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Coenzyme Q10 (CoQ10) plays an important role in improving mitochondrial function and has many beneficial effects on the kidney. However, whether CoQ10 protects against diquat (DQ)‐induced acute kidney injury (AKI) remains unclear. In this study, we investigated the protective effects and mechanism of action of CoQ10 against DQ‐induced AKI. Institute of Cancer Research (ICR) mice were intraperitoneally injected with DQ to induce AKI. The expression levels of serum creatinine (Cr), urea, and kidney injury molecule‐1 (KIM‐1) increased, those of aquaporin 1 (AQP‐1) decreased, and those of mitochondrial reactive oxygen species (ROS) increased with increased depolarization of mitochondrial membranes and mitochondrial rupture. In contrast, treatment with CoQ10 significantly improved DQ‐induced AKI. CoQ10 treatment reduced serum Cr, urea, and KIM‐1 contents, increased the AQP‐1 expression, and reduced ROS contents in mice with DQ poisoning. Our results suggest that AKI caused by DQ poisoning may be related to the disruption of mitochondrial homeostasis and that CoQ10 treatment protects against AKI caused by DQ poisoning by improving mitochondrial kinetic homeostasis. Thus, CoQ10 represents a new therapeutic option for the prevention and treatment of AKI caused by DQ poisoning. [ABSTRACT FROM AUTHOR]

Diquat (DQ) is a nonselective bipyridine herbicide with a structure resembling paraquat (PQ). In recent years, the utilization of DQ as a substitute for PQ has grown, leading to an increase in DQ poisoning cases. While the toxicity mechanism of DQ remains unclear, it is primarily attributed to the intracellular generation of reactive oxygen species (ROS) and reactive nitrogen species (RNS) through the process of reduction oxidation. This results in oxidative stress, leading to a cascade of clinical symptoms. Notably, recent reports on DQ poisoning have highlighted a concerning trend: an upsurge in cases involving neurological damage caused by DQ poisoning. These patients often present with severe illness and a high mortality rate, with no effective treatment available thus far. Imaging findings from these cases have shown that neurological damage tends to concentrate on the brainstem. However, the specific mechanisms behind this poisoning remain unclear, and no specific antidote exists. This review summarizes the research progress on DQ poisoning and explores potential mechanisms. By shedding light on the nerve damage associated with DQ poisoning, we hope to raise awareness, propose new avenues for investigating the mechanisms of DQ poisoning, and lay the groundwork for the development of treatment strategies for DQ poisoning. Trial registration number: 2024PS174K. [ABSTRACT FROM AUTHOR]

Oxidative stress is an important contributor to gastrointestinal diseases in multiple ways. Taurodeoxycholic acid (TDCA) is a metabolite of bile acids and has anti-inflammatory and protective effects on the intestinal tract. However, whether TDCA can alleviate oxidative stress in the intestine is still unclear. Here, we investigated the effects of TDCA on diquat-induced oxidative stress in the jejunum and its mechanism. The results revealed that TDCA increased the concentrations of antioxidant enzymes in the serum, jejunal tissue and intestinal epithelial cells of the mice, as did the expression of tight junction-associated proteins and the Nrf2 protein in the jejunal epithelial tissue and intestinal epithelial cells. We then explored the mechanism of Nrf2 with ML385 (a specific Nrf2 inhibitor). The results showed that after ML385 treatment, the levels of antioxidant enzymes were significantly decreased in the serum, jejunum, and intestinal epithelial tissues of the mice. The expression of tight junction proteins in jejunum epithelial tissues and intestinal epithelial cells was also decreased. In conclusion, our study suggests that TDCA alleviates oxidative stress to improve intestinal barrier function through the Nrf2-mediated signaling pathway. These findings help elucidate the role of TDCA in protecting the intestinal barrier and its mechanism of action, providing insights for the prevention and treatment of intestinal diseases caused by oxidative stress. [ABSTRACT FROM AUTHOR]

