Heavy metal toxicity has become an impediment to agricultural productivity, which presents major human health concerns in terms of food safety. Among them, arsenic (As) a non-essential heavy metal has gained worldwide attention because of its noxious effects on agriculture and public health. The increasing rate of global warming and anthropogenic activities have promptly exacerbated As levels in the agricultural soil, thereby causing adverse effects to crop genetic and phenotypic traits and rendering them vulnerable to other stresses. Conventional breeding and transgenic approaches have been widely adapted for producing heavy metal resilient crops; however, they are time-consuming and labor-intensive. Hence, finding new mitigation strategies for As toxicity would be a game-changer for sustainable agriculture. One such promising approach is harnessing plant microbiome in the era of ‘omics’ which is gaining prominence in recent years. The use of plant microbiome and their cocktails to combat As metal toxicity has gained widespread attention, because of their ability to metabolize toxic elements and offer an array of perquisites to host plants such as increased nutrient availability, stress resilience, soil fertility, and yield. A comprehensive understanding of below-ground plant-microbiome interactions and their underlying molecular mechanisms in exhibiting resilience towards As toxicity will help in identifying elite microbial communities for As mitigation. In this review, we have discussed the effect of As, their accumulation, transportation, signaling, and detoxification in plants. We have also discussed the role of the plant microbiome in mitigating As toxicity which has become an intriguing research frontier in phytoremediation. This review also provides insights on the advancements in constructing the beneficial synthetic microbial communities (SynComs) using microbiome engineering that will facilitate the development of the most advanced As remedial tool kit in sustainable agriculture.

Cadmium (Cd) is a toxic heavy metal that initiates diverse chronic diseases through food chains. Developing a biotechnology for manipulating Cd uptake in plants is beneficial to reduce environmental and health risks. Here, we identified a novel epigenetic mechanism underlying Cd accumulation regulated by an uncharacterized metallochaperone namely Heavy Metal Responsive Protein (HMP) in rice plants. OsHMP resides in cytoplasm and nucleus, dominantly induced by Cd stress and binds directly to Cd ions. OsHMP overexpression enhanced the rice growth under Cd stress but accumulated more Cd, whereas knockout or knockdown of OsHMP showed a contrasting effect. The enhanced Cd accumulation in the transgenic lines was confirmed by a long-term experiment with rice growing at the environmentally realistic Cd concentration in soil. The bisulfite sequencing and chromatin immunoprecipitation assessments revealed that Cd stress reduced significantly the DNA methylation at CpG (Cytosine-Guanine) and histone H3K9me2 marks in the upstream of OsHMP. By identifying a couple of mutants defective in DNA methylation and histone modification (H3K9me2) such as Osmet1 (methylatransfease1) and Ossdg714 (kryptonite), we found that the Cd-induced epigenetic hypomethylation at the region was associated with OsHMP overexpression, which consequently led to Cd detoxification in rice. The causal relationship was confirmed by the GUS reporter gene coupled with OsHMP and OsMET1 whereby OsMET1 repressed directly the OsHMP expression. Our work signifies that expression of OsHMP is required for Cd detoxification in rice plants, and the Cd-induced hypomethylation in the specific region is responsible for the enhanced OsHMP expression. In summary, this study gained an insight into the epigenetic mechanism for additional OsHMP expression which consequently ensures rice adaptation to the Cd-contaminated environment.

Insufficient evidence exists regarding the visible physiological toxic endpoints of MPs exposures on zebrafish larvae due to their small sizes. Herein, the impacts of micro-polystyrene particles (μ-PS) and 100 nm polystyrene particles (n-PS) on the toxicity of cadmium (Cd) through altering neutrophil expressions were identified and quantified in the transgenic zebrafish (Danio rerio) larvae Tg(lyz:DsRed2), and the effects were size-dependent. When exposed together with μ-PS, the amount of neutrophils in Cd treated zebrafish larvae decreased by 25.56% through reducing Cd content in the larvae. By contrast, although n-PS exposure caused lower Cd content in the larvae, the expression of neutrophils under their combined exposure remained high. The mechanism of immune toxicity was analyzed based on the results of metabonomics. n-PS induced high oxidative stress in the larvae, which promoted taurine metabolism and unsaturated fatty biosynthesis in n-PS + Cd treatment. This observation was accordance with the significant inhibition of the activities of superoxide dismutase and catalase enzymes detected in their combined treatment. Moreover, n-PS promoted the metabolic pathways of catabolic processes, amino acid metabolism, purine metabolism, and steroid hormone biosynthesis in Cd treated zebrafish larvae. Nanoplasctis widely coexist with other pollutants in the environment at relatively low concentrations. We conclude that more bio-markers of immune impact should be explored to identify their toxicological mechanisms and mitigate the effects on the environment.

