Dichlorvos is a common crop insecticide widely used by people which causes extensive and serious environmental pollution. However, it has been shown that organophosphorus poisoning causes energy metabolism and neural disorders. The overall purpose of this study was to investigate the damage to brain tissue and the changes in AMPK signaling pathway-related gene expression after dichlorvos poisoning in chickens. White-feathered broiler chickens, as the research subjects of this experiment, were divided into three groups: control group, low-dose group (77.5% dichlorvos at 1.13 mg/kg dose) and high-dose group (77.5% dichlorvos at 10.2 mg/kg dose). Clinical symptoms were observed after modeling, and an integrative analysis was conducted using HE staining microscopy, immune-histochemical microscopy, electron microscopy and PCR arrays. The results showed that the high-dose group had more obvious dyspnea, salivation, convulsion and other neurological phenomena. Pathological sections showed that nuclear disintegration of neurons was most obvious in the low-dose group, and apoptosis of brain cells was most obvious in the high-dose group, and the mitochondrial structure was destroyed in the two poisoned group, i.e. low-dose group and high-dose group. PCR arrays showed that AMPK signaling pathway was inhibited and the expressions of genes involved in energy metabolism (ACACA and PRKAA1) were significantly changed. Furthermore, genes associated with protein synthesis (EIF4EBP1) were significantly upregulated. FASN and HMGCR expressions were significantly increased. There were significant changes in the expressions of cell cycle-related genes (STK11, TP53 and FOXO3). Organophosphate poisoning can cause a lot of nuclear disintegration of brain neurons, increases cell apoptosis, disrupts the energy metabolism of mitochondrial structure, and inhibits the AMPK signaling pathway. These results provide a certain idea and basis for studying the mechanism of AMPK signaling after organophosphorus poisoning and provide a research basis for the prevention and treatment of organophosphorus poisoning.

Recently, the essentiality and fatalness of cardiovascular diseases is attracting much attention. Polybrominated diphenyl ethers (PBDEs) are persistent environmental pollutants, which could induce the toxic effect and have been implicated in the occurrence and development of cardiovascular diseases. However, it is unclear how autophagy and apoptosis induced by BDE-209 in endothelial cells are regulated. The aim of the present study was to investigate the effects of BDE-209 on human umbilical vein endothelial cells (HUVECs) and elucidate the mechanisms involved. HUVECs were treated with a wide range concentration of BDE-209 for 24 h. The appearance of autophagy was tested by the testing index such as outcomes of monodansylcadaverine (MDC) staining and lysotracker staining, observation of autophagosomes and conversion between autophagy marker light chain 3 (LC3)-I and LC3-II. Besides, the apoptotic cell rate was detected with flow cytometry. In addition, BDE-209 induced endoplasmic reticulum (ER) stress was detected by transmission electron microscopy (TEM). Our data suggest that the exposure of BDE-209 could induce autophagy, which was confirmed by MDC staining, transmission electron microscopy observation, lysotracker staining and LC3-I/LC3-II conversion. Besides, the ER stress-related inositol-requiring enzyme 1α (IRE1α)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) signaling pathway could be activated by reactive oxygen species (ROS) to regulate autophagy. Moreover, the apoptosis of endothelial cells was alleviated when autophagy was blocked by 3-Methyladenine (3-MA). The results demonstrated that BDE-209 could induce the production of ROS and ER stress, activate autophagy through IRE1α/AKT/mTOR signaling pathway and ultimately induce apoptosis of vascular endothelial cells. These findings indicate that exposure to PBDE is possible to be a potential risk factor for cardiovascular diseases.