Growing demand for pesticides has created an environment prone to deceptive activities, where counterfeit or adulterated pesticide products infiltrate the market, often escaping rapid detection. This situation presents a significant challenge for sensor technology, crucial in identifying authentic pesticides and ensuring agricultural safety practices. Raman spectroscopy emerges as a powerful technique for detecting adulterants. Coupling the electrochemical techniques allows a more specific and selective detection and compound identification. In this study, we evaluate the efficacy of spectroelectrochemical measurements by coupling a potentiostat and Raman spectrograph to identify paraquat, a nonselective herbicide banned in several countries. Our findings demonstrate that applying −0.70 V during measurements yields highly selective Raman spectra, highlighting the primary vibrational bands of paraquat. Moreover, the selective Raman signal of paraquat was discernible in complex samples, including tap water, apple, and green cabbage, even in the presence of other pesticides such as diquat, acephate, and glyphosate. These results underscore the potential of this technique for reliable pesticide detection in diverse and complex matrices. [ABSTRACT FROM AUTHOR]

The experiment was conducted to investigate the effects of silymarin on growth performance, liver weight and liver antioxidant capacity of layer chickens induced with diquat (DQ). A total of two hundred and forty one-day-old Hy-Line White layer chickens were randomly divided into 4 groups: control group (group C) and diquat group (group D) were fed a basal diet, and silymarin group (group S) and silymarin + diquat group (group SD) were fed the basal diet supplemented with 1 g/kg of silymarin. Group C and group S were intraperitoneally injected with 1 mL/kg normal sodium, and group D and group SD were intraperitoneally injected with 1 mL/kg diquat solution at 20 day. The experiment was lasted for 21 days. The results showed as follows: ① at 1 to 20 days of age, the average daily gain of groups S and SD was significantly higher than that of groups C and D (P<0.05). At 20 to 21 days of age, the average daily gain and weight change rate of group S were significantly higher than that of group C (P<0.05). And the final weight, average daily gain and weight change rate in the SD group were significantly higher than that in group D (P<0.05). ② Compared with group D, absolute liver weight and relative liver weight was significantly lower in group S (P<0.05) and relative liver weight was significantly lower in group SD (P<0.05). ③ The total antioxidant capacity (T-AOC) and the activity of superoxide dismutase (SOD) in liver of layer chickens in the group S were significantly higher (P<0.05) than that of group C. Compared with group D, the T-AOC in liver of layer chickens in the group SD was significantly increased (P<0.05), and the content of malondialdehyde (MDA) was significantly decreased (P<0.05). In summary, dietary supplementation with silymarin can improve the growth performance, liver weight and liver antioxidant capacity of layer chickens under DQ-induced oxidative stress. [ABSTRACT FROM AUTHOR]

Abstract Oxidative stress is an important contributor to gastrointestinal diseases in multiple ways. Taurodeoxycholic acid (TDCA) is a metabolite of bile acids and has anti-inflammatory and protective effects on the intestinal tract. However, whether TDCA can alleviate oxidative stress in the intestine is still unclear. Here, we investigated the effects of TDCA on diquat-induced oxidative stress in the jejunum and its mechanism. The results revealed that TDCA increased the concentrations of antioxidant enzymes in the serum, jejunal tissue and intestinal epithelial cells of the mice, as did the expression of tight junction-associated proteins and the Nrf2 protein in the jejunal epithelial tissue and intestinal epithelial cells. We then explored the mechanism of Nrf2 with ML385 (a specific Nrf2 inhibitor). The results showed that after ML385 treatment, the levels of antioxidant enzymes were significantly decreased in the serum, jejunum, and intestinal epithelial tissues of the mice. The expression of tight junction proteins in jejunum epithelial tissues and intestinal epithelial cells was also decreased. In conclusion, our study suggests that TDCA alleviates oxidative stress to improve intestinal barrier function through the Nrf2-mediated signaling pathway. These findings help elucidate the role of TDCA in protecting the intestinal barrier and its mechanism of action, providing insights for the prevention and treatment of intestinal diseases caused by oxidative stress.

Abstract The indiscriminate use of pesticides makes us susceptible to the toxicity of these chemical compounds, which may be present in high quantities in our food. It is crucial to develop inexpensive and rapid methods for determining these pesticides for government control or even for the general population. In this study, we investigated the fabrication of self-assembled LbL films using multi-walled carbon nanotubes (MWCNT) and nickel tetrasulphonated phthalocyanine (NiTsPc) as an electrochemical sensor for the herbicide Diquat (DQ). The Layer-by-Layer (LbL) assembly of the (MWCNT/NiTsPc) film was examined, along with its structural and morphological characteristics. The effect of the number of layers in DQ detection was evaluated by cyclic voltammetry, followed by the detection through differential pulse voltammetry. The achieved limit of detection was 9.62 × 10−7 mol L−1. A ~ 30% decrease in sensitivity was observed in the presence of Paraquat, a banned herbicide and electrochemical interferent due to the structural similarities, which is regularly neglected in the most published studies. The sensor was tested in real samples, demonstrating a recovery of 98.5% in organic apples.

