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.

Bacteria are important components of bioaerosols with the potential to influence human health and atmospheric dynamics. However, information on the concentrations and influencing factors of viable bacteria is poorly understood. In this study, size-segregated bioaerosol samples were collected from Aug. 2017 to Feb. 2018 in the coastal region of Qingdao, China. The total microbes and viable/non-viable bacteria in the samples were measured using an epifluorescence microscope after staining with the DAPI (4′, 6-diamidino-2-phenylindole) and LIVE/DEAD® BacLight™ Bacterial Viability Kit, respectively. The concentrations of non-viable bacteria increased when the air quality index (AQI) increased from <50 to 300, with the proportion of non-viable bacteria to total microbes increasing from (11.1 ± 12.0)% at an AQI of <50 to (18.4 ± 14.7)% at an AQI of >201. However, the concentrations of viable bacteria decreased from (2.12 ± 2.04) × 10⁴ cells·m⁻³ to (9.00 ± 1.72) × 10³ cells·m⁻³ when the AQI increased from <50 to 150. The ratio of viable bacteria to total bacteria (viability) decreased from (31.0 ± 14.7)% at 0 < AQI<50 to (8.6 ± 1.0)% at 101 < AQI<150 and then increased to (9.6 ± 5.3)% at an AQI of 201–300. The results indicated that the bacterial viability decreased when air pollution occurred and increased again when pollution became severe. The mean size distribution of non-viable bacteria exhibited a bimodal distribution pattern at an AQI<50 with two peaks at 2.1–3.3 μm and >7.0 μm, while the viable bacteria had two peaks at 1.1–2.1 μm and >7 μm. When the AQI increased from 101 to 300, the size distribution of viable/non-viable bacteria varied with an increased proportion of fine particles. The multiple linear regression analysis results verified that the AQI and PM₁₀ had important effects on the concentrations of non-viable bacteria. These results highlight impacts of air pollution on viable/non-viable bacteria and the interactions between complex environmental factors and bacteria interactions, improving our understanding of bioaerosols under air pollution conditions.

T-2 toxin is an unavoidable contaminant in human food, animal feeds, and agricultural products. T-2 toxin has been found to impair male reproductive function. But, few data is available that reveals the reproductive toxicity mechanism. In the study, male Kunming mice were orally administrated with T-2 toxin at the doses of 0, 0.5, 1 or 2 mg/kg body weight for 28 days. The body and reproductive organs weight, the concentration, malformation rate and ultrastructure of sperm in cauda epididymis were detected. Oxidative stress biomarkers and apoptosis were also measured in testes. Histological change of testes was performed by H&E and TUNEL staining. T-2 toxin down-regulated body and reproductive organs (testis, epididymis and seminal vesicle) weight, sperm concentration, increased sperm malformation rate and damaged the ultrastructure of sperm and structure of testes. T-2 toxin treatment increased the reactive oxygen species (ROS) and malondialdehyde content, while, decreased the total anti-oxidation capacity (T-AOC) and the superoxide dismutase activity in testes. T-2 toxin exposure increased the TUNEL-positive germ cells, the activities and mRNA expressions of caspase-3, caspase-8 and caspase-9, the mRNA expression of Bax, and inhibited the Bcl-2 mRNA expression. Furthermore, the expressions of caspase-3, caspase-8 caspase-9 and Bax were positively correlated with ROS level, but negatively correlated with T-AOC in testis. In summary, T-2 toxin caused spermatogenesis disorder associated with the germ cell apoptosis medicated by oxidative stress, impairing the male reproductive function.

Cadmium is one of the most serious metal pollutants in the Bohai Sea. Previous studies revealed that mitochondrion might be the target organelle of Cd toxicity. However, there is a lack of a global view on the mitochondrial responses in marine animals to Cd. In this work, the mitochondrial responses were characterized in clams Ruditapes philippinarum treated with two concentrations (5 and 50 μg/L) of Cd for 5 weeks using tetraethylbenzimidazolylcarbocyanine iodide (JC-1) staining, ultrastructural observation and quantitative proteomic analysis. Basically, a significant decrease of mitochondrial membrane potential (△Ψm) was observed in clams treated with the high concentration (50 μg/L) of Cd. Cd treatments also induced specific morphological changes indicated by elongated mitochondria. Furthermore, iTRAQ-based mitochondrial proteomics showed that a total of 97 proteins were significantly altered in response to Cd treatment. These proteins were closely associated with multiple biological processes in mitochondria, including tricarboxylic acid (TCA) cycle, oxidative phosphorylation, fatty acid β-oxidation, stress resistance and apoptosis, and mitochondrial fission. These findings confirmed that mitochondrion was one of the key targets of Cd toxicity. Moreover, dynamical regulations, such as reconstruction of energy homeostasis, induction of stress resistance and apoptosis, and morphological alterations, in mitochondria might play essential roles in Cd tolerance. Overall, this work provided a deep insight into the mitochondrial toxicity of Cd in clams based on a global mitochondrial proteomic analysis.

Epidemiological evidence showed that the particulate matter exposure is associated with atherosclerotic plaque progression, which may be related to foam cell formation, but the mechanism is still unknown. The study was aimed to investigate the toxic effects and possible mechanism of PM2.5 on the formation of macrophage foam cells induced by oxidized low density lipoprotein (ox-LDL). Results showed that PM2.5 induced cytotoxicity by decreasing the cell viability and increasing the LDH level in macrophage foam cells. PM2.5 aggravated the lipid accumulation in ox-LDL-stimulated macrophage RAW264.7 within markedly increasing level of intracellular lipid by Oil red O staining. The level of ROS increased obivously after co-exposure to PM2.5 and ox-LDL than single exposure group. In addition, serious mitochondrial damage such as the mitochondrial swelling, cristae rupturing and disappearance were observed in macrophage foam cells. The loss of the mitochondrial membrane potential (MMP) further exacerbated the mitochondrial damage in PM2.5-induced macrophage foam cells. The apoptotic rate increased more severely via up-regulated protein level of Bax, Cyt C, Caspase-9, Caspase-3, and down-regulated that of Bcl-2, indicating that PM2.5 activated the mitochondrial-mediated apoptosis pathway. In summary, our results demonstrated that PM2.5 aggravated the lipid accumulation, mitochondrial damage and apoptosis in macrophage foam cells, suggesting that PM2.5 was a risk factor of atherosclerosis progression.