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.

Nickel and cobalt are essential elements that become toxic at high concentrations. Little is known about nickel and cobalt toxicity in aquatic animals. This study aimed to investigate acute and chronic toxicity of nickel and cobalt in Japanese flounder (Paralichthys olivaceous), with emphasis on oxidative stress reactions, histopathological changes, and differences in gene expression. The lethal concentration for 50% mortality (LC₅₀) in 3 and 8 cm Japanese flounder exposed to nickel for 96 h was found to be 86.2 ± 0.018 and 151.3 ± 0.039 mg/L; for cobalt exposure, LC₅₀ was 47.5 ± 0.015 and 180.4 ± 0.034 mg/L, respectively. Chronic nickel and cobalt exposure caused different degrees of oxidative enzyme activity changes in gill, liver, and muscle tissues. Erythrocyte deformations were detected after acute or chronic exposure to nickel and cobalt. the nickel and cobalt exposure also caused pathological changes such as spherical swelling over other gill patches, rod-like proliferations in the gill patch epithelial cell layer, and disorder in hepatocyte arrangement, cell swelling, and cytoplasm loosening. RNA-Seq indicated that there were 184 upregulated and 185 downregulated genes in the liver of Japanese flounder exposed to 15 mg/L nickel for 28 d. For cobalt, 920 upregulated and 457 downregulated genes were detected. Among these differentially expressed genes, 162 were shared by both nickel and cobalt exposure. In both nickel and cobalt, pathways including fatty acid elongation, steroid biosynthesis, unsaturated fatty acid biosynthesis, fatty acid metabolism, PPAR signaling, and ferroptosis were significantly enriched. Taken together, these results aided our understanding of the toxicity of nickel and cobalt in aquatic animals.

The ubiquity of pollutants, such as agrochemicals and heavy metals, constitute a serious risk to human health. To evaluate the induction of DNA damage and programmed cell death (PCD), root cells of Allium cepa and Vicia faba were treated with two organophosphate insecticides (OI), fenthion and malathion, and with two heavy metal (HM) salts, nickel nitrate and potassium dichromate. An alkaline variant of the comet assay was performed to identify DNA breaks; the results showed comets in a dose-dependent manner, while higher concentrations induced clouds following exposure to OIs and HMs. Similarly, treatments with higher concentrations of OIs and HMs were analyzed by immunocytochemistry, and several structural characteristics of PCD were observed, including chromatin condensation, cytoplasmic vacuolization, nuclear shrinkage, condensation of the protoplast away from the cell wall, and nuclei fragmentation with apoptotic-like corpse formation. Abiotic stress also caused other features associated with PCD, such as an increase of active caspase-3-like protein, changes in the location of cytochrome C (Cyt C) toward the cytoplasm, and decreases in extracellular signal-regulated protein kinase (ERK) expression. Genotoxicity results setting out an oxidative via of DNA damage and evidence the role of the high affinity of HM and OI by DNA molecule as underlying cause of genotoxic effect. The PCD features observed in root cells of A. cepa and V. faba suggest that PCD takes place through a process that involves ERK inactivation, culminating in Cyt C release and caspase-3-like activation. The sensitivity of both plant models to abiotic stress was clearly demonstrated, validating their role as good biosensors of DNA breakage and PCD induced by environmental stressors.

In bacteria a metal may be defined as bioavailable if it crosses the cytoplasmic membrane to reach the cytoplasm. Once inside the cell, specific metal resistance systems may be triggered. In this research, specific metal resistance genes were used to estimate metal bioavailability in sediment microbial communities. Gene levels were measured by quantitative PCR and correlated to metals in sediments using five different protocols to estimate dissolved, particle-adsorbed and occluded metals. The best correlations were obtained with czcA (a Cd/Zn/Co efflux pump) and Cd/Zn adsorbed or occluded in particles. Only adsorbed Co was correlated to czcA levels. We concluded that the measurement of czcA gene levels by quantitative PCR is a promising tool which may complement the classical approaches used to estimate Cd/Zn/Co bioavailability in sediment compartments.

