1,2-Dichloroethane (1,2-DCE) is a highly toxic neurotoxicity, and the brain tissue is the main target organ. At present, long-term exposure to 1,2-DCE has been shown to cause cognitive dysfunction in some studies, but the mechanism is not clear. The results of this study showed that long-term 1,2-DCE exposure decreased learning and memory abilities in mice and impaired the structure and morphology of neurons in the hippocampal region. Moreover, except for the mRNA level of PAG, the enzymatic activities and protein levels of GS and PAG, as well as the mRNA level of GS were inhibited. With increasing dose of exposure, the protein and mRNA expression of GLAST and GLT-1 also decreased. Contrarily, there were protein and mRNA expression upregulation of GluN1, GluN2A and GluN2B in the hippocampus, as well as increased levels of extracellular Glu and intracellular Ca²⁺. In addition, 1,2-DCE exposure also downregulated the protein expression levels of CaM, CaMKII and CREB. Taken together, our results suggest that long-term 1,2-DCE exposure impairs the learning and memory capacity in mice, which may be attributed to the disruption of Glu metabolism and the inhibition of CaM- CaMKII-CREB signaling pathway in the hippocampus.

An emerging stress of pesticides in plant and soil is closely watched as it affects crop antioxidant systems, nutritional quality, and flavor. Although selenium (Se) can enhance the resistance of plants, the protective mechanism of nanoselenium is still not known under the long-term pesticide stress in tea trees. In this study, we investigated the potential effects of foliar application of nanoselenium for a two-year field experiment on tea plants under pesticide-induced oxidative stress. Compared to control, nano-Se (10 mg/L) markedly enhanced the protein, soluble sugar, carotenoid, tea polyphenols, and catechins contents. High levels of theanine, glutamic acid, proline, and arginine were found to be induced most likely by adjusting the GS-GOGAT cycle. Se-supplementation may promote tea leaves’ secondary metabolism, thus increasing the accumulation of total phenols and flavonoids (apigenin, kaempferol, quercetin, myricetin, and rutin). It also minimized the accumulation of malondialdehyde, hydrogen peroxide, and superoxide anion by activating the antioxidants enzymes including in the AsA-GSH cycle. Selenium-rich tea also showed better fragrance and flavor. In summary, nano-Se can ameliorate the nutrients quality and abiotic stresses resistance of crops.

We investigated physiological responses including calcification, photosynthesis and alterations to polar metabolites, in the scleractinian coral Stylophora pistillata exposed to different concentrations of polyethylene microplastics. Results showed that at high plastic concentrations (50 particles/mL nominal concentration) the photosynthetic efficiency of photosystem II in the coral symbiont was affected after 4 weeks of exposure. Both moderate and high (5 and 50 particles/mL nominal) concentrations of microplastics caused subtle but significant alterations to metabolite profiles of coral, as determined by Nuclear Magnetic Resonance (NMR) spectroscopy. Specifically, exposed corals were found to have increased levels of phosphorylated sugars and pyrimidine nucleobases that make up nucleotides, scyllo-inositol and a region containing overlapping proline and glutamate signals, compared to control animals. Together with the photo-physiological stress response observed and previously published literature, these findings support the hypothesis that microplastics disrupt host-symbiont signaling and that corals respond to this interference by increasing signaling and chemical support to the symbiotic zooxanthellae algae. These findings are also consistent with increased mucus production in corals exposed to microplastics described in previous studies. Considering the importance of coral reefs to marine ecosystems and their sensitivity to anthropogenic stressors, more research is needed to elucidate coral response mechanisms to microplastics under realistic exposure conditions.

Leaf is an important organ in responding to environmental stresses. To date, chlorophyll metabolism under polycyclic aromatic hydrocarbon (PAH) stress is still unclear. Here we reveal, for the first time, the chlorophyll metabolism of wheat seedling leaves in response to phenanthrene (a model PAH) exposure. In this study, the hydroponic experiment was employed, and the wheat seedlings were exposed to phenanthrene to observe the response at day 1, 3, 5, 7 and 9. Over the exposure time, wheat leaf color turns light. With the accumulation of phenanthrene, the concentrations of glutamate, 5-aminolevulinic acid, uroporphyrinogen III, protoporphyrin IX, Mg-protoporphyrin IX and protochlorophyllide increase while the concentrations of porphobilinogen and Chlorophyll b decrease. Also chlorophyll a content rises initially and then declines. Uroporphyrinogen III synthase and chlorophyllase are activated and porphobilinogen deaminase activity declines in the treatments. Both chlorophyll synthesis and degradation are enhanced, but the degradation rate is faster. Phenanthrene accumulation has significant and positive effects on increase of glutamate, 5-aminolevulinic acid, uroporphyrinogen III, protoporphyrin IX, Mg-protoporphyrin IX and protochlorophyllide concentrations. There is a negative correlation between phenanthrene accumulation and total chlorophyll. Additionally, the leaf moisture increases. Therefore, it is concluded that wheat leaf chlorosis results from a combination of accelerated chlorophyll degradation and elevated leaf moisture under phenanthrene exposure. Our results are helpful not only for better understanding the toxicity of PAHs to plants and crop PAH-adaptive mechanism in the environment, but also for potentially employing the changes of the chlorophyll-synthesizing precursors and enzyme activities in plant leaves as indicators of plant response to PAH pollution.