Our previous study showed that the tea extract, epigallocatechin-3-gallate (EGCG), protects against microcystin-LR (MC-LR) -mediated apoptosis of human umbilical vein endothelial cells (HUVECs); however, the mechanism underlying MC-LR-induced HUVEC apoptosis remains incompletely understood. In this study, we investigated whether the nuclear factor erythroid-like 2 (NRF2)/heme oxygenase-1 (HO-1) pathway, which regulates antioxidant transcriptional regulation of oxidative stress and apoptosis, is involved in this process. Mitochondrial membrane potential (MMP) and caspase-3/-9 activities were evaluated in HUVECs by JC-1 staining and colorimetric activity assay, and a DCFH-DA fluorescent probe assay was used to quantitate reactive oxygen species (ROS) generation. The effects of MC-LR, EGCG, NF2, and HO-1 on HUVEC apoptosis were explored by western blotting and small interfering RNA (siRNA) analyses. MC-LR treatment downregulated HUVEC mitochondrial membrane potential, and decreased levels of cytochrome c release and activated caspase-3/-9, ROS generation, consequently inducing HUVEC apoptosis. EGCG treatment attenuated MC-LR-mediated HUVEC oxidative stress and mitochondria-related apoptosis. EGCG induced NRF2/HO-1 expression and activation in MC-LR treated HUVECs, while downregulation of NRF2/HO-1 by specific siRNAs revealed that NRF2/HO-1 signaling was involved in EGCG attenuation of MC-LR-induced HUVEC apoptosis. Our findings indicate that EGCG treatment protects against MC-LR-mediated HUVEC apoptosis via activation of NRF2/HO-1 signaling.

Microplastics (MPs) are the most numerous debris reported in marine environments and assessment of the amounts of MPs that accumulate in wild organisms is necessary for risk assessment. Our objective was to assess MP contamination in mussels collected around the coast of Scotland (UK) to identify characteristics of MPs and to evaluate risk of human exposure to MPs via ingestion of mussels. We deployed caged mussels (Mytilus edulis) in an urbanised estuary (Edinburgh, UK) to assess seasonal changes in plastic pollution, and collected mussels (Mytilus spp and subtidal Modiolus modiolus) from eight sampling stations around Scotland to enumerate MP types at different locations. We determined the potential exposure of humans to household dust fibres during a meal to compare with amounts of MPs present in edible mussels. The mean number of MPs in M. modiolus was 0.086 ± 0.031 (SE, n = 6)/g ww (3.5 ± 1.29 (SE) per mussel). In Mytilus spp, the mean number of MPs/g ww was 3.0 ± 0.9 (SE, n = 36) (3.2 ± 0.52 (SE) per mussel), but weight dependent. The visual accuracy of plastic fibres identification was estimated to be between 48 and 50%, using Nile Red staining and FT-IR methodologies, respectively, halving the observed amounts of MPs in wild mussels. We observed an allometric relationship between the number of MPs and the mussels wet weight. Our predictions of MPs ingestion by humans via consumption of mussels is 123 MP particles/y/capita in the UK and can go up to 4620 particles/y/capita in countries with a higher shellfish consumption. By comparison, the risk of plastic ingestion via mussel consumption is minimal when compared to fibre exposure during a meal via dust fallout in a household (13,731–68,415 particles/Y/capita).

Chlorinated polyfluorinated ether sulfonate (Cl-PFESA) is a novel alternative compound for perfluorooctane sulfonate (PFOS), with its environmental risk not well known. The bioaccumulation and toxic effects of Cl-PFESA in the freshwater alga is crucial for the understanding of its potential hazards to the aquatic environment. Scenedesmus obliquus was exposed to Cl-PFESA at ng L⁻¹ to mg L⁻¹, with the exposure regime beginning at the environmentally relevant level. The total log BAF of Cl-PFESA in S. obliquus was 4.66, higher than the reported log BAF of PFOS in the freshwater plankton (2.2–3.2). Cl-PFESA adsorbed to the cell surface accounted for 33.5–68.3% of the total concentrations. The IC50 of Cl-PFESA to algal growth was estimated to be 40.3 mg L⁻¹. Significant changes in algal growth rate and chlorophyll a/b contents were observed at 11.6 mg L⁻¹ and 13.4 mg L⁻¹ of Cl-PFESA, respectively. The sample cell membrane permeability, measured by the fluorescein diacetate hydrolyzation, was increased by Cl-PFESA at 5.42 mg L⁻¹. The mitochondrial membrane potential, measured by Rh123 staining, was also increased, indicating the hyperpolarization induced by Cl-PFESA. The increasing ROS and MDA contents, along with the enhanced SOD, CAT activity, and GSH contents, suggested that Cl-PFESA caused oxidative damage in the algal cells. It is less possible that current Cl-PFESA pollution in surface water posed obvious toxic effects on the green algae. However, the bioaccumulation of Cl-PFESA in algae would contribute to its biomagnification in the aquatic food chain and its effects on membrane property could potentially increase the accessibility and toxicity of other coexisting pollutants.

