Biotechnological strategies have become effective in the remediation of polluted soils as they are cost-effective and do not present a risk of secondary pollution. However, using a single bioremediation technique (microorganism or plant) is not suitable for achieving a high remediation rate of polluted saline-alkali soils with heavy metals. Therefore, the present study aims to assess the effects and mechanisms of combined ryegrass and Fusarium incarnatum on the zinc (Zn)-polluted saline-alkali soil over 45 days. According to the obtained results, the combined Fusarium incarnatum-ryegrass showed the highest remediation rate of 49.35% after 45 days, resulting in a significantly lower soil Zn concentration than that observed in the control group. In addition, the inoculation of Fusarium incarnatum showed a positive effect on the soil EPS secretion. The soil protein contents ranged from 0.035 to 0.055 mg/kg, while the soil polysaccharide contents increased from 0.25 to 0.61 mg/g. The soil microbial flora and ryegrass showed resistance to saline and alkaline stresses through the secretion of extracellular polysaccharides. The three-dimensional fluorescence spectrum (3D-EEM) confirmed that EPS in the soil was mainly a fulvic acid-like substance. The fluorescein diacetate (FDA) hydrolase activity in the saline-alkali soil was first increased due to the effect of Fusarium incarnatum and then decreased to a minimum value of 96 μg/(g·h). In addition, the Fusarium incarnatum inoculation improved the diversity and richness of soil fungi. Although the Fusarium incarnatum inoculation had a slight effect on the germination of ryegrass, it increased the biomass and enrichment coefficient. The results revealed a translocation factor (TF) value of 0.316 at 45 days after ryegrass sowing, showing significant enrichment of the soil Zn heavy metal zinc in the ryegrass roots.

Titanium dioxide nanoparticles (TiO₂ NPs) easily combine with other pollutants such as heavy metals because of their excellent physiochemical properties. However, how such an interaction may affect the binding behavior of metals onto biofilms remains largely unclear. This study, examined the effects of TiO₂ NPs on Cd²⁺ accumulation and toxicity for natural periphytic biofilms were examined. The adsorption kinetics showed that adding 0.1 and 1 mg/L TiO₂–NPs increased the Cd²⁺ adsorption of biofilms at equilibrium by 23.5% and 35.8%, respectively. However, adding 10 mg/L TiO₂ NPs increased the Cd²⁺ adsorption of biofilms at equilibrium by only 1.9%. The adsorption isotherms indicate that the presence of TiO₂ NPs considerably increased the Cd²⁺ adsorption capacity of the biofilms; however, this effect became less prominent at high TiO₂ NP concentrations. The optimum pH for Cd²⁺ adsorption increased with increasing Cd²⁺ and TiO₂ NP contents. At low concentrations, the coexistence of Cd²⁺ and TiO₂ NPs may facilitate their respective accumulation by stimulating the secretion of extracellular polymeric substances and enhancing the microbial activity of the biofilm. The presence of TiO₂ NPs increases the surface binding energy between Cd²⁺ and functional groups such as carboxyl groups, enhancing the Cd²⁺ accumulation on the biofilm.

Systemic studies on the bioremediation of co-contaminated PAHs and heavy metals are lacking, and this paper provides an in-depth review on the topic. The released sources and transport of co-contaminated PAHs and heavy metals, including their co-occurrence through formation of cation-π interactions and their adsorption in soil are examined. Moreover, it is investigated that co-contamination of PAHs and heavy metals can drive a synergistic positive influence on bioremediation through enhanced secretion of extracellular polymeric substances (EPSs), production of biosynthetic genes, organic acid and enzymatic proliferation. However, PAHs molecular structure, PAHs-heavy metals bioavailability and their interactive cytotoxic effects on microorganisms can exert a challenging influence on the bioremediation under co-contaminated conditions. The fluctuations in bioavailability for microorganisms are associated with soil properties, chemical coordinative interactions, and biological activities under the co-contaminated PAHs-heavy metals conditions. The interactive cytotoxicity caused by the emergence of co-contaminants includes microbial cell disruption, denaturation of DNA and protein structure, and deregulation of antioxidant biological molecules. Finally, this paper presents the emerging strategies to overcome the bioavailability problems and recommends the use of biostimulation and bioaugmentation along with the microbial immobilization for enhanced bioremediation of PAHs-heavy metals co-contaminated sites. Better knowledge of the bioremediation potential is imperative to improve the use of these approaches for the sustainable and cost-effective remediation of PAHs and heavy metals co-contamination in the near future.

