Atrazine (ATR) is a widely utilized herbicide that has been demonstrated to exert a multitude of deleterious effects on the environment, particularly with regard to water and soil contamination. Moreover, its disruption of endocrine function and implications for antibiotic resistance underscore the urgent need to prioritize alternative solutions for both ecosystems and human health. Therefore, the objective of this study was to investigate a range of neurotoxic effects associated with atrazine-induced damage in the prefrontal lobe of mice. The results of this study indicate that treatment with ATR in C57BL/6 J mice resulted in cognitive-related behavioral deficits, including anxiety and depression, as well as motor impairments. In vivo analyses demonstrated that ATR exposure resulted in a reduction in neuronal synapse density at the microstructural level, while also compromising prefrontal morphological integrity, nociceptor count, and overall neuronal health within the brain. These findings collectively suggest that synaptic deficits are implicated in ATR-induced behavioral abnormalities observed in these mice. Furthermore, our findings revealed that ATR exposure resulted in elevated TDP-43 expression levels that were ectopically localized within the cytoplasm. This alteration led to impaired functionality of mRNP granules and contributed to the development of abnormal synaptic defects. Conversely, TDP43 has the potential to localize ectopically to mitochondria, where it activates the mitochondrial unfolded protein response (UPRmt), which ultimately results in mitochondrial dysfunction. These findings collectively indicate a strong correlation between TDP-43 dysregulation and the progression of neurodegenerative diseases. Further investigation into the potential neurotoxicity of atrazine may foster heightened awareness, leading to more stringent regulatory measures, research into safer alternatives, and the adoption of sustainable practices, which are essential for safeguarding environmental integrity alongside human health.

Microplastics (MPs) are newly emerged pollutants found in water and soil, while microcystin-leucine arginine (MC-LR) is often detected in drinking water and water products, both posing serious threats to aquatic environment and food safety. MPs can serve as carriers of MC-LR. These pollutants are often found together, rather than separately. This study focused on assessing the neurotoxicity of co-exposure to MC-LR and PS in Caenorhabditis elegans (C. elegans) after combined exposure to these two pollutants. Exposure to varying concentrations of polystyrene (PS) and MC-LR individually caused a dose-dependent decrease in the locomotion behaviors of C. elegans. Exposure to either of these substances alone caused damage to the phenotypic indicators of the C. elegans. To further explore the additional damage caused by the combined exposure of PS and MC-LR, the low, medium, and high combined dose groups were selected based on the locomotion behaviors and survival results. Combined exposure increased the level of oxidative stress indicators and resulted in neuronal loss. It also reduced serotonin, glutamate, GABA, and dopamine neurotransmitters levels, without affecting cholinergic neurons. The expression of neurotransmitter-related genes also decreased. The high-dose group showed the most significant effects. This article is the first to study the combined effect of PS and MC-LR on C. elegans nervous systems, offering novel insights into the risks posed by co-occurring contaminants and their implications for aquatic ecosystems and food safety.

Polybrominated diphenyl ethers (PBDEs) are synthetic halogen compounds, industrially used as flame retardants in many flammable products. PBDEs are environmentally persistent and bioaccumulative substances that were used from the 1970s and discontinued in the 1990s. PBDEs are present in air, soil, water, and food, where they remain stable for a long time. Chronic exposure to PBDEs is associated with adverse human health effects, including cancer, immunotoxicity, hepatotoxicity, reproductive and metabolic disorders, motor and hormonal impairments, and neurotoxicity, especially in children. It has been demonstrated that PBDE exposure can cause mitochondrial and DNA damage, apoptosis, oxidative stress, epigenetic modifications, and changes in calcium and neurotransmitter levels. Here, we conduct a comprehensive review of the molecular mechanisms of the neurotoxicity of PBDEs using different approaches. We discuss the main neurotransmitter pathways affected by exposure to PBDEs in vitro and in vivo in different mammalian models. Excitatory and inhibitory signaling pathways are the putative target where PBDEs carry out their neurotoxicity. Based on this evidence, environmental PBDEs are considered a risk to human public health and a hazard to biota, underscoring the need for environmental monitoring to mitigate exposure to PBDEs.

