Smoke from plastic waste incineration in an open air travels worldwide and is a major source of air pollution particulate matter (PM) that is very withstand to degradation and hazard to human health. Suspension of smoke aerosol components in water occurs during rains and fire extinguishing. Here, water-suspended plastic smoke aerosol (WPS) preparations suitable for biotesting were synthesized. It has been revealed using dynamic light scattering that WPS contained major nano-sized (∼30 nm) PM fraction, and this result was confirmed by electron microscopy. Optical absorption of WPS was in the UV region and an increase in λₑₓ led to a red-shift in fluorescence emission with a corresponding decrease in fluorescence intensity. WPS was analyzed in neurotoxicity studies in vitro using presynaptic rat cortex nerve terminals (synaptosomes). Generation of spontaneous reactive oxygen species (ROS) detected using fluorescent dye 2′,7-dichlorofluorescein in nerve terminals was decreased by WPS (10–50 μg/ml) in a dose-dependent manner. WPS also reduced the H₂O₂-evoked ROS production in synaptosomes, thereby influencing cellular oxidative processes and this effect was similar to that for carbon nanodots. WPS (0.1 mg/ml) decreased the synaptosomal membrane potential and synaptic vesicle acidification in fluorimetric experiments. WPS (1.0 mg/ml) attenuated the synaptosomal transporter-mediated uptake of excitatory and inhibitory neurotransmitters, L-[¹⁴C]glutamate and [³H]GABA, respectively. This can lead to an excessive increase in the glutamate concentration in the synaptic cleft and neurotoxicity via over activation of ionotropic glutamate receptors. Therefore, WPS was neurotoxic and provoked presynaptic malfunction through changes of oxidative activity, reduction of the membrane potential, synaptic vesicle acidification, and transporter-mediated uptake of excitatory and inhibitory neurotransmitters in nerve terminals. In summary, synthesis and emission to the environment of ultrafine PM occur during combustion of plastics, thereby polluting air and water resources, and possibly triggering development of neuropathologies.

Perfluorobutanesulfonate (PFBS), an aquatic pollutant of emerging concern, is found to disturb the neural signaling along gut-brain axis, whereas probiotic additives have been applied to improve neuroendocrine function of teleosts. Both PFBS and probiotics can commonly target nervous system. However, whether and how probiotic bacteria can modulate the neurotoxicities of PFBS remain not explored. It is thus necessary to elucidate the probiotic modulation of PFBS neurotoxicity, which can provide implications to the application of probiotic bacteria in aquaculture industry. In the present study, adult zebrafish were exposed to 0, 10 and 100 μg/L PFBS with or without dietary administration of probiotic Lactobacillus rhamnosus. Interaction between PFBS and probiotic along gut-brain axis was examined, covering three dominant pathways (i.e., neurotransmission, immune response and hypothalamic-pituitary-adrenal (HPA) axis). The results showed that, compared to the single effects, PFBS and probiotic coexposure significantly altered the acetylcholinesterase activity and neurotransmitter profiles in gut and brain of zebrafish, with mild effects on neuronal integrity. Neurotransmitters closely correlated reciprocally in intestines, which, however, was distinct from the correlation profile in brains. In addition, PFBS and probiotic were combined to impact brain health through absorption of bacterial lipopolysaccharides and production of inflammatory cytokines. Relative to neurotransmission and immune signaling, HPA axis was not involved in the neurotoxicological interaction between PFBS and probiotic. Furthermore, it needs to point out that interactive modes between PFBS and probiotic varied a lot, depending on exposure concentrations, sex and toxic indices. Overall, the present study provided the first evidence that probiotic supplement could dynamically modulate the neurotoxicities of PFBS in teleost.

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.

Cypermethrin is a frequently used insecticide in agriculture and households but its chronic and molecular effects are poorly known are . Here we describe effects of sublethal cypermethrin exposure on the global transcriptome in the brain of honey bees determined by RNA-sequencing. Exposure for 48 h to 0.3 ng/bee cypermethrin (3 ng/mL sucrose solution) causes 38 differentially expressed genes (DEGs), of which 29 are up-regulated and 9 down-regulated. Exposure to 3 ng/bee causes differential expression of 265 DEGs (209 up-, 56 down-regulated). Among the 24 DEGs shared by both concentrations are genes encoding muscular structure, muscular processes and esterase B1. Functional analysis (GO term analysis) confirms the enrichment of muscular development, structure and function among the 89 and 35 significantly altered GO terms at the low and high concentration, respectively. Up-regulation of nine DEGs determined by RT-qPCR showed a good correlation with RNA-sequence data. Among them are genes including esterase B1, titin, twitchin, mucin-19, insulin like growth factor binding protein, golgin like protein and helix loop protein. Our study demonstrates for the first time molecular effects of cypermethrin at environmental concentrations, which include expressional induction of genes encoding muscular and cellular processes and metabolism enzymes. Further studies should demonstrate the physiological consequences in bees.

