondrial dysfunction due to PM₂.₅ exposure is essential for further cardiotoxic effects. Here, the mechanism of PM₂.₅-induced cardiac hypertrophy through calcium overload and mitochondrial dysfunction was investigated in vivo and in vitro. Male and female BALB/c mice were given 1.28, 5.5, and 11 mg PM₂.₅/kg bodyweight weekly through oropharyngeal inhalation for four weeks and were assigned to low, medium, and high dose groups, respectively. PM₂.₅-induced myocardial edema and cardiac hypertrophy were detected in the high-dose group. Mitochondria were scattered and ruptured with abnormal ultrastructural morphology. In vitro experiments on human cardiomyocyte AC16 showed that exposure to PM₂.₅ for 24 h caused opened mitochondrial permeability transition pore --leading to excessive calcium production, decreased mitochondrial membrane potential, weakened mitochondrial respiratory metabolism capacity, and decreased ATP production. Nevertheless, the administration of calcium chelator ameliorated the mitochondrial damage in the PM₂.₅-treated group. Our in vivo and in vitro results confirmed that calcium overload under PM₂.₅ exposure triggered mTOR/AKT/GSK-3β activation, leading to mitochondrial bioenergetics dysfunction and cardiac hypertrophy.

We investigated the in vitro effects of pyriproxyfen on ionic balance in the testis of the zebrafish by measuring ⁴⁵Ca²⁺ influx. In vivo pyriproxyfen treatment was carried out to study oxidative stress, and conduct morphological analysis of the testis and liver. Whole testes were incubated in vitro with/without pyriproxyfen (10⁻¹², 10⁻⁹ or 10⁻⁶ M; 30 min) and ⁴⁵Ca²⁺ influx determined. To study pyriproxyfen’s mechanism of action, inhibitors/activators of ionic channels or pumps/exchangers, protein kinase inhibitors or a calcium chelator were added 15 min before the addition of ⁴⁵Ca²⁺ and pyriproxyfen. We evaluated the in vivo effects of 7 day exposure to waterborne pyriproxyfen (10⁻⁹ M) on reactive oxygen species (ROS) formation, lipid peroxidation, and reduced glutathione content (GSH), glutathione S-transferase (GST), superoxide dismutase (SOD), catalase (CAT) and γ-glutamyltransferase (GGT) activity. Morphological analyses of the testis and liver were carried out after in vivo exposure of D. rerio to pyriproxyfen. Pyriproxyfen increased ⁴⁵Ca²⁺ influx by opening the voltage-dependent T-type channels (T-type VDCC), inhibiting sarco/endoplasmic reticulum ⁴⁵Ca²⁺-ATPase (SERCA) and the NCX exchanger (forward mode) and by mobilizing calcium from stores. The involvement of potassium channels and protein kinase C (PKC) was also demonstrated in pyriproxyfen-induced intracellular calcium elevation. In vivo pyriproxyfen treatment of D. rerio increased lipid peroxidation, decreased GSH content and increased GST activity in testes, in addition to increasing the number and size of spermatogonia cysts and inducing hepatocyte basophilia and dilation of blood vessels in the liver. The toxicity of pyriproxyfen is mediated by calcium overload, increased lipid peroxidation, and a diminished antioxidant capacity in the testis, due to GSH depletion, and altered spermatogenesis. The development of high basophilia in the liver suggests that pyriproxyfen may have estrogenic activity, possibly acting as an endocrine-disruptor. These findings indicate that these alterations may contribute to pyriproxyfen toxicity and spermatogenesis disruption.

PM2.5 is becoming a worldwide environmental problem, which profoundly endangers public health, thus progressively capturing public attention this decade. As a fragile target of PM2.5, the underlying mechanisms of endothelial cell damage are still obscure. According to the previous microarray data and signaling pathway analysis, a new form of cell death termed ferroptosis in the current study is proposed following PM2.5 exposure. In order to verify the vital role of ferroptosis in PM2.5-induced endothelial lesion and further understand the potential mechanism involved, intracellular iron content, ROS release and lipid peroxidation, as well as biomarkers of ferroptosis were detected, respectively. As a result, uptake of particles increases cellular iron content and ROS production. Meanwhile, GSH depletion, and the decrease of GSH-Px and NADPH play significant roles in PM2.5-induced endothelial cell ferroptosis. Moreover, significantly changed expression of TFRC, FTL and FTH1 hinted that dysfunction of iron uptake and storage is a major inducer of ferroptosis. Importantly, index monitored above can be partially rescued by lipid peroxidation inhibitor ferrostatin-1 and iron chelator deferoxamine mesylate, which mediated antiferroptosis activity mainly depends on the restoration of antioxidant activity and iron metabolism. In conclusion, our data basically show that PM2.5 enhances ferroptosis sensitivity with increased ferroptotic events in endothelial cells, in which iron overload, lipid peroxidation and redox imbalance act pivotal roles.

Organic complexing agents, such as ethylenediaminetetraacetic acid (EDTA), nitrilotriacetic acid (NTA) and picolinic acid, have been widely used at nuclear sites and are therefore found as common co-contaminants in radioactive contaminated land. This study has explored the mechanisms by which these three complexing agents affect the sorption of Th(IV) to pure silica and a natural sand. EDTA, NTA and, to a lesser extent, picolinic acid decreased the sorption of Th to silica, demonstrating the formation and solubility of Th complexes. However, Th sorption to sand was kinetically controlled and complexation enhanced the rate of Th sorption. EDTA and NTA did not sorb significantly to the sand, and metal desorption indicated that the mechanism involved exchange with sand-associated metals. At equilibrium, however, Th sorption was not affected by the presence of the ligands, and modelling suggested that the interaction between Th and the surface binding sites controlled Th sorption thermodynamically.