Cardiovascular diseases is related to environmental pollution. Endosulfan is an organochlorine pesticide and its toxicity has been reported. However, the relationship between oxidative stress and autophagy induced by endosulfan and its underlying mechanism remain confusing. In this study, human umbilical vein endothelial cells (HUVECs) were chosen to explore the toxicity mechanism and were treated with 0, 1, 6, 12 μg/mL−1 endosulfan for 24 h, respectively. The present results showed that autophagy could be induced by endosulfan, which was verified by the monodansylcadaverine staining, autophagic ultrastructural observation, and LC3-I/LC3-II conversion. In addition, the levels of adenosine triphosphate (ATP), the mitochondria membrane potential (MMP) were significantly decreased in a dose-dependent way. The expression of proinflammatory cytokines (tumor necrosis factor α, interleukin-1β, and interleukin-6) were significantly elevated, and the index of endothelial function such as monocyte chemotactic protein 1 (MCP-1), intercellular cell adhesion molecule-1 (ICAM-1) increased. Moreover, endosulfan had an activation effect on the 5′AMP-activated protein kinase (AMPK)/rapamycin (mTOR) signaling pathway. Our findings demonstrated that endosulfan could induce oxidative stress and mitochondria injury, activate autophagy, induce inflammatory response, and eventually lead to endothelial dysfunction via the AMPK/mTOR pathway. This indicates that exposure to endosulfan is a potential risk factor for cardiovascular diseases.

Melatonin is a hormone which is generated from pineal gland, and it is responsible for the regulation of wake-sleep cycle. Melatonin is a well-known antioxidant and free radical scavenger to protect against multiple type of tissue damage. While ochratoxin A (OTA) is a mycotoxin found widely in contaminated food and foodstuffs, which causes nephrotoxicity, hepatotoxicity, immunotoxicity, and reproductive damage in humans and animals. In present study we report the toxicity of OTA on porcine oocyte quality and the protective effects of melatonin on OTA-exposed oocytes. Using transcriptome analysis our results show that OTA exposure alters the expression of multiple genes in oocytes, indicating its effect on oocyte maturation. The cellular changes following OTA treatment are examined, and the results show that OTA adversely affects oocyte polar body extrusion, which is confirmed by the delay of Cdc2-mediated cell cycle progression. OTA exposure also disrupts meiotic spindle formation, which is confirmed by altered phosphorylated MAPK expression. RNA-seq screening and further fluorescence staining results show that OTA induces aberrant mitochondria distribution and oxidative phosphorylation defects, which then causes oxidative stress, followed by early apoptosis and autophagy. Treatment with melatonin significantly ameliorates oxidative stress and apoptosis, which further protects cell cycle and spindle formation in OTA-exposed oocytes. Collectively, these results show the protective effects of melatonin against defects induced by OTA during porcine meiotic oocyte maturation.

