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.

Atrazine, a herbicide used for controlling broadleaf weeds, has been one of the predominant pollutants constituting 80-90% of detection frequency in the samples collected from rivers, estuaries, oceans, sediments, agricultural lands, and crops. The fate of atrazine is highly unpredictable depending on the physio-chemical, physiological and geographical conditions. Range of metabolites such as deethylatrazine (DEA), deisopropyl atrazine (DIA), and didealkylatrzine (DDA) are formed as a result of biotic as well as abiotic degradation process in the environment following cyanuric acid, ammelide, CO2 and NH3 are formed as final products. Atrazine degraded products has shown more hazardous nature than the parent compound, atrazine. Atrazine is banned in Italy, India, Germany and European union but widely used in China, Australian, Canadian and US agriculture. To date, reviews evaluating the assimilation of synerigistic treatment technologies and comparative degration mechanism have not been highlighted. This work focuses on (1) the spatiotemporal distribution of atrazine and its metabolites globally and the factors governing it (2) provides an in-depth discussion about the various studies showing the toxicity of atrazine in microbes, cattle, human, terrestrial and aquatic organisms; (3) discusses the contaminants of emerging concern which are continuously replacing atrazine like terbuthylazine and their intermediate compounds posing more risk to wildlife and humans; (4) summarises the different treatment technologies which have been predominantly applied for the removal of atrazine in water and soil systems and also discusses the synergistic or mutualistic aspects of treatment methods in degrading atrazine.

Atrazine, a commonly employed herbicide for corn production, can leave residues in soil, resulting in photosynthetic toxicity and impeding growth in subsequent alfalfa (Medicago sativa L.) crops within alfalfa-corn rotation systems. The molecular regulatory mechanisms by which atrazine affects alfalfa growth and development, particularly its impact on the microbial communities of the alfalfa rhizosphere, are not well understood. This study carried out field experiments to explore the influence of atrazine stress on the biomass, chlorophyll content, antioxidant system, and rhizosphere microbial communities of the atrazine-sensitive alfalfa variety WL-363 and the atrazine-resistant variety JN5010. The results revealed that atrazine significantly reduced WL-363 growth, decreasing plant height by 8.58 cm and root length by 5.42 cm (p < 0.05). Conversely, JN5010 showed minimal reductions, with decreases of 1.96 cm in height and 1.26 cm in root length. Chlorophyll content in WL-363 decreased by 35% under atrazine stress, while in JN5010, it was reduced by only 10%. Reactive oxygen species (ROS) accumulation increased by 60% in WL-363, compared to a 20% increase in JN5010 (p < 0.05 for both). Antioxidant enzyme activities, such as superoxide dismutase (SOD) and catalase (CAT), were significantly elevated in JN5010 (p < 0.05), suggesting a more robust defense mechanism. Although the predominant bacterial and fungal abundances in rhizosphere soils remained generally unchanged under atrazine stress, specific microbial groups exhibited variable responses. Notably, Promicromonospora abundance declined in WL-363 but increased in JN5010. FAPROTAX functional predictions indicated shifts in the abundance of microorganisms associated with pesticide degradation, resistance, and microbial structure reconstruction under atrazine stress, displaying different patterns between the two varieties. This study provides insights into how atrazine residues affect alfalfa rhizosphere microorganisms and identifies differential microbial responses to atrazine stress, offering valuable reference data for screening and identifying atrazine-degrading bacteria.

Nickel oxide nanoparticles (NiO-NPs) are common nanomaterials that may be released into the environment, affecting the toxicity of other contaminants. Atrazine (ATZ) is a commonly used herbicide that can harm organisms due to its persistence and bioaccumulation in the environment. Although the toxicity of ATZ to earthworms is well-documented, the risk of co-exposure with NiO-NPs increases as more nanoparticles accumulate in the soil. In this study, we investigated the effects and mechanisms of NiO-NPs on the accumulation of ATZ in earthworms. The results showed that after day 21, the antioxidant system of the cells under ATZ treatment alone was adversely affected, with ROS content 36.05 % higher than that of the control (CK) group. However, the addition of NiO-NPs reduced the ROS contents in the earthworms by 0.6 %- 32.3 %. Moreover, analysis of earthworm intestinal sections indicates that NiO-NPs mitigated cellular and tissue damage caused by ATZ. High-throughput sequencing revealed that NiO-NPs in earthworm intestines increased the abundance of Pseudomonas aeruginosa and Aeromonas aeruginosa. Additionally, the enhanced function of the ABC transport system in the gut resulted in lower accumulation of ATZ in earthworms. In summary, NiO-NPs can reduce the accumulation and thus the toxicity of ATZ in earthworms. Our study contributes to a deeper understanding of the effects of NiO-NPs on co-existing pollutants.