Thiacloprid is widely used in agriculture and may affect pollinators. However, its molecular effects are poorly known. Here, we report the global gene expression profile in the brain of honey bee foragers assessed by RNA-sequencing. Bees were exposed for 72 h to nominal concentrations of 25 and 250 ng/bee via sucrose solution. Determined residue concentrations by LC-MS/MS were 0.59 and 5.49 ng/bee, respectively. Thiacloprid exposure led to 5 and 71 differentially expressed genes (DEGs), respectively. Nuclear genes encoding mitochondrial ribosomal proteins and enzymes involved in oxidative phosphorylation, as well as metabolism enzymes and transporters were altered at 5.49 ng/bee. Kyoto Encylopedia of Genes and Genomes (KEGG) analysis revealed that mitochondrial ribosome proteins, mitochondrial oxidative phosphorylation, pyrimidine, nicotinate and nicotinamide metabolism and additional metabolic pathways were altered. Among 21 genes assessed by RT-qPCR, the transcript of farnesol dehydrogenase involved in juvenile hormone III synthesis was significantly down-regulated. Transcripts of cyp6a14-like and apolipophorin-II like protein, cytochrome oxidase (cox17) and the non-coding RNA (LOC102654625) were significantly up-regulated at 5.49 ng/bee. Our findings indicate that thiacloprid causes transcriptional changes of genes prominently associated with mitochondria, particularly oxidative phosphorylation. This highlight potential effects of this neonicotinoid on energy metabolism, which may compromise bee foraging and thriving populations at environmentally relevant concentrations.

Present study demonstrates permethrin induced oxidative damage in fish brain and explores effectiveness of melatonin to ameliorate brain function. Adult female Notopterus notopterus were exposed to nominal permethrin concentrations at 1/20th (0.34 μg/l) and 1/10th (0.68 μg/l) of LC₅₀ for 15 days. The measured permethrin concentrations using gas chromatography (GC-ECD) were 0.28 μg/l and 0.57 μg/l, respectively. Some fish were sacrificed to collect brain tissue after 15 days of exposure. Remaining fish from both groups were administered exogenous melatonin (50 μg/kg, 100 μg/kg body weight) for 7 days and brain tissues were collected. Brain enzymes, ntioxidant factors, HSP70, HSP90, nuclear factor-kappa binding (NFkB), melatonin receptor (MT1R) proteins were measured. Permethrin treatment significantly (P < 0.05) decreased the levels of glutathione and brain enzymes. Malondialdehyde (MDA), xanthine oxidase (XO), HSPs increased at each concentration of permethrin. However, superoxide dismutase, glutathione s-transferase levels increased at low permethrin concentration followed by sharp decrease at higher concentration. Expression of NFkB and MT1R increased significantly (P < 0.05). Melatonin administration reinstated activity of brain enzymes, reduced MDA, XO levels and modulated HSPs. Melatonin also increased expression of NFkB and MT1R. Exogenous melatonin improves oxidative status in permethrin stressed fish brain. Melatonin modulates expression of HSPs that enables brain to become stress tolerant and survive by initiating NFkB translocation. Melatonin could act through melatonin receptor protein to induce synthesis of antioxidant proteins. Therefore the study successfully evaluates the potential of melatonin application for better culture and management of fish against pesticide toxicity.

Polychlorinated biphenyls (PCBs) are persistent organic pollutants that are linked to adverse health outcomes. PCB tissue levels are determinants of PCB toxicity; however, it is unclear how factors, such as an altered metabolism and/or a fatty liver, affect PCB distribution in vivo. We determined the congener-specific disposition of PCBs in mice with a liver-specific deletion of cytochrome P450 reductase (KO), a model of fatty liver with impaired hepatic metabolism, and wild-type (WT) mice. Eight-week-old male WT (MWT, n = 3), male KO (MKO, n = 5), female WT (FWT, n = 4), and female KO mice (FKO, n = 4) were exposed orally to Aroclor 1254. PCBs were quantified in adipose, blood, brain, and liver tissues by gas chromatography-mass spectrometry. The ΣPCB levels followed the rank order adipose > liver ∼ brain > blood in WT and adipose ∼ liver > brain > blood in KO mice. PCB levels were much higher in the liver of KO than WT mice, irrespective of the sex. A comparison across exposure groups revealed minor genotype and sex-dependent differences in the PCB congener profiles (cos Θ > 0.92). Within each exposure group, tissue profiles showed small differences between tissues (cos Θ = 0.85 to 0.98). These differences were due to a decrease in metabolically more labile PCB congeners and an increase in congeners resistant to metabolism. The tissue-to-blood ratio of PCBs decreased for adipose, increased for the brain, and remained constant for the liver with an increase in chlorination. While these ratios did not follow the trends predicted using a composition-based model, the agreement between experimental and calculated partition coefficients was reasonable. Although the distribution of PCBs differs between KO and WT mice, the magnitude of the partitioning of PCBs from the blood into tissues can be approximated using composition-based models.