1H-HRMAS NMR-based metabolomics was used to better understand the toxic effects on maize root tips of organochlorine pesticides (OCPs), namely lindane (γHCH) and chlordecone (CLD). Maize seedlings were exposed to 2.5 μM γHCH (mimicking basic environmental contaminations) for 7 days and compared to 2.5 μM CLD and 25 μM γHCH for 7 days (mimicking hot spot contaminations). The 1H-HRMAS NMR-based metabolomic profiles provided details of the changes in carbohydrates, amino acids, tricarboxylic acid (TCA) cycle intermediates and fatty acids with a significant separation between the control and OCP-exposed root tips. First of all, alterations in the balance between glycolysis/gluconeogenesis were observed with sucrose depletion and with dose-dependent fluctuations in glucose content. Secondly, observations indicated that OCPs might inactivate the TCA cycle, with sizeable succinate and fumarate depletion. Thirdly, disturbances in the amino acid composition (GABA, glutamine/glutamate, asparagine, isoleucine) reflected a new distribution of internal nitrogen compounds under OCP stress. Finally, OCP exposure caused an increase in fatty acid content, concomitant with a marked rise in oxidized fatty acids which could indicate failures in cell integrity and vitality. Moreover, the accumulation of asparagine and oxidized fatty acids with the induction of LOX3 transcription levels under OCP exposure highlighted an induction of protein and lipid catabolism. The overall data indicated that the effect of OCPs on primary metabolism could have broader physiological consequences on root development. Therefore, 1H-HRMAS NMR metabolomics is a sensitive tool for understanding molecular disturbances under OCP exposure and can be used to perform a rapid assessment of phytotoxicity.

Research over the last three decades showed that chromium, particularly the oxyanion chromate Cr(VI) behaves as a toxic environmental pollutant that strongly damages plants due to oxidative stress, disruption of nutrient uptake, photosynthesis and metabolism, and ultimately, represses growth and development. However, mild Cr(VI) concentrations promote growth, induce adventitious root formation, reinforce the root cap, and produce twin roots from single root meristems under conditions that compromise cell viability, indicating its important role as a driver for root organogenesis. In recent years, considerable advance has been made towards deciphering the molecular mechanisms for root sensing of chromate, including the identification of regulatory proteins such as SOLITARY ROOT and MEDIATOR 18 that orchestrate the multilevel dynamics of the oxyanion. Cr(VI) decreases the expression of several glutamate receptors, whereas amino acids such as glutamate, cysteine and proline confer protection to plants from hexavalent chromium stress. The crosstalk between plant hormones, including auxin, ethylene, and jasmonic acid enables tissues to balance growth and defense under Cr(VI)-induced oxidative damage, which may be useful to better adapt crops to biotic and abiotic challenges. The highly contrasting responses of plants manifested at the transcriptional and translational levels depend on the concentration of chromate in the media, and fit well with the concept of hormesis, an adaptive mechanism that primes plants for resistance to environmental challenges, toxins or pollutants. Here, we review the contrasting facets of Cr(VI) in plants including the cellular, hormonal and molecular aspects that mechanistically separate its toxic effects from biostimulant outputs.

The main objective of the study was to assess if joint application of melatonin (MT, 0.1 mM) and salicylic acid (SA 0.5 mM) could improve tolerance of pepper plants to arsenic (As) as sodium hydrogen arsenate heptahydrate (0.05 mM). The imposition of arsenic stress led to accumulation of As in roots and leaves, and increased contents of leaf proline, phytochelatins, malondialdehyde (MDA) and H₂O₂, but it reduced plant biomass, chlorophylls (Chl), PSII maximum efficiency (Fv/Fm) and leaf water potential. Melatonin and SA applied jointly or alone enhanced nitrogen metabolism by triggering the activities of glutamate synthase, glutamine synthetase, and nitrite reductases and nitrate. In comparison with a single treatment of MT or SA, the joint treatment of MT and SA had better impact on enhancing growth and key biological events and decreasing tissue As content. This clearly shows a cooperative function of both agents in enhancing tolerance to As-toxicity in pepper plants.