Diquat (DQ) poisoning can cause multiple organ damage, and the kidney is considered to be the main target organ. Increasing evidence shows that alleviating oxidative stress and inflammatory response has promising application prospects. Epigallocatechin gallate (EGCG) has potent antioxidant and anti-inflammatory effects. In this study, red blood cell membrane (RBCm)- camouflaged polylactic-co-glycolic acid (PLGA) nanoparticles (NPs) were synthesized to deliver EGCG (EGCG-RBCm/NPs) for renal injury induced by DQ. Human renal tubular epithelial cells (HK-2 cells) were stimulated with 600 μM DQ for 12 h and mice were intraperitoneally injected with 50 mg/kg b.w. DQ, followed by 20 mg/kg b.w./day EGCG or EGCG-RBCM/NPs for 3 days. The assessment of cellular vitality was carried out using the CCK-8 assay, while the quantification of reactive oxygen species (ROS) was performed through ROS specific probes. Apoptosis analysis was conducted by both flow cytometry and TUNEL staining methods. Pathological changes in renal tissue were observed. The expressions of NLRP3, IL-1β, IL-18, NFκB and Caspase1 were detected by quantitative reverse transcription polymerase chain reaction (qRT-PCR), immunohistochemistry, immunofluorescence, and Western blot. The results showed that the DQ group had increased ROS expression, increased the level of oxidative stress, and increased apoptosis rate compared with the control group. Histopathological analysis of mice in the DQ group showed renal tubular injury and elevated levels of blood urea nitrogen (BUN), serum creatinine (SCr), kidney injury molecule-1 (KIM-1), and cystatin C (Cys C). Furthermore, the DQ group exhibited heightened expression of NLRP3, p-NFκB p65, Caspase1 p20, IL-1β, and IL-18. However, EGCG-RBCm/NPs treatment mitigated DQ-induced increases in ROS, apoptosis, and oxidative stress, as well as renal toxicity and decreases in renal biomarker levels. Meanwhile, the expression of the above proteins were significantly decreased, and the survival rate of mice was ultimately improved, with an effect better than that of the EGCG treatment group. In conclusion, EGCG-RBCm/NPs can improve oxidative stress, inflammation, and apoptosis induced by DQ. This effect is related to the NF-κB/NLRP3 inflammasome pathway. Overall, this study provides a new approach for treating renal injury induced by DQ. [ABSTRACT FROM AUTHOR]

The indiscriminate use of pesticides makes us susceptible to the toxicity of these chemical compounds, which may be present in high quantities in our food. It is crucial to develop inexpensive and rapid methods for determining these pesticides for government control or even for the general population. In this study, we investigated the fabrication of self-assembled LbL films using multi-walled carbon nanotubes (MWCNT) and nickel tetrasulphonated phthalocyanine (NiTsPc) as an electrochemical sensor for the herbicide Diquat (DQ). The Layer-by-Layer (LbL) assembly of the (MWCNT/NiTsPc) film was examined, along with its structural and morphological characteristics. The effect of the number of layers in DQ detection was evaluated by cyclic voltammetry, followed by the detection through differential pulse voltammetry. The achieved limit of detection was 9.62 × 10−7 mol L−1. A ~ 30% decrease in sensitivity was observed in the presence of Paraquat, a banned herbicide and electrochemical interferent due to the structural similarities, which is regularly neglected in the most published studies. The sensor was tested in real samples, demonstrating a recovery of 98.5% in organic apples. [ABSTRACT FROM AUTHOR]

