Environmental obesogens contributed significantly to the obesity prevalence. Recently, antibiotics joined the list of environmental obesogens, while the underlying mechanisms remained to be explored. In the present study, effects of erythromycin (ERY), one widely used macrolide antibiotic, were measured on C. elegans to investigate the obesogenic mechanism. Results showed that ERY at 0.1 μg/L significantly increased the fat content by 17.4% more than the control and also stimulated triacylglycerol (TAG) levels by 25.7% more than the control. Regarding the obesogenic mechanisms, ERY provoked over-eating by stimulation on the pharyngeal pumping and reduction on the satiety quiescence percentage and duration. Such effects were resulted from stimulation on the neurotransmitters including serotonin (5-HT), dopamine (DA) and acetylcholine (ACh). The nervous responses involved the up-regulation of Gsα (e.g., ser-7, gsa-1, acy-1 and kin-2) signaling pathway and the down-regulation of TGFβ (daf-7) but not via cGMP-dependent regulations (e.g., egl-4). Moreover, ERY stimulated the activities of fatty acid synthase (FAS) and glycerol-3-phosphateacyl transferases (GPAT) that catalyze lipogenesis, while ERY inhibited those of acyl-CoA synthetase (ACS), carnitine palmitoyl transferase (CPT) and acyl-CoA oxidase (ACO) that catalyze lipolysis. The unbalance between lipogenesis and lipolysis resulted in the fat accumulation which was consistent with up-regulation on mgl-1 and mgl-3 which are the down-steam of TGFβ regulation. Such consistence supported the close connection between nervous regulation and lipid metabolism. In addition, ERY also disturbed insulin which connects lipid with glucose in metabolism.

Hydrogen peroxide (H₂O₂), as a common disinfectant, has been extensively used in aquaculture. The toxicity of high ambient H₂O₂ for gills and liver of fish has received attention from many researchers. However, whether H₂O₂ exposure induced brain injury and neurotoxicity has not been reported in fish. Therefore, this study aimed to explore the potential mechanism of H₂O₂ toxicity in brain of common carp via transcriptome analysis and biochemical parameter detection. The fish were exposed to 0 (control) and 1 mM of H₂O₂ for 1 h per day lasting 14 days. The results showed that H₂O₂ exposure caused oxidative damage in brain evidenced by decreased glutathione (GSH), total antioxidant capacity (T-AOC) and nicotinamide adenine dinucleotide (NAD⁺) levels, and increased formation of malondialdehyde (MDA) and 8-hydroxy-2′-deoxyguanosine (8-OHdG). Meanwhile, H₂O₂ exposure reduced 5-hydroxytryptamine (5-HT) level, and down-regulated tryptophan hydroxylase 1 (tph1a), tph2, 5-hydroxytryptamine receptor 1A-beta (htr1ab) and htr2b expression in brain. Transcriptome analysis showed that H₂O₂ exposure up-regulated 604 genes and down-regulated 1209 genes in brain. Go enrichment displayed that the differently expressed genes (DEGs) were enriched mainly in cellular process, single-organism process, metabolic process, and biological regulation in the biological process category. Further, KEGG enrichment indicated that H₂O₂ exposure led to dysregulation of neurotransmitter signals including depression of glutamatergic synapse, GABAergic synapse and endocannabinoid signaling. Also, we found the alteration of three key pathways including calcium, cAMP and HIF-1 in brain after H₂O₂ exposure. In conclusion, our data indicated that H₂O₂ exposure induced oxidative damage and neurotoxicity, possibly related to dysregulation of neurotransmitters and calcium, cAMP and HIF-1 signaling pathways, which may adversely affect learning, memory and social responses of common carp. This study provided novel insight into biological effects and underlying mechanism of H₂O₂ toxicity in aquatic animal, and contributed to proper application of H₂O₂ in aquaculture.