Volcanoes, during their explosive and post-explosive phases, as well as through continuous degassing processes, release a range of pollutants hazardous to human health, including toxic gases, fine particulate matter, and heavy metals. These emissions impact over 14% of the global population living in proximity to volcanoes, with effects that can persist for days, decades, or even centuries. Living conditions in these regions often involve chronic exposure to contaminants in the air, water, and soil, significantly increasing the risk of developing neurological disorders. Prolonged exposure to elements such as lead (Pb), mercury (Hg), and cadmium (Cd), among others, results in the accumulation of metals in the brain, which increases oxidative stress and causes neuronal damage and severe neurotoxicity in animals. An examination of metal accumulation in brain cells, particularly astroglia, provides valuable insights into the developmental neurotoxicity of these metals. Moreover, microglia may activate itself to protect from cytotoxicity. In this review, we consider the implications of living near an active volcano for neurotoxicity and the common neurodegenerative diseases. Additionally, we encourage governments to implement public health strategies and mitigation measures to protect vulnerable communities residing near active volcanoes.

Fosthiazate (FOS) is a widely used organophosphorus insecticide effective against soil root-knot nematodes. However, its ecotoxicity to non-target soil organisms, particularly in combination with microplastics (MPs), is unclear. This study explores the toxic-effects and molecular mechanisms of co-exposure to FOS and MPs on earthworms (Eisenia fetida) using multilevel toxicity endpoints and transcriptomics. Results showed that both FOS and MPs elevated the intracellular levels of reactive oxygen species (ROS), malondialdehyde (MDA), and 8-hydroxy-2-deoxyguanosine (8-OHdG) in earthworms' cells. The superoxide dismutase (SOD) and catalase (CAT) activities followed a similar trend in all treatments, with changes observed at 14 and 28 days, indicating that co-exposure to FOS and MPs increased DNA oxidative damage. Notably, the co-exposure more significantly inhibited Ca2+-ATPase activity and exacerbated neurotoxicity compared to individual treatments, closely associated with changes in intracellular ROS levels that mediate neuroinhibition and lead to neurotoxicity. KEGG enrichment analysis revealed that MPs and FOS disrupted pathways related to metabolism, immunity, and apoptosis, while co-exposure primarily impaired endocrine and receptor pathways, showing higher toxicity. Our study offers novel insights into the ecotoxicological effects and mechanisms of pesticides and microplastics on earthworms, providing valuable data for evaluating the soil environmental health risks associated with compound pollution.

Fluxapyroxad, an emerging succinate dehydrogenase inhibitor fungicide, is widely used due to its excellent properties. Given its persistence in soil with a 50 % disappearance time of 183-1000 days, it is crucial to evaluate the long-term effects of low-dose fluxapyroxad on non-target soil organisms such as earthworms ( Eisenia fetida). The present study investigated the impacts of fluxapyroxad (0.01, 0.1, and 1 mg kg(-1 )) on Eisenia fetida over 56 days, focusing on oxidative stress, digestive and nervous system functions, and histopathological changes. We also explored the mechanisms of fluxapyroxad-enzyme interactions through molecular docking and dynamics simulations. Results demonstrated a significant dose-response relationship in the integrated biomarker response of 12 biochemical indices. Fluxapyroxad altered expression levels of functional genes and induced histopatho- logical damage in earthworm epidermis and intestines. Molecular simulations revealed that fluxapyroxad is directly bound to active sites of critical enzymes, potentially disrupting their structure and function. Even at low doses, long-term fluxapyroxad exposure significantly impacted earthworm physiology, with effects becoming more pronounced over time. Our findings provide crucial insights into the chronic toxicity of fluxapyroxad and emphasize the importance of long-term, low-dose studies in pesticide risk assessment in soil. This research offers valuable guidance for the responsible management and application of fungicides.