Most laboratory studies have focused on the effects of nanoplastics instead of plastics at the micrometer scale, which are the major microplastics (MPs) discarded in marine environments. Knowledge on the potential effects of micrometer scale plastics on marine microalgae remains limited. It remains unknown whether the micrometer scale plastics also affect microalgal growth, lipid accumulation and resistance to organic contaminants? In addition, the role of polymer-size on the potential hazardous effects of MPs on microalgae is unknown. In the present study, cell populations of a marine diatom, Phaeodactylum tricornutum, were treated with micrometer scale polyethylene (PEMP, 150 μm) and unplasticized polyvinyl chloride (uPVCMP, 250 μm) powders in the laboratory. Growth was assessed using a hemacytometer and neutral lipid concentrations were evaluated using the Nile Red staining method under short-term (four days) and long-term (nine days) exposure. The effects of combined PEMP and phenanthrene (Phe), and uPVCMP and Phe exposures over four days on growth were investigated. Importance scores and SHapley Additive exPlanations (SHAP) values were calculated to assess the contributions of seven factors in exposure systems to the hazardous effects of MPs on microalgae using a machine-learning prediction based on 165 data sets. Both MP types did not influence algal growth and lipid accumulation but minimized algal inhibition by the action of Phe at four days. In addition, lipid accumulation was induced at nine days. Both importance scores and SHAP values indicated that MP polymer-size was the key factor influencing MP toxicity in microalgae. In conclusion, MPs had adverse effects only in chronic tests and the potential adsorption of MPs could have led to the lower levels of toxicity in a combined MP–Phe exposure system. Compared to nanoplastics, MPs in the hundred-micrometer range do not significantly affect growth and their adsorption would not be influenced by size. Therefore, MP size is the most critical factor that should be considered in future laboratory tests and eco-toxicological risk assessments for microalgae.

Biofilms containing pathogenic organisms from the water supply are a potential source of protozoan parasite outbreaks and a significant public health concern. The aim of the present study was to demonstrate the simultaneous and multi-spatial occurrence of waterborne protozoan pathogens (WBPP) in substrate-associated biofilms (SAB) and compare it to surface water (SW) and sediments with bottom water (BW) counterparts using manual filtration and elution from low-volume samples. For scenario purposes, simulated environmental biofilm contamination was created from in-situ grown one-month-old SAB (OM-SAB) that were spiked with Cryptosporidium parvum oocysts. Samples were collected from the largest freshwater reservoirs in Luzon, Philippines and a University Lake in Thailand. A total of 69 samples (23 SAB, 23 SW, and 23 BW) were evaluated using traditional staining techniques for Cryptosporidium, and Immunofluorescence staining for the simultaneous detection of Cryptosporidium and Giardia. WBPP were found in 43% SAB, 39% SW, and 39% BW of the samples tested in the present study with SAB results reflecting SW and BW results. Further highlights were demonstrated in the potential of using low-volume samples for the detection of parasites in source water. Scanning electron microscopy of OM-SAB samples revealed a naturally-associated testate amoeba shell, while Cryptosporidium oocysts spiked samples provided a visual profile of what can be expected from naturally contaminated biofilms. This study provides the first evidence for the simultaneous and multi-spatial occurrence of waterborne protozoan pathogens in low-volume aquatic matrices and further warrants SAB testing along with SW and BW matrices for improved water quality assessment strategies (iWQAS).

Microplastics (particle size <5 mm) are an emerging contaminant for aquatic environmental, which have attracted increasing attention in worldwide range. In this study, an improved fluorescent staining method for detection and quantification of microplastics was developed based on thermal expansion and contraction. This method is effective in detection of polyethylene, polystyrene, polyvinyl chloride and polyethylene terephthalate plastic particles. In order to avoid error statistics caused by pretreatment, various characterizations of microplastics were measured after heated, such as microstructure, compositions and thermostability. The results showed that there was no significant damage to microplastics even under heating condition at 75 °C for 30 min, and the stained microplastics had strong stability for up to two months. Moreover, this method has been successfully applied to the quantification of microplastics in biological samples and result showed there were about 54 particles g⁻¹ (dry weight) microplastics in the Sipunculus nudus. This new method provides a reliable method for quantitative analysis of microplastics in environment and biological tissue.