Herein, magnetic biochar coupled with Acinetobacter lwoffii DNS32 immobilized pellets (DMBC-P) were synthesized through sodium alginate embedding and fixation, which could fast and completely eliminate atrazine from contaminated farmland soil. Characterization results revealed that DMBC-P exhibited a significant abundance of three-dimensional network porous structures, thereby enhancing the stability and specific surface area of DMBC-P. The application of 0.5 % DMBC-P could completely remove 22 mg/kg atrazine from soil within 4 d under the condition of moisture content of 60 % and soil pH of 7.4. After 5 d of remediation, DMBC-P could be easily extracted from the soil by magnetic separation and still had 100 % removal efficiency for atrazine after 3 rounds of recycling. Moreover, DMBC-P effectively alleviated the oxidative damage of atrazine to soybean seedlings through significantly decreasing the activities of various plants antioxidant enzymes by 27 % to 79 %. Meanwhile, analysis of 16S rRNA revealed a significant increase in the relative abundance of functional microflora such as Acidobacteriota and Chloroflexi at the phylum level, which promoted the growth of soybean seedlings. Additionally, pore filling, hydrogen bonding, and 7C -7C stacking were identified as the primary mechanisms responsible for atrazine adsorption onto DMBC-P. Subsequently, the degrading bacteria DNS32 immobilized on DMBC-P was employed to catalyze the decomposition of atrazine into non-toxic cyanuric acid based on LC -MS. Overall, this study provided a reasonable design of magnetic carbon -based bacterial pellet for atrazinecontaminated soil remediation, which could efficiently remove atrazine and be effectively recycled after remediation.

In this study, the sustainability of the electrokinetic remediation soil flushing (EKSFs) process integrated without and with adsorption barriers (EKABs) have been evaluated for the treatment of four soils contaminated with Atrazine, Oxyfluorfen, Chlorosulfuron and 2,4-D. To this purpose, the environmental effects of both procedures (EKSFs and EKABs) have been determined through a life cycle assessment (LCA). SimaPro 9.3.0.3 was used as software tool and Ecoinvent 3.3 as data base to carry out the inventory of the equipment of each remediation setup based on experimental measurements. The environmental burden was quantified using the AWARE, USEtox, IPPC, and ReCiPe methods into 3 Endpoint impact categories (and damage to human health, ecosystem and resources) and 7 Midpoints impact categories (water footprint, global warming potential, ozone depletion, human toxicity (cancer and human non-cancer), freshwater ecotoxicity and terrestrial ecotoxicity). In general terms, the energy applied to treatment (using the Spanish energy mix) was the parameter with the greatest influence on the carbon footprint, ozone layer depletion and water footprint accounting for around 70 % of the overall impact contribution. On the other hand, from the point of view of human toxicity and freshwater ecotoxicity of soil treatments with 32 mg kg(-1) of the different pesticides, the EKSF treatment is recommended for soils with Chlorosulfuron. In this case, the carbon footprint and water footprint reached values around 0.36 kg of CO2 and 114 L of water per kg of dry soil, respectively. Finally, a sensitivity analysis was performed assuming different scenarios.

Atrazine (ATR) is a widely used herbicide worldwide that can cause kidney damage in humans and animals by accumulation in water and soil. Lycopene (LYC), a carotenoid with numerous biological activities, plays an important role in kidney protection due to its potent antioxidant and anti-inflammatory effects. The current study sought to investigate the role of interactions between mtDNA and the cGAS-STING signaling pathway in LYC mitigating PANoptosis and inflammation in kidneys induced by ATR exposure. In our research, 350 mice were orally administered LYC (5 mg/kg BW/day) and ATR (50 or 200 mg/kg BW/day) for 21 days. Our results reveal that ATR exposure induces a decrease in mtDNA stability, resulting in the release of mtDNA into the cytoplasm through the mPTP pore and the BAX pore and the mobilization of the cGAS-STING pathway, thereby inducing renal PANoptosis and inflammation. LYC can inhibit the above changes caused by ATR. In conclusion, LYC inhibited ATR exposure-induced histopathological changes, renal PANoptosis, and inflammation by inhibiting the cGAS-STING pathway. Our results demonstrate the positive role of LYC in ATR-induced renal injury and provide a new therapeutic target for treating renal diseases in the clinic.