Penconazole is a widely used chiral triazole bactericide that may adversely affect the environment. It contains two corresponding enantiomers and there may be differences in toxicity between the isomers. Therefore, in this study, we exposed zebrafish embryos to different concentrations of the penconazole enantiomer to study the developmental toxicity and neurotoxicity of penconazole on zebrafish and the difference in toxicity between enantiomers. The results showed that penconazole exposure caused adverse effects on zebrafish embryos, such as autonomous motor abnormalities, heart rate slowing, and increased deformity, resulting in significant developmental toxicity. Meanwhile, also caused the zebrafish larvae to slow movement, the neurotransmitter content and nervous system related gene expression significantly changed, which proved that penconazole also caused neurotoxicity to zebrafish. Interestingly, our results also clearly show that (+)-penconazole is significantly more toxic to zebrafish than (−)-penconazole at the same concentration, whether it is developmental toxicity or neurotoxicity, which suggests that we should focus on (+)-penconazole more when conducting toxicological studies on penconazole.

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.

There are serious concerns over the adverse impacts of microplastics (MPs) on living organisms. The main objective of this study was to test the effects of MPs on the total length, weight, condition factor (CF), transcriptional level of antioxidant, anti and pro-apoptotic, and neurotransmitter genes, and the histopathology of the gill, liver, brain, kidney, and intestine in the larvae of zebrafish (Danio rerio). Fish were exposed to one of three levels of pristine low-density polyethylene (LDPE) fragments (5, 50, or 500 μg/L) for 10 or 20 days. No significant changes were observed in any of the selected biomarkers across MP concentrations at days 10 or 20. The expression of casp9 (caspase 9, apoptosis-related cysteine protease), casp3a (caspase 3, apoptosis-related cysteine protease a) and cat (catalase), however, were significantly lower in the larvae sampled at day 20 than day 10. We provide evidence that virgin short-term exposure to LDPE fragments has minimal impact on biomarker responses in D. rerio larvae.

Risk assessments of the ecotoxicological effects insecticides impose on ectotherms have increasingly considered temperature. However, the changes toxicants induce in thermoregulatory behavioral traits may lead to a divergence of thermal selection and temperature-dependent changes of contaminant toxicity. This study demonstrated the interaction of behavioral thermoregulation and temperature-dependent toxicity of beta-cyfluthrin (BC) in the lizard Eremias argus. Based on the negative relationship between temperature and BC toxicity, seeking a warming environment was assumed to represent a self-rescue behavior (and vice versa). The results showed that BC-treated lizards (0–20 μg/g body weight (bw)) showed such self-rescue behavior, while lizards exposed to an extremely high BC dose (200 μg/g bw) sought a cooler environment. Biochemical assays showed that BC affected neurotransmitter systems, caused oxidative stress, and interfered with ion-transport in the central nervous system. Biomarkers of the cholinergic and glutamatergic system, ion-transport function, and oxidative stress were identified as potential biochemical variables related to thermoregulatory behavior. Apparently, seeking a warmer environment is a survival strategy with the aim to neutralize BC toxicity, while seeking a cooler environment aims to attenuate the harmful effects of metabolic and oxidative stress, and to decelerate internal BC diffusion. This phenomenon could be also explained by the concept of the “cooling trap”, i.e., a behavior where cooler temperatures are sought. This impairs survival after exposure to BC at it has a negative temperature coefficient, derived from a dysfunction of the central nervous system regarding thermoregulation caused by the high dosage of neurotoxicant and resulting temperature maladaptation. Implications of the interaction between thermoregulatory behavior and temperature-dependent toxicity are presented, which may aid further temperature-dependent risk assessments.

Fumonisin B1 (FB1) is a neurodegenerative mycotoxin synthesized by Fusarium spp., but the potential neurobehavioral toxicity effects in organisms have not been characterized clearly. Caenorhabditis elegans (C. elegans) has emerged as a promising model organism for neurotoxicological studies due to characteristics such as well-functioning nervous system and rich behavioral phenotypes. To investigate whether FB1 has neurobehavioral toxicity effects on C. elegans, the motor behavior, neuronal structure, neurotransmitter content, and gene expression related with neurotransmission of C. elegans were determined after exposed to 20–200 μg/mL FB1 for 24 h and 48 h, respectively. Results showed that FB1 caused behavioral defects, including body bends, head thrashes, crawling distance, mean speed, mean amplitude, mean wavelength, foraging behavior, and chemotaxis learning ability in a dose-, and time-dependent manner. In addition, when C. elegans was exposed to FB1 at a concentration of 200 μg/mL for 24 h and above 100 μg/mL for 48 h, the GABAergic and serotonergic neurons were damaged, but no effect on dopaminergic, glutamatergic, and cholinergic neurons. The relative content of GABA and serotonin decreased significantly. Furthermore, abnormal expression of mRNA levels associated with GABA and serotonin were found in nematodes treated with FB1, such as unc-30, unc-47, unc-49, exp-1, mod-5, cat-1, and tph-1. The neurobehavioral toxicity effect of FB1 may be mediated by abnormal neurotransmission of GABA and serotonin. This study provides useful information for understanding the neurotoxicity of FB1.