Exposure to tobacco smoke during pregnancy has been associated with a series of adverse reproductive outcomes; however, the underlying molecular mechanisms are not well-established. We conducted an untargeted metabolome-wide association study to identify the metabolic perturbations and molecular mechanisms underlying the association between cotinine, a widely used biomarker of tobacco exposure, and adverse birth outcomes. We collected early and late pregnancy urine samples for cotinine measurement and serum samples for high-resolution metabolomics (HRM) profiling from 105 pregnant women from the Atlanta African American Maternal-Child cohort (2014–2016). Maternal metabolome perturbations mediating prenatal tobacco smoke exposure and adverse birth outcomes were assessed by an untargeted HRM workflow using generalized linear models, followed by pathway enrichment analysis and chemical annotation, with a meet-in-the-middle approach. The median maternal urinary cotinine concentrations were 5.93 μg/g creatinine and 3.69 μg/g creatinine in early and late pregnancy, respectively. In total, 16,481 and 13,043 metabolic features were identified in serum samples at each visit from positive and negative electrospray ionization modes, respectively. Twelve metabolic pathways were found to be associated with both cotinine concentrations and adverse birth outcomes during early and late pregnancy, including tryptophan, histidine, urea cycle, arginine, and proline metabolism. We confirmed 47 metabolites associated with cotinine levels, preterm birth, and shorter gestational age, including glutamate, serine, choline, and taurine, which are closely involved in endogenous inflammation, vascular reactivity, and lipid peroxidation processes. The metabolic perturbations associated with cotinine levels were related to inflammation, oxidative stress, placental vascularization, and insulin action, which could contribute to shorter gestations. The findings will support the further understanding of potential internal responses in association with tobacco smoke exposures, especially among African American women who are disproportionately exposed to high tobacco smoke and experience higher rates of adverse birth outcomes.

Cadmium (Cd) and lead (Pb) are the major toxic heavy metals accumulated in rice and pose a serious threat to human health. The most important remediation strategy is to reduce the translocation of these heavy metals from polluted soil to rice. Bioremediation using microorganisms had been widely used for preventing environmental heavy metal pollution, and the interaction between microorganisms and plants is critical to reduce the heavy metal stress. In this study, we demonstrated that an extremophile Deinococcus radiodurans, especially its mutant strain-Δdr2577 which is deficient in cell surface-layer, could efficiently prevent the translocation and damages of Cd or Pb in rice. The bacterial cells efficiently removed Cd or Pb from culture medium. Following colonization of Δdr2577 cells in rice root, Cd level decreased to 71.6% in root and 60.9% in shoot, comparing to the plants treated with Cd alone; Pb level decreased to 73.3% in root and 56.9% in shoot, comparing to the plants treated with Pb alone. Meanwhile, the bacterial cells released their intracellular antioxidant-related molecules including glutamate and manganese ions into culture medium. Accumulation of glutamate and manganese ions detected in rice root and shoot ameliorate Cd/Pb-induced oxidative stress as indicated by reduced levels of ROS and enhanced activities of antioxidant enzymes in rice. Our results provide a potential application of an extremophile bacterium in alleviating heavy metal toxicity in rice.The main findings of the work reveal the interaction between the D. radiodurans and rice, as well as the alleviating mechanism of Cd and Pb toxicity through suppressing heavy metal accumulation and improving the antioxidant system in rice by the extremophile bacterium.

Exposure to ambient fine particular matter (PM2.5) are linked to an increased risk of metabolic disorders, leading to enhanced rate of many diseases, such as inflammatory bowel disease (IBD), cardiovascular diseases, and pulmonary diseases; nevertheless, the underlying mechanisms remain poorly understood. In this study, BALB/c mice were exposed to filtered air (FA) or concentrated ambient PM2.5 (CPM) for 2 months using a versatile aerosol concentration enrichment system(VACES). We found subchronic CPM exposure caused significant lung and intestinal damage, as well as systemic inflammatory reactions. In addition, serum and BALFs (bronchoalveolar lavage fluids) metabolites involved in many metabolic pathways in the CPM exposed mice were markedly disrupted upon PM2.5 exposure. Five metabolites (glutamate, glutamine, formate, pyruvate and lactate) with excellent discriminatory power (AUC = 1, p < 0.001) were identified to predict PM2.5 exposure related toxicities. Furthermore, subchronic exposure to CPM not only significantly decreased the richness and composition of the gut microbiota, but also the lung microbiota. Strong associations were found between several gut and lung bacterial flora changes and systemic metabolic abnormalities. Our study showed exposure to ambient PM2.5 not only caused dysbiosis in the gut and lung, but also significant systemic and local metabolic alterations. Alterations in gut and lung microbiota were strongly correlated with metabolic abnormalities. Our study suggests potential roles of gut and lung microbiota in PM2.5 caused metabolic disorders.