Reversible protein phosphorylation regulates various cellular mechanisms in eukaryotes by altering the conformation, activity, localization, and stability of substrate proteins. In Arabidopsis thaliana root meristems, histone post-translational modifications are crucial for proper cell division, and they are also involved in oxidative stress signaling. To investigate the link between reactive oxygen species (ROS) and mitosis, we treated various Arabidopsis genotypes, including wild-types and mutants showing dysfunctional PP2A, with the ROS-inducing herbicide diquat (DQ). Studying the c3c4 double catalytic subunit mutant and fass regulatory subunit mutants of PP2A provided insights into phosphorylation-dependent mitotic processes. DQ treatment reduced mitotic activity in all genotypes and caused early mitotic arrest in PP2A mutants, likely due to oxidative stress-induced damage to essential mitotic processes. DQ had a minimal effect on reversible histone H3 phosphorylation in wild-type plants but significantly decreased phospho-histone H3 levels in PP2A mutants. Following drug treatment, the phosphatase activity decreased only in the stronger phenotype mutant plants (fass-5 and c3c4). Our findings demonstrate that (i) the studied PP2A loss-of-function mutants are more sensitive to increased intracellular ROS and (ii) DQ has indirect altering effects of mitotic activities and histone H3 phosphorylation. All these findings underscore the importance of PP2A in stress responses. [ABSTRACT FROM AUTHOR]

Many factors induced by environmental toxicants have made oxidative stress a risk factor for the intestinal barrier injury and growth restriction, which is serious health threat for human and livestock and induces significant economic loss. It is well‐known that diquat‐induced oxidative stress is implicated in the intestinal barrier injury. Although some studies have shown that mitochondria are the primary target organelle of diquat, the underlying mechanism remains incompletely understood. Recently, mitochondria‐associated endoplasmic reticulum membranes (MAMs) have aroused increasing concerns among scholars, which participate in mitochondrial dynamics and signal transduction. In this study, we investigated whether MAMs involved in intestinal barrier injury and mitochondrial dysfunction induced by diquat‐induced oxidative stress in piglets and porcine intestinal epithelial cells (IPEC‐J2 cells). The results showed that diquat induced growth restriction and impaired intestinal barrier. The mitochondrial reactive oxygen species (ROS) was increased and mitochondrial membrane potential was decreased following diquat exposure. The ultrastructure of mitochondria and MAMs was also disturbed. Meanwhile, diquat upregulated endoplasmic reticulum stress marker protein and activated PERK pathway. Furthermore, loosening MAMs alleviated intestinal barrier injury, decrease of antioxidant enzyme activity and mitochondrial dysfunction induced by diquat in IPEC‐J2 cells, while tightening MAMs exacerbated diquat‐induced mitochondrial dysfunction. These results suggested that MAMs may be associated with the intestinal barrier injury and mitochondrial dysfunction induced by diquat in the jejunum of piglets. [ABSTRACT FROM AUTHOR]

Diquat (DQ) is a widely utilized nonselective herbicide that is primarily used to control a wide range of weeds and crop residues. It also has significant environmental implications. DQ exposure can cause severe damage to the central nervous system (CNS), a critical symptom of acute poisoning that endangers patients. Despite its severity, the underlying mechanisms of DQ-induced toxic encephalopathy remain unclear, hindering the development of precise treatments. Our research demonstrated that acute DQ exposure in mice significantly increases oxidative stress and triggers neuroinflammation in the hippocampus. Furthermore, in vitro findings indicate that the detrimental effects of DQ are mediated by its disruption of autophagic processes, leading to exacerbated neural damage. DQ initially promotes autophagy in BV2 microglia for self-protection against oxidative stress and inflammation. However, this process is subsequently blocked, intensifying neural damage. Crucially, our results show that the activation of autophagy can reverse these adverse effects. This study not only sheds light on the intricate mechanisms of DQ neurotoxicity but also provides potential therapeutic targets for mitigating DQ-induced toxic encephalopathy.

