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.

Cadmium (Cd) and lead (Pb) are ubiquitously present in surface soils, due to anthropogenic activities, causing threat to ecological and human health because of their carcinogenic nature. They accumulate in large quantities in the environment and affect negatively soil microbiota, plants, animals, and humans. For the cleanup of Cd/Pb polluted soils, different plant species have been studied. Many plants have shown the potential to hyperaccumulate Cd/Pb in their above-ground tissues. These plants decrease soil pH by root exudation or by releasing H⁺ ions, and this, in turn, increases the bioavailability of Cd/Pb for plant uptake. Different environmental processes related to soil organic matter, microorganisms, pH, genetic modifications, and various soil-borne chelating agents affect the potential of phytoremediation technology. Review papers trying to identify a single factor influencing the phytoremediation of heavy metals are available in the literature. However, an integrated approach dealing with different factors involved in the remediation of both metals is scarcely discussed. The main focus of this review is to discuss the phytoextraction technique for Cd/Pb removal from contaminated sites along with detoxification mechanisms. Further, the challenges in the Cd/Pb phytoextraction and different options available to cope with these challenges are also discussed. The update on the relevant findings on the use of microorganisms and amendments in enhancing the Cd/Pb phytoextraction is also provided. Finally, the areas to be explored in future research for the removal of Cd/Pb by integrated strategies have been discussed.

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.

Municipal solid wastes (MSW) can be composted to become an organic fertilizer. However, besides plant nutrients, it can also contain high concentration of some toxic metals than can pollute agricultural soils, contaminate food, animals and human being. A greenhouse experiment was carried out for two purposes: i) to evaluate the concentrations of cadmium, copper, chromium, nickel, lead and zinc in four Brazilian MSW composts, and, ii) to know which is the best solution for extracting those metals in phytoavailable form from the composts. In order to evaluate the phytoavailability of metals, they were extracted with six chemical extractants: i) water, ii) 0.05 mol L⁻¹ Ca(NO₃)₂, iii) 0.1 mol L⁻¹ HCl, iv) 0.005 mol L⁻¹ DTPA at pH 7.3, v) 0.05 mol L⁻¹ CaCl₂ and vi) Mehlich 3 solution. In addition, lettuces were cultivated as a test plant in pots containing 1.8 kg of MSW compost as substrate. Fifty-six days later, lettuce plants were harvested. New lettuces were then planted for a second cycle, and then harvested after fifty-six days. Semi-total concentration of metals in composts and total in plants was also determined through an extraction with nitric-perchloric acid. Semi–total concentration of Cd and Pb exceeded the intervention limits from Brazil in the four studied composts, and lettuce plants were polluted by those two elements. Therefore, compost made of MSW must be characterized before being used for agricultural soils. Copper and nickel in phytoavailable were effectively extracted with the strongest chelating agents used, HCl and Mehlich 3, probably because most metal is bound to organic matter in the compost. Cadmium, chromium, lead and zinc were no efficiently extracted with any of the tested extractants.

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.

Incubation and pot experiments using poplar (Populus nigra L. cv. Wolterson) were performed in order to evaluate the questionable efficiency of EDDS-enhanced phytoextraction of Cu from contaminated soils. Despite the promising conditions of the experiment (low contamination of soils with a single metal with a high affinity for EDDS, metal tolerant poplar species capable of producing high biomass yields, root colonization by mycorrhizal fungi), the phytoextraction efficiency was not sufficient. The EDDS concentrations used in this study (3 and 6 mmol kg-1) enhanced the mobility (up to a 100-fold increase) and plant uptake of Cu (up to a 65-fold increase). However, despite EDDS degradation and the competition of Fe and Al for the chelant, Cu leaching cannot be omitted during the process. Due to the low efficiency, further research should be focused on other environment-friendly methods of soil remediation.

Three experiments were conducted to optimize the use of ethylenediaminetetraacetic acid (EDTA) for reclaiming urban soils contaminated with trace metals. As compared to Na2EDTA, (NH4)2EDTA extracted 60% more Zn and equivalent amounts of Cd, Cu and Pb from a sandy loam. When successively saturating and draining loamy sand columns during a washing cycle, which submerged it once with a (NH4)2EDTA wash and four times with deionised water, the post-wash rinses largely contributed to the total cumulative extraction of Cd, Co, Cr, Cu, Mn, Ni, Pb and Zn. Both the washing solution and the deionised water rinses were added in a 2:5 liquid to soil (L:S) weight ratio. For equal amounts of EDTA, concentrating the washing solution and applying it and the ensuing rinses in a smaller 1:5 L:S weight ratio, instead of a 2:5 L:S weight ratio, increased the extraction of targeted Cr, Cu, Ni, Pb and Zn. A single EDTA addition is best utilised in a highly concentrated washing solution given in a small liquid to soil weight ratio.

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.

The toxicity of commercially-available CuO and ZnO nanoparticles (NPs) to pathogenic bacteria was compared for a beneficial rhizosphere isolate, Pseudomonas chlororaphis O6. The NPs aggregated, released ions to different extents under the conditions used for bacterial exposure, and associated with bacterial cell surface. Bacterial surface charge was neutralized by NPs, dependent on pH. The CuO NPs were more toxic than the ZnO NPs. The negative surface charge on colloids of extracellular polymeric substances (EPS) was reduced by Cu ions but not by CuO NPs; the EPS protected cells from CuO NPs-toxicity. CuO NPs-toxicity was eliminated by a Cu ion chelator, suggesting that ion release was involved. Neither NPs released alkaline phosphatase from the cells’ periplasm, indicating minimal outer membrane damage. Accumulation of intracellular reactive oxygen species was correlated with CuO NPs lethality. Environmental deposition of NPs could create niches for ion release, with impacts on susceptible soil microbes.