Azoxystrobin (AZ) and pyraclostrobin (PY) are strobilurin fungicides that inhibit fungal mitochondrial respiration. In this study, a representative model, zebrafish (Danio rerio), was used as a test species for acute and developmental toxicity. Survival and malformation rates were observed only PY-treated embryos, with an LC₅₀ value of 77.75 ppb accompanied by a dramatic decrease in hatching rate, while AZ did not show great mortality. Morphological changes were observed in PY-treated embryos with the occurrence of pericadial edema at 25 ppb. A delay in growth was observed after treatment with pyraclostrobin at 50 ppb. Use of genetically engineered Tg(cmlc:EGFP) allowed fluorescence observation during heart development. PY interfered with normal heart development via upregulation of the nppa gene responsible for the expression of natriuretic peptides. Heart function was dramatically reduced as indicated by reduced heart rates. Increased expression of the nppa gene was also seen in AZ-treated embryos. The expression level of cyp24a1 was also up-regulated, while ugt1a1 and sult1st6 were down-regulated after treatment of zebrafish embryos with AZ or PY. Overall, strobilurin fungicides might inhibit normal heart formation and function within the range of concentrations tested.

Triclosan (TCS) is an organic compound with a wide range of antibiotic activity and has been widely used in items ranging from hygiene products to cosmetics; however, recent studies suggest that it has several adverse effects. In particular, TCS can be passed to both fetus and infants, and while some evidence suggests in vitro neurotoxicity, there are currently few studies concerning the mechanisms of TCS-induced developmental neurotoxicity. Therefore, this study aimed to clarify the effect of TCS on neural development using zebrafish models, by analyzing the morphological changes, the alterations observed in fluorescence using HuC-GFP and Olig2-dsRED transgenic zebrafish models, and neurodevelopmental gene expression. TCS exposure decreased the body length, head size, and eye size in a concentration-dependent manner in zebrafish embryos. It increased apoptosis in the central nervous system (CNS) and particularly affected the structure of the CNS, resulting in decreased synaptic density and shortened axon length. In addition, it significantly up-regulated the expression of genes related to axon extension and synapse formation such as α1-Tubulin and Gap43, while decreasing Gfap and Mbp related to axon guidance, myelination and maintenance. Collectively, these changes indicate that exposure to TCS during neurodevelopment, especially during axonogenesis, is toxic. This is the first study to demonstrate the toxicity of TCS during neurogenesis, and suggests a possible mechanism underlying the neurotoxic effects of TCS in developing vertebrates.

How to evaluate the ecological risk of transgenic technology is a focus of scientists because of the safety concerns raised by genetically modified (GM) organisms. Nevertheless, most studies are based on individual chemicals and always analyze the GM organism as a type of toxicant. In this study, we changed the approach and used GM organisms as the test objects with normal chemical exposure. Three types of chemicals (two substituted phenols, 4-chlorophenol and 4-nitrophenol; two ionic liquids, 1-butylpyridinium chloride and 1-butylpyridinium bromide; two pesticides, dichlorvos and glyphosate) were used to construct a six-component mixture system. The lethality to wild-type (N2) and sod-3::GFP (SOD-3) Caenorhabditis elegans was determined when they were exposed to the same mixture system after 12 and 24 h. The results showed that the pEC50 values of all of the single chemicals on SOD-3 were greater than those on N2 at 24 h. The toxicities of the single chemicals and nine mixture rays on the two strains increased with time. Notably, we discovered a significant difference between the two strains; time-dependent synergism occurred in mixtures on N2, but time-dependent antagonism occurred in mixtures on SOD-3. Finally, the strength of the synergism or antagonism turned to additive action on the two strains as the exposure time increased. These findings illustrated that the GM factor of the nematode influenced the mixture toxicological interaction at some exposure times. Compared with N2, SOD-3 were more sensitive to stress or toxic reactions. Therefore, the influence of the GM factor on mixture toxicological interactions in environmental risk assessment must be considered.