Fluorine, an environmental toxicant in our daily life, has been reported to have adverse effects on nervous system. Previous studies demonstrated that fluorine exposure could induce brain injury in fish and human. However, the possible mechanism remains unclear. In the present study, we aimed to reveal the mechanism of fluorine exposure on brain injury of common carp through transcriptome analysis. In the fluorine-exposed carp, 444 brain genes were up-regulated, whereas 742 genes were down-regulated. DNA-templated (regulation of transcription) and multicellular organism development in the GO function annotation accounted for the most biological processes. Nucleus and membrane accounted for the most cellular components and DNA binding and metal ion binding accounted for the most molecular function. Meanwhile, 196 metabolic pathways were identified in Kyoto Encyclopedia of Genes and Genomes (KEGG) Pathway significant enrichment analysis, including long-term depression, Cushing syndrome, nuclear receptors, vascular smooth muscle contraction, Ion channels, and other pathways. Furthermore, we found that the up-regulated and down-regulated trends were similar between the quantitative real-time-PCR and RNA-Seq results, which indicate the transcriptome sequencing data is reliable. In conclusion, our data may provide insights into the mechanisms underlying brain injury induced by fluorine exposure.

With increasing demand for aquaculture products, water reuse is likely to increase for aquaculture operations around the world. Herein, wastewater stabilization ponds (WSP) represents low cost and sustainable treatment technologies to reduce nutrients and various contaminants of emerging concern from effluent. In the present study, we examined bioaccumulation of selected pharmaceuticals from several therapeutic classes by two important fish species in aquaculture with different feeding preferences (Cyprinus carpio and Sander lucioperca) and their common prey to test whether species specific accumulation occurs. Forty and nineteen from 66 selected pharmaceuticals and their metabolites were positively found in water and sediment samples, respectively from the representative WSP. After a six-month study, which corresponds to aquaculture operations, fourteen pharmaceuticals and their metabolites were detected (at a frequency of higher than 50% of samples) in at least one fish tissue collected from the WSP. We observed striking differences for species and organ specific BAFs among study compounds. Though muscle tissues consistently accumulated lower levels of the target analytes, several substances were elevated in brain, liver and kidney tissues (e.g., sertraline) of both species. Low residual concentrations of these target analytes in aquaculture products (fish fillets) suggest WSPs are promising to support the water-food nexus in aquaculture.

There is little information about the residue levels and congener composition of organic contaminants (OCs) in cetaceans. In the present study, we investigated the polychlorinated biphenyls (PCBs), polycyclic aromatic hydrocarbons (PAHs) and organochlorine pesticides (OCPs) in the blubber, blood, brain and testes of Indo-Pacific humpback dolphins (Sousa chinensis) stranded in the Pearl River Estuary (PRE), China. The lowest blubber/tissue partition coefficients were found for sum hexachlorocyclohexanes (ΣHCHs) and ΣPAHs, while the highest were in ΣPCBs and sum dichlorodiphenyltrichloroethanes (ΣDDTs), likely attributing to the octanol-water partition features. The low levels of OCs in brain and testes theoretically resulted from the blood-brain barrier, blood-testes barrier, contaminant molecule dimensions and unique lipid compositions in the brain and testes. Compared with other contaminants, the higher mean brain/blood and testes/blood partition coefficients found for mirex, heptachlor, dieldrin and endrin would increase the risks associated with exposure-related toxicity and the bioavailability of contaminants within these tissues. Observations also suggest that as lipid mobilizes from blubber, contaminants may redistribute, leading to elevated tissue (such as brain) concentrations. Therefore, dolphins with less blubber may be more susceptible to health risks. The Indo-Pacific humpback dolphins living in PRE are at great risk due to variety of OCs in indirect contact with non-target organisms, affecting the health of animals (toxic effects and accumulation). Our findings contribute to the knowledge of the potential effects of OCs exposure on developmental neurotoxicity and reproductive damage in marine mammals.