Nanoplastics (NPs), the emerging contaminants in recent years, widely distributed in the environment and are bioaccumulated and biomagnified in organisms through food chain. A growing number of studies have detected plastic particulates in human placenta and blood. However, few studies have focused on their effects during human pregnancy. Herein, human trophoblast HTR-8/Svneo cells were used to evaluate the effects and the possible mechanism of 100-nm polystyrene NPs on placental trophoblasts at the maternal-fetal interface. The results showed that NPs entered the trophoblastic cytoplasm, decreased cell viability, caused cell cycle arrest, reduced the cell migration and invasion abilities, increased level of intracellular reactive oxygen species and the production of proinflammatory cytokines (TNF-α and IFN-γ) in a dose-dependent manner. Furthermore, global transcriptome sequencing (RNA-Seq) was performed on HTR-8/Svneo cells with or without 100 μg/mL PS-NP exposure for 24 h. A total of 344 differentially expressed genes were detected. The gene functions for regulation of leukocyte differentiation, response to stimulus, cell cycle, apoptotic process, and cell adhesion were enriched. Thyroid hormone, Hippo, TGF-β and FoxO signaling pathways were activated. Collectively, our data provided evidences for the adverse consequences of NPs on the biological functions of trophoblasts, which provided new insights into the potential trophoblast toxicity of NPs in mammals.

Chinese cabbage (Brassica rapa ssp. pekinensis) is one of the most popular and frequently consumed leafy vegetables. It was found that atmospheric PM₂.₅-Pb contributes to Pb accumulation in the edible leaves of Chinese cabbage via stomata in North China during haze seasons with high concentrations of fine particulate matter in autumn and winter. However, it is unclear whether both stomata and trichomes co-regulate foliar transfer of PM₂.₅-Pb from atmospheric deposition to the leaf of Chinese cabbage genotypes with trichomes. Field and hydroponic experiments were conducted to investigate the effects of foliar uptake of PM₂.₅-Pb on Pb accumulation in leaves using two genotypes of Chinese cabbage, one without trichomes and one with trichomes. It was verified that open stoma is a prominent pathway of foliar PM₂.₅-Pb transfer in the short-term exposure for 6 h, contributing 74.5% of Pb accumulation in leaves, whereas Pb concentrations in the leaves of with-trichome genotype in the rosette stage were 6.52- and 1.04-fold higher than that of without-trichome genotype in greenhouse and open field, respectively, which suggests that stomata and trichomes co-regulate foliar Pb uptake of from atmospheric PM₂.₅. Moreover, subcellular Pb in the leaves was distributed in the following order of cytoplasm (53.8%) > cell wall (38.5%)> organelle (7.8%), as confirmed through high-resolution secondary ion mass spectrometry (NanoSIMS). The Leadmium™ Green AM dye manifested that Pb in PM₂.₅ entered cellular space of trichomes and accumulated in the basal compartment, enhancing foliar Pb uptake in the edible leaves of cabbage. The results of these experiments are evidence that both stomata and trichomes are important pathways in the regulation of foliar Pb uptake and translocation in Chinese cabbage.

To understand the fate of plastic in oceans and the interaction with marine organisms, we investigated the incorporation of (bio)polymers and microplastics in selected benthic foraminiferal species by applying FTIR (Fourier Transform Infrared) microscopy. This experimental methodology has been applied to cultured benthic foraminifera Rosalina globularis, and to in situ foraminifera collected in a plastic remain found buried into superficial sediment in the Mediterranean seafloor, Rosalina bradyi, Textularia bocki and Cibicidoides lobatulus. In vitro foraminifera were treated with bis-(2-ethylhexyl) phthalate (DEHP) molecule to explore its internalization in the cytoplasm. Benthic foraminifera are marine microbial eukaryotes, sediment-dwelling, commonly short-lived and with reproductive cycles which play a central role in global biogeochemical cycles of inorganic and organic compounds. Despite the recent advances and investigations into the occurrence, distribution, and abundance of plastics, including microplastics, in marine environments, there remain relevant knowledge gaps, particularly on their effects on the benthic protists. No study, to our knowledge, has documented the molecular scale effect of plastics on foraminifera.Our analyses revealed three possible ways through which plastic-related molecules and plastic debris can enter a biogeochemical cycle and may affect the ecosystems: 1) foraminifera in situ can grow on plastic remains, namely C. lobatulus, R. bradyi and T. bocki, showing signals of oxidative stress and protein aggregation in comparison with R. globularis cultured in negative control; 2) DEHP can be incorporated in the cytoplasm of calcareous foraminifera, as observed in R. globularis; 3) microplastic debris, identified as epoxy resin, can be found in the cytoplasm and the agglutinated shell of T. bocki.We hypothesize that plastic waste and their associated additives may produce modifications related to the biomineralization process in foraminifera. This effect would be added to those induced by ocean acidification with negative consequences on the foraminiferal biogenic carbon (C) storage capacity.