Global water scarcity entailed the use of treated wastewater (TWW) in agriculture, however, this water can vehiculate numerous pollutants into soil and further crops such as microplastics (MPs). To date, few studies had quantified the accumulation of MPs in soils and earthworms after irrigation with TWW as well as their toxicological effects. Hence, the main objective of the present work is to evaluate the toxicity of MPs using Lumbricus sp. earthworms collected from TWW irrigated soils with an increasing gradient of time (5 years, 16 years and 24 years). MPs determination in soil, as well as in earthworms were performed. The intestinal mucus was quantified, and cytotoxicity (Lysosomal membrane stability (LMS), Catalase (CAT) and glutathione-S-Transferase (GST) activities), neurotoxicity (Acetylcholinesterase activity (AChE)) and genotoxicity (Micronuclei frequency (MNi)) biomarker were assessed. Our results revealed that the use of TWW rendered MPs accumulation in earthworms' tissues and induce alteration on the intestinal mucus. An important cytotoxicity time-depending was observed being associated with an increase on genotoxicity. Overall, the present investigation highlights the ecotoxicological risk associated with the use of TWWs as an important driver of MPs and consequently measures are necessary to reduce MPs in wastewater treatment plans to improve this non-conventional water quality.

Arsenic is one of the toxic metalloid that is ubiquitously distributed in environment that exerts toxic effects by contaminating air, water, soil, and other resources. Groundwater is thought to be the major source of arsenic-induced mammalian toxicity. The current work sheds light on the antioxidant and anti-inflammatory properties of silymarin against arsenic-induced neurotoxicity in rats. Male albino wistar rats were categorized into 4 groups i.e., control, silymarin-treated (50 mg/kg), arsenic-treated (25ppm), and arsenic + silymarin-treated. Arsenic and silymarin were given intragastrically for 28 days. The study found that as compared to the control rats, animals that received arsenic treatment had lower levels of total antioxidants inside their brain tissues. Additionally, a notable rise in malondialdehyde level, protein oxidation, and inflammation was observed in the group of arsenic treatment suggesting oxidative stress generation inside brain tissue of rats leading to neuronal damage. However, silymarin reversed the damage caused by arsenic in rats, demonstrating its anti-inflammatory and antioxidant potential. The electron microscopic and histological results also showed that silymarin reversed the neuronal damage induced by arsenic exposure providing additional evidence of its antioxidative nature. The present study highlights the therapeutic efficacy of silymarin as an antioxidant against arsenic-induced toxicity in rats' brain.

As a major alternative to the brominated flame retardants, the production and use of organophosphorus flame retardants (OPFRs) are increasing. And tris (1,3-dichloro-2-propyl) phosphate (TDCPP), one of the most widely used OPFRs, is now commonly found in a variety of products, such as building materials, furniture, bedding, electronic equipment, and baby products. TDCPP does not readily degrade in the water and tends to accumulate continuously in the environment. It has been detected in indoor dust, air, water, soil, and human samples. Considered as an emerging environmental pollutant, increasing studies have demonstrated its adverse effects on environmental organisms and human beings, with the nerve system identified as a sensitive target organ. This paper systematically summarized the progress of TDCPP application and its current exposure in the environment, with a focus on its neurotoxicity. In particular, we highlighted that TDCPP can be neurotoxic (including neurodevelopmentally toxic) to humans and animals, primarily through oxidative stress, neuroinflammation, mitochondrial damage, and epigenetic regulation. Additionally, this paper provided an outlook for further studies on neurotoxicity of TDCPP, as well as offered scientific evidence and clues for rational application of TDCPP in daily life and the prevention and control of its environmental impact in the future.

Fosthiazate is a widely used organophosphorus nematicide that resides in the soil and controls soil root-knot nematodes. However, whether it has toxic effects on non-target soil organisms such as earthworms is unclear. Therefore, in this study, a 28-day experiment of fosthiazate exposure was conducted using the Eisenia fetida as the model organism. The results showed that fosthiazate stress caused excessive production of reactive oxygen species (ROS), increased the levels of malondialdehyde (MDA) and 8-hydroxy-2-deoxyguanosine (8-OHdG), and decreased the activities of superoxide dismutase (SOD) and catalase (CAT), suggesting that fosthiazate induced oxidative stress and DNA damage in E. fetida. Acetylcholinesterase (AChE) activity was significantly reduced, and the expression of its related functional genes was also altered, demonstrating that fosthiazate damaged the nervous system of E. fetida, which was further confirmed by AlphaFold2 modeling and molecular docking simulations. Furthermore, Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis indicated that fosthiazate exposure may induce apoptosis, inflammation, and viral infection in E. fetida, which adversely affect the organism. This study provides reference data for the ecotoxicity of fosthiazate.