Selenium engineered nanomaterials (Se ENMs)-enabled agriculture has developed rapidly, however, the roles of surface charge in the bioavailability and enrichment efficiency of Se ENMs are still unknown. Herein, various Se ENMs of homogenous size (40–60 nm) and different surface charges (3.2 ± 0.7, −29.0 ± 0.4, and 45.5 ± 1.3 mV) were prepared to explore the Se content and nutritional quality in Brassica chinensis L. The results demonstrated that soil application of various Se ENMs (0.05 mg kg⁻¹) displayed different bio-availabilities via modulating the secretion of root exudates (e.g., tartaric, malic, and citric acids), microbial community composition (e.g., Flavobacterium, Pseudomonas, Paracoccus, Bacillus and Rhizobium) and root cell wall. Negatively charged Se ENMs (Se (−)) showed the highest Se content in the shoot of B. chinensis (3.7-folds). Se (−) also significantly increased yield (156.9%) and improved nutritional quality (e.g., ascorbic acid, amino acids, flavonoids, fatty acids, and tricarboxylic acid) of B. chinensis. Moreover, after harvest, the Se (−) did not lead to significant change in Se residue in soil, but the amount of Se residue in soil was increased by 5.5% after applying the traditional Se fertilizer (selenite). Therefore, this study provides useful information for producing Se-fortified agricultural products, while minimizing environmental risk.

Cigarette smoke (CS) affects immune functions, leading to severe outcomes in smokers. Robust evidence addresses the immunotoxic effects of combustible tobacco products. As heat-not-burn tobacco products (HNBT) vaporize lower levels of combustible products, we here compared the effects of cigarette smoke (CS) and HNBT vapor on Jurkat T cells. Cells were exposed to air, conventional cigarettes or heatsticks of HNBT for 30 min and were stimulated or not with phorbol myristate acetate (PMA). Cell viability, proliferation, reactive oxygen species (ROS) production, 8-OHdG, MAP-kinases and nuclear factor κB (NFκB) activation and metallothionein expression (MTs) were assessed by flow cytometry; nitric oxide (NO) and cytokine levels were measured by Griess reaction and ELISA, respectively. Levels of metals in the exposure chambers were quantified by inductively coupled plasma mass spectrometry. MT expressions were quantified by immunohistochemistry in the lungs and liver of C57Bl/6 mice exposed to CS, HNBT or air (1 h, twice a day for five days: via inhalation). While both CS and HBNT exposures increased cell death, CS led to a higher number of necrotic cells, increased the production of ROS, NO, inflammatory cytokines and MTs when compared to HNBT-exposed cells, and led to a higher expression of MTs in mice. CS released higher amounts of metals. CS and HNBT exposures decreased PMA-induced interleukin-2 (IL-2) secretion and impaired Jurkat proliferation, effects also seen in cells exposed to nicotine. Although HNBT vapor does not activate T cells as CS does, exposure to both HNBT and CS suppressed proliferation and IL-2 release, a pivotal cytokine involved with T cell proliferation and tolerance, and this effect may be related to nicotine content in both products.

Polychlorinated biphenyls (PCBs) are one of the most refractory organic environmental pollutants that ubiquitous existence in nature. Due to the polymorphism of their metabolic pathway and corresponding downstream metabolites, PCBs’ toxicities are complicated and need extended investigation. In the present study, we discovered a novel regulatory mechanism of PCB quinone metabolite-driven programmed cell death (PCD), namely, necroptosis. We first confirmed that PCB quinone induces cancerous HeLa and MDA-MB-231 cells necroptosis via the phosphorylation of mixed lineage kinase domain-like MLKL (p-MLKL). Then, we found that PCB quinone-stimulated p-MLKL enhances exosome biogenesis and secretion. Exosome interacts with p-MLKL and releases p-MLKL to the outside of the cell, and ultimately alleviating PCB quinone-induced necroptosis. The inhibition of exosome secretion by GW4869 significantly elevated necroptotic level, indicating the establishment of a short negative feedback loop of MLKL-exosome secretion upon PCB quinone challenge. Since exosome-mediated signaling showed great implications in various human diseases, this work may provide a new mechanism for PCBs-associated toxicity.

Low pH and aluminum (Al)-toxicity often coexist in acidic soils. Citrus sinensis seedlings were treated with nutrient solution at a pH of 2.5, 3.0, 3.5 or 4.0 and an Al concentration of 0 or 1 mM for 18 weeks. Thereafter, malate, citrate, isocitrate, acid-metabolizing enzymes, and nonstructural carbohydrates in roots and leaves, and release of malate and citrate from roots were measured. Al concentration in roots and leaves increased under Al-toxicity, but it declined with elevating nutrient solution pH. Al-toxicity increased the levels of glucose, fructose, sucrose and total soluble sugars in leaves and roots at each given pH except for a similar sucrose level at pH 2.5–3.0, but it reduced or did not alter the levels of starch and total nonstructural carbohydrates (TNC) in leaves and roots with the exception that Al improved TNC level in roots at pH 4.0. Levels of nonstructural carbohydrates in roots and leaves rose with reducing pH with a few exceptions with or without Al-toxicity. A potential model for the possible role of root organic acid (OA) metabolism (anions) in C. sinensis Al-tolerance was proposed. With Al-toxicity, the elevated pH upregulated the OA metabolism, and increased the flow of carbon to OA metabolism, and the accumulation of malate and citrate in roots and subsequent release of them, thus reducing root and leaf Al and hence eliminating Al-toxicity. Without Al-toxicity, low pH stimulated the exudation of malate and citrate, an adaptive response of Citrus to low pH. The interactive effects of pH and pH on OA metabolism were different between roots and leaves.