Epidemiological studies and animal experiments have suggested that exposure to Di-(2-ethylhexyl) phthalate (DEHP) is strongly associated with an increase in blood pressure. However, the mechanisms that result in the detrimental effects of DEHP exposure on blood pressure are unclear. In our study, mice were orally exposed to DEHP dosages of 0.1, 1, 10 mg/kg/day for 6 weeks. The results showed that DEHP could induce a significant increase in systolic blood pressure (SBP) and heart rate, and a significant thickening of the ventricular wall. To explore the underlying mechanism, we measured the level of: angiotensin converting enzyme (ACE); bradykinin B2 receptor (BK2R); endothelial nitric oxide synthase (eNOS); bradykinin and Ca²⁺ in cardiac cytoplasm as well as in serum nitric oxide (NO). The results suggested that DEHP could induce an increase in ACE levels, and a decrease in bradykinin levels. Moreover, BK2R, Ca²⁺, eNOS and NO decreased when mice were exposed to 10 mg/kg/day DEHP. Interestingly, 5 mg/kg/day angiotensin converting enzyme inhibitor (ACEI) treatment inhibited the increase in blood pressure, and inhibited the decrease in the levels of BK2R, Ca²⁺, eNOS, and NO, that were induced by DEHP exposure. Our results suggest that DEHP might increase blood pressure by activating ACE expression, and inhibiting the bradykinin-NO pathway.

Carbon nanotubes (CNTs) are considered promising materials in nanotechnology. We quantified CNT accumulation by the alga Desmodesmus subspicatus. Cells were exposed to radiolabeled CNTs (14C-CNTs; 1 mg/L) to determine uptake and association, as well as elimination and dissociation in clear media. Attenuated total reflection Fourier-transform infrared spectroscopy (ATR-FTIR) was used to detect effects of CNTs on algae. CNT-cell interactions were visualized by electron microscopy and related to alterations in their cell composition. A concentration factor of 5000 L/kg dry weight was calculated. Most of the material agglomerated around the cells, but single tubes were detected in the cytoplasm. Computational analyses of the ATR-FTIR data showed that CNT treated algae differed from controls at all sampling times. CNT exposure changed the biochemical composition of cells. The fact that CNTs are bioavailable for algae and that they influence the cell composition is important with regard to environmental risk assessment of this nanomaterial.

Microplastics (MPs) have become a global concern as a key environmental pollutant. MPs are widely found in oceans, rivers, bottled water, plastic-packaged foods, and toiletries. The ocular surface is the exposed mucosal tissue, which comes in contact with MP particles contained in toiletries, tap water, cosmetics, and air. However, the effects of MPs on ocular surface health are still unclear. In this study, the toxic effects of polystyrene MPs (PS-MPs) on the ocular surface in vivo and in vitro were explored. The results demonstrated that 50 nm or 2 μm PS-MPs, following exposure for 48 h appeared in the cytoplasm of two kinds of eye cells in vitro and caused a concentration dependent reduction in cell viability, further causing oxidative stress and cell apoptosis. In addition, after treatment for 2 or 4 weeks, 50 nm and 2 μm PS-MPs were deposited in the conjunctival sac of mice. After 2 and 4 weeks of PS-MP treatment, the number of goblet cells in the lower eyelid conjunctival sac decreased to 65% and 40% of that in the control group, respectively. Moreover, dry eye like ocular surface damage and inflammation of conjunctiva and lacrimal gland in mice were observed. In conclusion, this study revealed that PS-MPs could cause ocular surface dysfunctions in mice, thus providing a new perspective for the toxic effects of MPs on ocular surface.