As an environmental endocrine disruptor, atrazine (ATR) can produce serious health damage to humans. This study aimed to assess the exposure and health risks associated with ATR among Chinese adults by analyzing data on ATR concentrations in various environmental media across China. Literatures were retrieved from 5 databases and finally identified 65 eligible studies. The concentrations of ATR in environmental media ranged from 0 to 0.12 mg/kg. The average daily doses (ADD) of ATR for Chinese males and females were estimated at 2.58 x 10-5 mg/kg/d and 2.53 x 10-5 mg/kg/d, respectively. The ADD values did not exceed the reference dose -0.035 mg/kg/d. Sensitivity analysis revealed that body weight and ATR concentrations in various food items such as vegetables, grains, and fruits, along with factors like drinking water intake rate, were the primary influencing factors. Furthermore, the hazard index (HI) values were less than 1 and over 0.32% of cancer risk (CR) values were higher than 10-4, indicating that exposure to ATR could pose a potential risk. The HI and CR values did not exhibit statistically significant differences across genders or among various age groups. This study illustrated that exposed to ATR can pose potential risk to Chinese adults health and dietary intake (including drinking water, and food) was the major pathway by which most humans are exposed to ATR.

The global prevalence of Neurological disorders has increased alarmingly in response to environmental and lifestyle changes. Atrazine (ATZ) is a difficult to degrade soil and water pollutant with well-known neurotoxicity. Melatonin (MT), an antioxidant with chemoprotective properties, has a potential therapeutic effect on cerebellar damage caused by ATZ exposure. The aim of this study was to explore the effects and underlying mechanisms of MT on the cerebellar inflammatory response and pyroptosis induced by ATZ exposure. In this study, C57BL/6J mice were treated with ATZ (170 mg/kg BW/day) and MT (5 mg/kg BW/day) for 28 days. Our results revealed that MT alleviated the histopathological changes, ultrastructural damage, oxidative stress and decrease of mitochondrial membrane potential (Delta psi m) in the cerebellum induced by ATZ exposure. ATZ exposure damaged the mitochondria leading to release of mitochondrial DNA (mtDNA) to the cytoplasm, MT activated the cyclic GMP-AMP synthetase interferon gene stimulator (cGAS-STING) axis to alleviate inflammation and pyroptosis caused by ATZ exposure. In general, our study provided new evidence that the cGAS-STING-NLRP3 axis plays an important role in the treatment of ATZ-induced cerebellar injury by MT.

Atrazine (ATR), a water-soluble herbicide commonly used to control broad-leaf and monocotyledonous weeds, presents a significant risk to environmental soil and water quality. Exposure to ATR adversely affects human and animal health, frequently resulting in cardiac impairment. Curcumin (Cur), an acidic polyphenol derivative from plants acclaimed for its pronounced anti-inflammatory and antioxidant properties, has garnered interest as a potential therapeutic agent. However, whether it has the potential to ameliorate ATR-induced cardiac toxicity via modulation of endoplasmic reticulum stress (ERS) and apoptosis pathways in mice remains unclear. Our results showed that Cur supplementation attenuates ATR-induced cardiotoxicity, evidenced by decrease in creatine kinase and lactate dehydrogenase, key biochemical markers of myocardial injury, which have a more significant protecting effect in high-dose ATR induced injury. Histopathological and electron microscopy examinations further solidified these findings, demonstrating an amelioration in organellar damage, particularly in endoplasmic reticulum swelling and subsequent mitochondrial impairment. Additionally, ATR exposure augments ERS and triggers apoptotic pathways, as indicated by the upregulation of ERS-related gene expression (ATF6, CHOP, IRE1, GRP78) and pro-apoptotic markers (BAX, BAK1, Caspase3, Caspase. Intriguingly, Cur counteracts this detrimental response, significantly reducing ERS and pro-apoptotic signals at both transcriptional and translational levels. Collectively, our findings illuminate Cur's cardioprotective effect against ATRinduced injury, primarily through its anti-ERS and anti-apoptotic activities, underscoring Cur's potential as a therapeutic for ATR-induced cardiotoxicity.