Arsenic is a well-recognized environmental contaminant that occurs naturally through geogenic processes in the aquifer. More than 200 million people around the world are potentially exposed to the elevated level of arsenic mostly from Asia and Latin America. Many adverse health effects including skin diseases (i.e., arsenicosis, hyperkeratosis, pigmentation changes), carcinogenesis, and neurological diseases have been reported due to arsenic exposure. In addition, arsenic has recently been shown to contribute to the onset of non-communicable diseases, such as diabetes mellitus and cardiovascular diseases. The mechanisms involved in arsenic-induced diabetes are pancreatic β-cell dysfunction and death, impaired insulin secretion, insulin resistance and reduced cellular glucose transport. Whereas, the most proposed mechanisms of arsenic-induced hypertension are oxidative stress, disruption of nitric oxide signaling, altered vascular response to neurotransmitters and impaired vascular muscle calcium (Ca²⁺) signaling, damage of renal, and interference with the renin-angiotensin system (RAS). However, the contributions of arsenic exposure to non-communicable diseases are complex and multifaceted, and little information is available about the molecular mechanisms involved in arsenic-induced non-communicable diseases and also no suitable therapeutic target identified yet. Therefore, in the future, more basic research is necessary to identify the appropriate therapeutic target for the treatment and management of arsenic-induced non-communicable diseases. Several reports demonstrated that a daily balanced diet with proper nutrient supplements (vitamins, micronutrients, natural antioxidants) has shown effective to reduce the damages caused by arsenic exposure. Arsenic detoxication through natural compounds or nutraceuticals is considered a cost-effective treatment/management and researchers should focus on these alternative options. This review paper explores the scenarios of arsenic contamination in groundwater with an emphasis on public health concerns. It also demonstrated arsenic sources, biogeochemistry, toxicity mechanisms with therapeutic targets, arsenic exposure-related human diseases, and onsets of cardiovascular diseases as well as feasible management options for arsenic toxicity.

Chemical pollutants, such as pesticides, often leach into aquatic environments and impact non-target organisms. Marine invertebrates have complex life cycles with multiple life-history stages. Exposure to pesticides during one life-history stage potentially influences subsequent stages; a process known as a carry-over effect. Here, we investigated carry-over effects on the jellyfish Aurelia coerulea. We exposed polyps to individual and combined concentrations of atrazine (2.5 μg/L) and chlorpyrifos (0.04 μg/L) for four weeks, after which they were induced to strobilate. The resultant ephyrae were then redistributed and exposed to either the same conditions as their parent-polyps or to filtered seawater to track potential carry-over effects. The percentage of deformities, ephyrae size, pulsation and respiration rates, as well as the metabolic profile of the ephyrae, were measured. We detected a subtle carry-over effect in two metabolites, acetoacetate and glycerophosphocholine, which are precursors of the neurotransmitter acetylcholine, important for energy metabolism and osmoregulation of the ephyrae. Although these carry-over effects were not reflected in the other response variables in the short-term, a persistent reduction of these two metabolites could have negative physiological consequences on A. coerulea jellyfish in the long-term. Our results highlight the importance of considering more than one life-history stage in ecotoxicology, and measuring a range of variables with different sensitivities to detect sub-lethal effects caused by anthropogenic stressors. Furthermore, since we identified few effects when using pesticides concentrations corresponding to Australian water quality guidelines, we suggest that future studies consider concentrations detected in the environment, which are higher than the water quality guidelines, to obtain a more realistic scenario by possible risk from pesticide exposure.