Diquat, glufosinate and the combination of the latter with carfentrazone or saflufenacil are believed to be as effective for pre-harvest desiccation of soybean plants as paraquat. This work was developed with the objective of evaluating the efficacy of paraquat, diquat, and glufosinate alone or at mixtures of carfentrazone or saflufenacil in pre-harvest desiccation of soybean. Soybean defoliation, maturity and yield were evaluated. Similar efficacy was observed between glufosinate and paraquat in soybean defoliation and maturity, in addition to a greater flexibility of use, in which it could be an anticipator and standardizing agent of the harvest. The application of diquat (200 g of active ingredient [a.i.] ha-1), paraquat (200 g a.i. ha-1) or glufosinate (400 or 500 g a.i. ha-1) was effective for pre-harvest desiccation of soybean at the R7.2 stage. As well, it was observed promising results for application of glufosinate + saflufenacil (300 + 24.5 g a.i. ha-1), glufosinate + carfentrazone (200 + 25 g a.i. ha-1), glufosinate + saflufenacil (200 + 35 g a.i. ha-1). Diquat and glufosinate can replace paraquat in pre-harvest desiccation of soybean plants, and glufosinate also provide greater management flexibility, in anticipating the harvest.

Introduction: Severe diquat poisoning often leads to acute kidney injury, gastrointestinal injury, paralytic ileus, rhabdomyolysis, respiratory failure, refractory circulatory failure, and brainstem damage. Case summary: A previously healthy 38-year-old man was admitted to our hospital with anuria, mild abdominal distension, and calf pain after ingesting diquat (200 g/L) 100 mL approximately 13 h before presentation. His blood diquat concentration was 8.14 µg/L on admission. Gastrointestinal catharsis, haemoperfusion, and haemodiafiltration were performed. Subsequently, he developed marked abdominal distention, impaired consciousness, hypotension, and respiratory failure, leading to death. Images: Computed tomography revealed gas accumulation in the portal venous system and mesenteric vessels. Moreover, gastrointestinal pneumatosis was present. Computed tomography also revealed changes in the lung, brainstem, and calf muscles. Conclusion: Diquat poisoning can result in acute kidney injury, hepatic injury, gastrointestinal injury, paralytic ileus, rhabdomyolysis, refractory circulatory failure, brainstem damage, and hepatic portal venous gas, all observed in this patient. [ABSTRACT FROM AUTHOR]

Abstract Diquat (DQ) is among the most widely used herbicides, and its intake can cause severe systemic toxicity that manifests rapidly. The resultant symptoms can cause the dysfunction of a range of tissues and organs,. As there is no specific antidote for diquat poisoning and the efficacy of extant treatments is suboptimal, physicians must acquire a more comprehensive understanding of the most effective approaches to managing affected patients. Relative few studies have been published to date focused on diquat poisoning in pediatric patients. In this report, we compare two similar cases of juvenile diquat poisoning with dynamic changes in clinical manifestations, laboratory values, and imaging results. For the first time, the difference in whether to perform blood flow perfusion and the time difference of initiation of hemoperfusion had a clear clinical difference in the subsequent effects of diquat poisoning in children with diquat poisoning. Limited evidence is available regarding the efficacy of early hemoperfusion for diquat poisoning; however, the differences in clinical outcomes articulated here highlight the benefits of early and timely hemoperfusion therapy in the treatment of DQ toxicity in children, in conjunction with primary supportive care in the management of DQ poisoning in children.

Objective To evaluate the clinical efficacy and safety of fractionated plasma separation and adsorption combined with continuous veno-venous hemofiltration (FPSA-CVVH) treatment in patients with acute bipyridine herbicide poisoning.Methods A retrospective analysis of 18 patients with acute bipyridine herbicide poisoning was conducted, of which 9 patients were poisoned by diquat and 9 patients by paraquat. All patients underwent FPSA-CVVH treatment. The serum cytokine levels in pesticide-poisoned patients were assessed. The efficacy of FPSA-CVVH in eliminating cytokines, the 90-d survival rate of poisoned patients, and adverse reactions to the treatment were observed.Results Fourteen patients (77.8%) had acute kidney injuries and 10 (55.6%) had acute liver injuries. The serum cytokine levels of high mobility group protein B-1 (HMGB-1), interleukin-6 (IL-6), IL-8, interferon-inducible protein-10 (IP-10), monocyte chemotactic protein-1 (MCP-1), and macrophage inflammatory protein-1β (MIP-1β) were significantly elevated. A total of 41 FPSA-CVVH treatment sessions were administered. After a single 8-h FPSA-CVVH treatment, the decreases in HMGB-1, IL-6, IL-8, IP-10, MCP-1, and MIP-1β were 66.0%, 63.5%, 73.3%, 63.7%, 53.9%, and 54.1%, respectively. During FPSA-CVVH treatment, one patient required a filter change due to coagulation in the plasma component separator, and one experienced a bleeding adverse reaction. The 90-d patient survival rate was 50%, with 4 patients with diquat poisoning and 5 patients with paraquat poisoning, and both liver and kidney functions were restored to normal.Conclusion Cytokine storms may play a significant role in the progression of multiorgan dysfunction in patients with acute bipyridine herbicide poisoning. FPSA-CVVH can effectively reduce cytokine levels, increase the survival rate of patients with acute bipyridine herbicide poisoning, and decrease the incidence of adverse events.