As an important part of extracellular secondary metabolites, extracellular polymeric substances (EPS) can play a significant role in protecting cells from the threat of exogenous substances, including nanoparticles (NPs). However, the regulation mechanisms of EPS secretion under NPs exposure remain largely unknown. This study investigated the signaling pathways and molecular responses related to EPS secretion of algae (Chlorella pyrenoidosa) upon the exposures to anatase and rutile TiO₂ NPs (nTiO₂-A and nTiO₂-R, respectively) at two similar toxic (20% and 50% of algal growth inhibition) concentrations. The results showed that EPS responded to nTiO₂ stress via excess secretion and compositional variation, and nTiO₂-A induced more EPS secretion than nTiO₂-R at similar toxicity concentrations. The up-regulation of the Ca²⁺ signaling pathway might play a greater role in promoting EPS secretion under nTiO₂-R exposure compared with nTiO₂-A exposure, while the significantly increased intracellular ROS could mainly account for the increased EPS secretion under nTiO₂-A exposure. The up-regulated genes related to biological synthesis and protein metabolism and the enhanced biosynthetic metabolism might be the direct causes of the increased EPS secretion. The increased ROS could have a greater effect on the amino acid metabolism and related genes upon the exposure to nTiO₂-A than nTiO₂-R to induce more EPS secretion. More serious membrane damage caused by nTiO₂-R than nTiO₂-A would affect the intracellular inositol phospholipid metabolism more severely, while the inositol phospholipid pathway and Ca²⁺ signaling pathway might agree and communicate with each other inherently to regulate EPS secretion upon nTiO₂-R exposure. The findings address the regulation mechanisms of algal EPS secretion under nTiO₂ exposure and provide new insights into algal bio-responses to nTiO₂ exposure.

A tropical soil Actinomycete, Gordonia amicalis HS-11, has been previously demonstrated to degrade unsaturated and saturated hydrocarbons (squalene and n-hexadecane, respectively) in an effective manner. In present study, G. amicalis HS-11 degraded 92.85 ± 3.42% of the provided diesel oil [1% (v/v)] after 16 days of aerobic incubation. The effect of different culture conditions such as carbon source, nitrogen source, pH, temperature, and aeration on degradation was studied. During degradation, this Actinomycete synthesized surface active compounds (SACs) in an extracellular manner that brought about a reduction in surface tension from 69 ± 2.1 to 30 ± 1.1 mN m⁻¹ after 16 days. The morphology of cells grown on diesel was monitored by using a Field Emission Scanning Electron Microscope. Diesel-grown cells were longer and clumped with smooth surfaces, possibly due to the secretion of SACs. The interaction between the cells and diesel oil was studied by Confocal Laser Scanning Microscope. Some cells were adherent on small diesel droplets and others were present in the non-attached form thus confirming the emulsification ability of this organism. The fatty acid profiles of the organism grown on diesel oil for 48 h were different from those on Luria Bertani Broth. The genotoxicity and cytotoxicity of diesel oil before and after degradation were determined. Cytogenetic parameters such as mitotic index (MI); mitosis distribution and chromosomal aberration (type and frequency) were assessed. Oxidative stress was evaluated by measuring levels of catalase, superoxide dismutase and concentration of malondialdehyde. On the basis of these studies it was deduced that the degradation metabolites were relatively non-toxic.

Perfluorooctanoic acid (PFOA) toxicity is of considerable concern due to its wide application, environmental persistence, and bioaccumulation. In the current study, we used a scaffold-free three-dimensional (3D) spheroid model of mouse liver cells (AML12) to explore the toxicity of PFOA and emerging alternatives (HFPO-DA and PFO4DA). Comparing the short-term (24 and 72 h treatment) toxicity of PFOA between conventional 2D monolayer cells and 3D spheroids, we found that spheroids had higher EC₅₀ values and lower ROS levels after treatment, indicating their greater resistance to PFOA. Cell viability (i.e., adenosine triphosphate (ATP) content and lactate dehydrogenase (LDH) leakage) and liver-specific function (i.e., albumin secretion) were stable in spheroids through 28 day of culture. However, under 100 and 200 μM-PFOA treatment for 28 day, ROS levels, LDH leakage, and caspase3/7 activity all increased significantly. As a sensitive parameter, ROS showed a significant increase at 21 day, even in the 50 μM-PFOA group. Consistent with the elevation of ROS and caspase3/7, the expressions of oxidative stress- and apoptosis-related genes, including Gsta2, Nqo1, Ho-1, caspase3, p53, and p21, were induced in dose- and time-dependent manners after PFOA exposure. The peroxisome proliferator-activated receptor alpha (PPARα) pathway was also activated after treatment, with significant induction of its target genes, Fabp4 and Scd1. Similar to PFOA, both HFPO-DA and PFO4DA activated the PPARα pathway, induced ROS levels, and initiated cell damage, though at a relatively lower extent than that of PFOA. Our results imply that the 3D spheroid model is a valuable tool in chronic toxicological studies.