Benthic invertebrates can uptake metals through diffusion of free ion solutes, or ingestion of sediment-bound forms. This study investigated the efficacy of the metal chelating resin SIR 300™ in adsorbing porewater metals and isolating pathways of metal exposure. A field experiment (Botany Bay, Sydney, Australia) and a laboratory toxicity test each manipulated the availability of porewater metals within contaminated and uncontaminated sediments. It was predicted that within contaminated sediments, the resin would adsorb porewater metals and reduce toxicity to invertebrates, but in uncontaminated sediments, the resin would not significantly affect these variables. Whereas in the laboratory, the resin produced the predicted results, in the field the resin increased porewater metal concentrations of contaminated sediments for at least 34 days and decreased abundances of four macroinvertebrate groups, and richness in all sediments. These contrasting findings highlight the limits of extrapolating the results of laboratory experiments to the field environment.

Two common sorrel (Rumex acetosa) accessions, one from a Zn–Pb contaminated site (CS accession) and the other from an uncontaminated site (UCS accession), were hydroponically exposed to a mixture of heavy metals (Pb2+ + Zn2+ + Cd2+) with and without EDTA at an equimolar rate. The metallicolous CS accession showed a higher tolerance to metal treatment in the absence of the chelating agent, whereas the UCS accession was especially tolerant to EDTA treatment alone. Combination of metal and EDTA treatment resulted in a higher Pb accumulation in shoots of both accessions although plants hardly showed phytotoxic symptoms. Cd and Zn uptake was not augmented by EDTA addition to the polymetallic medium. Chelant-assisted Pb accumulation was 70% higher in the CS accession than in the UCS accession, despite the fact that the former accession evapotranspired less water than the UCS accession. These results support the existence of a non-selective apoplastic transport of metal chelates by R. acetosa roots, not related to transpiration stream.

An integrated experimental program was conducted to remove Cd, Pb and Cu from contaminated soil. The chelate agents nitrilotriacetic acid (NTA), diethylenetriamine pentaacetic acid (DTPA) and ethyleneglycol tetraacetic acid (EGTA) were used as washing solutions under different pH conditions and concentrations. Results showed that the extraction efficiency for Cd in decreasing order was NTA > EGTA > DTPA, while for Pb and Cu it was DTPA > NTA > EGTA. The use of higher chelate concentrations did not necessarily result in greater extraction efficiency. Electrokinetic remediation was applied by conditioning anolyte–catholyte pH to neutral values in order to avoid any potential alterations to the physicochemical soil properties. The removal efficiency for Cd was 65–95%, for Cu 15–60%, but for Pb was less than 20%. The phytotoxicity of the treated soil showed that the soil samples from the anode section were less phytotoxic than the untreated soil, but the phytotoxicity was increased in the samples from the cathode section. Cadmium, lead and copper were extracted from contaminated soil by integrated electrokinetic and soil washing studies.

Ochratoxin A (OTA) is a frequent contaminant of feed and food worldwide. The toxicity of OTA on intestinal barrier was investigated in porcine intestinal epithelial cells (IPEC-J2). We observed that OTA induced intestinal barrier dysfunction as indicated by the reduction in transepithelial electrical resistance (TEER) and elevation in paracellular permeability to 4 kDa dextran. The barrier dysfunction was accompanied with tight junction disruption including a down-regulation in ZO-1 expression and redistribution of Occludin and ZO-1. Moreover, OTA exposure increased reactive oxygen species (ROS) generation, elevated the intracellular calcium level ([Ca²⁺]c) and activated myosin light chain kinase (MLCK). Simultaneously, NAC, a ROS scavenger, blocked OTA-induced ROS generation, [Ca²⁺]c elevation, barrier dysfunction and tight junction disruption, suggesting that OTA-induced ROS generation may act as a trigger. Next, we found that OTA-induced MLCK activation was inhibited by BAPTA-AM, the cytosolic Ca²⁺ chelator, demonstrating that OTA-induced MLCK activation is dependent on [Ca²⁺]c elevation. Furthermore, inhibition of MLCK with ML-7 or inhibition of [Ca²⁺]c elevation with BAPTA-AM markedly prevented OTA-induced barrier dysfunction and tight junction disruption. Taken together, our results indicated that OTA induces ROS generation, and then elevates the [Ca²⁺]c and MLCK activity in turn, which finally induces barrier dysfunction and disrupts tight junction in IPEC-J2 cell monolayers.

This study investigates the column leaching of a soil contaminated mainly with Cr and Ni by using two chelants: citric acid (biodegradable) and EDTA (non-biodegradable) followed with water rinse. The chelants lead to Cr and Ni leaching, in addition to major elements (Ca, Fe, Mg, Al, Mn and Zn) showing the dissolution of soil mineral constituents. EDTA leaches more major elements and Ni than citric acid related to the respective stability of metal–chelant complexes; citric acid leaches more Cr than EDTA, certainly because of a substitution reaction with Cr(VI). In the case of alternating chelant/water applications, leaching occurs during the chelant applications, but also during water applications. In the case of chelant/water applications followed by continuous water application, both Cr and Ni leach over time. This increased mobility could be due to the residual chelant present in soil as well as to the dissolution/mobilization of mineral or organic soil fractions.