Diquat (DQ), paraquat (PQ), glufosinate (GLU), and glyphosate (GLYP) are commonly used herbicides that have been confirmed to be toxic to humans. Rapid and accurate measurements of these toxicants in clinical practice are beneficial for the correct diagnosis and timely treatment of herbicide-poisoned patients. The present study aimed to establish an efficient, convenient, and reliable method to achieve the simultaneous quantification of DQ, PQ, GLU, and GLYP in human plasma using liquid chromatography-tandem mass spectrometry (LC-MS/MS) without using derivatization or ion-pairing reagents. DQ, PQ, GLU, and GLYP were extracted by the rapid protein precipitation and liquid-liquid extraction method and then separated and detected by LC-MS/MS. Subsequently, linearity, limit of detection (LOD), limit of quantification (LOQ), precision, accuracy, extraction recovery, matrix effect, dilution integrity, and stability were evaluated to validate the method based on the FDA criteria. Finally, the validated method was applied to real plasma samples collected from 166 Chinese patients with herbicide poisoning. The results showed satisfactory linearity with low LOD (1 ng/mL for DQ and PQ, 5 ng/mL for GLU, and 10 ng/mL for GLYP, respectively) and low LOQ (5 ng/mL for DQ and PQ, 25 ng/mL for GLU and GLYP, respectively). In addition, the precision, accuracy, extraction recovery, and stability of the method were acceptable. The matrix effect was not observed in the analyzed samples. Moreover, the developed method was successfully applied to determine the target compounds in real plasma samples. These data provided reliable evidence for the application of this LC-MS/MS method for clinical poisoning detection. [ABSTRACT FROM AUTHOR]

Diquat (DQ) is among the most widely used herbicides, and its intake can cause severe systemic toxicity that manifests rapidly. The resultant symptoms can cause the dysfunction of a range of tissues and organs,. As there is no specific antidote for diquat poisoning and the efficacy of extant treatments is suboptimal, physicians must acquire a more comprehensive understanding of the most effective approaches to managing affected patients. Relative few studies have been published to date focused on diquat poisoning in pediatric patients. In this report, we compare two similar cases of juvenile diquat poisoning with dynamic changes in clinical manifestations, laboratory values, and imaging results. For the first time, the difference in whether to perform blood flow perfusion and the time difference of initiation of hemoperfusion had a clear clinical difference in the subsequent effects of diquat poisoning in children with diquat poisoning. Limited evidence is available regarding the efficacy of early hemoperfusion for diquat poisoning; however, the differences in clinical outcomes articulated here highlight the benefits of early and timely hemoperfusion therapy in the treatment of DQ toxicity in children, in conjunction with primary supportive care in the management of DQ poisoning in children. [ABSTRACT FROM AUTHOR]

Diquat, glufosinate and the combination of the latter with carfentrazone or saflufenacil are believed to be as effective for pre-harvest desiccation of soybean plants as paraquat. This work was developed with the objective of evaluating the efficacy of paraquat, diquat, and glufosinate alone or at mixtures of carfentrazone or saflufenacil in pre-harvest desiccation of soybean. Soybean defoliation, maturity and yield were evaluated. Similar efficacy was observed between glufosinate and paraquat in soybean defoliation and maturity, in addition to a greater flexibility of use, in which it could be an anticipator and standardizing agent of the harvest. The application of diquat (200 g of active ingredient [a.i.] ha-1 ), paraquat (200 g a.i. ha-1 ) or glufosinate (400 or 500 g a.i. ha-1 ) was effective for pre-harvest desiccation of soybean at the R7.2 stage. As well, it was observed promising results for application of glufosinate + saflufenacil (300 + 24.5 g a.i. ha-1 ), glufosinate + carfentrazone (200 + 25 g a.i. ha-1 ), glufosinate + saflufenacil (200 + 35 g a.i. ha-1 ). Diquat and glufosinate can replace paraquat in pre-harvest desiccation of soybean plants, and glufosinate also provide greater management flexibility, in anticipating the harvest. [ABSTRACT FROM AUTHOR]