2,2′,4,4′-Tetrabromodiphenyl ether (BDE-47), a representative congener of polybrominated diphenyl ethers in the environment, is known to have reproductive toxicity. However, the underlying mechanisms remain to be clarified, especially in in vivo systems. In the present study, we employed Caenorhabditis elegans to study the effects of BDE-47 on reproduction. Our results showed that BDE-47 impaired worm fecundity and induced germ cell apoptosis. To elucidate the mechanisms, DNA damage and oxidative stress induction were investigated by determining the numbers of foci formation in transgenic worms expressing HUS-1::GFP and the levels of reactive oxygen species, respectively. We found that BDE-47 induced oxidative stress but not DNA damage, and treatment with the antioxidant, N-acetyl-L-cysteine, completely abrogated BDE-47-induced germ cell apoptosis. In addition, the apoptosis was blocked in mutants carrying mek-1, sek-1 or abl-1 loss-of-function alleles, but not in the p53/cep-1 deficient worms, suggesting that the mitogen-activated protein kinase (MAPK) signaling cascade was essential for BDE-47-induced germ cell apoptosis and p53/cep-1 was not required. Moreover, the apoptosis in the strains deficient for DNA damage response was not suppressed under BDE-47 treatment. Overall, we demonstrated that BDE-47 could induce oxidative stress and subsequent germ cell apoptosis in Caenorhabditis elegans through a MAPK-mediated p53-independent pathway.

Environmental pollution with petroleum products such as benzene, toluene, ethylbenzene, and xylenes (BTEX) has garnered increasing awareness because of its serious consequences for human health and the environment. We have constructed toluene bacterial biosensors comprised of two reporter genes, gfp and luxCDABE, characterized by green fluorescence and luminescence, respectively, and compared their abilities to detect bioavailable toluene and related compounds. The bacterial luminescence biosensor allowed faster and more-sensitive detection of toluene; the fluorescence biosensor strain was much more stable and thus more applicable for long-term exposure. Both luminescence and fluorescence biosensors were field-tested to measure the relative bioavailability of BTEX in contaminated groundwater and soil samples. The estimated BTEX concentrations determined by the luminescence and fluorescence bacterial biosensors were closely comparable to each other. Our results demonstrate that both bacterial luminescence and fluorescence biosensors are useful in determining the presence and the bioavailable fractions of BTEX in the environment. The choice of reporter genes for toluene bacterial biosensors to determine BTEX bioavailability is case-specific.

Insufficient evidence exists regarding the effects of microplastics (MPs) on the neuronal toxicity of heavy metals in the early stages of organisms. Herein, the effects of micro-polystyrene (μ-PS; 157 μm) and nano-polystyrene (n-PS; 100 nm) particles on the neurodevelopmental toxicity of mercury (Hg) in zebrafish embryos were compared. Zebrafish embryos exposed to Hg at the concentration of 0.1 mg L⁻¹ revealed blood disorders, delayed hatching, and malformations such as pericardial oedema and tail deformity. The length of the larval head was significantly reduced (P < 0.01) and in vivo expression of atoh1a in the cerebellum of neuron-specific transgenic zebrafish Tg(atoh1a:dTomato) larvae was inhibited by 29.46% under the Hg treatment. Most of the toxic effects were inhibited by the combined exposure to μ-PS or n-PS with Hg, and n-PS decreased the neurodevelopmental toxicity of Hg more significantly than μ-PS. Metabolomic analysis revealed that in addition to inhibiting the amino acid metabolism pathway as in the μ-PS+Hg treatment, the n-PS+Hg treatment inhibited unsaturated fatty acid metabolism in zebrafish larvae, likely because of a greater reduction in Hg bioavailability, thus reducing the oxidative damage caused by Hg in the larvae. The combined effects of MPs and heavy metals differ greatly among different species and their targeted effects. We conclude that the combined toxicity mechanisms of MPs and heavy metals require further clarification.

4-nitrobenzaldehyde (4-NBA) is a widely used chemical intermediate for industrial application and an important photodegradation product of chloramphenicol. This compound represents a substantial threat to human health and ecosystem due to its genotoxic and mutagenic effect. In this study, the 4-NBA detoxification by transgenic rice overexpressing a bacterial nitroreductase gene, ElNFS1, from Enterobacter ludwigii were investigated. The cytosol-targeted ElNFS1 transgenic plants were selected to comprehensively examine their physio-biochemical responses and phytoremediation potential to 4-NBA. Our results showed that the transgenic plants exhibited strong tolerance to 4-NBA. Overexpression of ElNFS1 could significantly alleviate 4-NBA-induced damages of photosynthetic apparatus and reactive oxygen species overproduction in transgenic plants. The phytoremediation assay revealed that transgenic plants could remove more 4-NBA from the medium than wild-type plants. HPLC and LC-MS assays showed that 4-aminobenzaldehyde was found in the reductive products of 4-NBA. Altogether, the function of ElNFS1 during 4-NBA detoxification was characterized for the first time, which provides a strong theoretical support for the application potential of ElNFS1 transgenic plants on the phytoremediation of 4-NBA.