BACKGROUND: Diquat is a common environmental pollutant, which can cause oxidative stress in humans and animals. Diquat exposure causes growth retardation and intestinal damage. Therefore, this study was performed to investigate the effects of melatonin on diquat‐challenged piglets. RESULTS: Dietary supplementation with 2 mg kg−1 melatonin significantly increased the average daily gain and feed conversion rate in piglets. Melatonin increased antioxidant capacity, and improved intestinal epithelial barrier function of duodenum and jejunum in piglets. Moreover, melatonin was found to regulated the expression of immune and antioxidant‐related genes. Melatonin also alleviated diquat‐induced growth retardation and anorexia in diquat‐challenged piglets. It also increased antioxidant capacity, and ameliorated diquat‐induced intestinal epithelial barrier injury. Melatonin also regulated the expression of MnSOD and immuner‐elated genes in intestinal. CONCLUSION: Dietary supplementation with 2 mg kg−1 melatonin increased antioxidant capacity to ameliorate diquat‐induced oxidative stress, alleviate intestinal epithelial barrier injury, and increase growth performance in weaned piglets. © 2023 Society of Chemical Industry. [ABSTRACT FROM AUTHOR]

Understanding non-target-site resistance (NTSR) to herbicides represents a pressing challenge as NTSR is widespread in many weeds. Using giant duckweed (Spirodela polyrhiza) as a model, we systematically investigated genetic and molecular mechanisms of diquat resistance, which can only be achieved via NTSR. Quantifying the diquat resistance of 138 genotypes, we revealed an 8.5-fold difference in resistance levels between the most resistant and most susceptible genotypes. Further experiments suggested that diquat uptake and antioxidant-related processes jointly contributed to diquat resistance in S. polyrhiza. Using a genome-wide association approach, we identified several candidate genes, including a homolog of dienelactone hydrolase, that are associated with diquat resistance in S. polyrhiza. Together, these results provide new insights into the mechanisms and evolution of NTSR in plants. [ABSTRACT FROM AUTHOR]

Diquat (DQ) is a commonly used bipyridine herbicide known for its toxic properties and adverse effects on individuals. However, the mechanism underlying DQ-induced damage remain elusive. Our research aimed to uncover the regulatory network involved in DQ-induced damage. We analyzed publicly accessible gene expression patterns and performed research using a DQ-induced damage animal model. The GSE153959 dataset from the Gene Expression Omnibus collection and the animal model of DQ-induced kidney injury were used to identify differentially expressed genes (DEGs). Pathways including the regulation of DNA-templated transcription in response to stress, RNA polymerase II transcription regulator complex and transcription coregulatory activity were shown to be enriched in 21 DEGs. We used least absolute shrinkage and selection operator (LASSO) regression analysis to find possible diagnostic biomarkers for DQ-induced damage. Then, we used an HK-2 cell model to confirm these results. Additionally, we confirmed that 3-hydroxy-3-methylglutaryl-CoA synthase 2 (HMGCS2) was the major gene associated with DQ-induced damage using multi-omics screening. The sample validation strongly suggested that HMGCS2 has promise as a diagnostic marker and may provide new targets for therapy in the context of DQ-induced damage.

Diquat dibromide (DQ) is a globally used herbicide in agriculture, and its overuse poses an important public health issue, including male reproductive toxicity in mammals. However, the effects and molecular mechanisms of DQ on testes are limited. In vivo experiments, mice were intraperitoneally injected with 8 or 10 mg/kg/ day of DQ for 28 days. It has been found that heme oxygenase-1 (HO-1) mediates DQ-induced ferroptosis in mouse spermatogonia, thereby damaging testicular development and spermatogenesis. Histopathologically, we found that DQ exposure caused seminiferous tubule disorders, reduced germ cells, and increased sperm malformation, in mice. Reactive oxygen species (ROS) staining of frozen section and transmission electron microscopy (TEM) displayed DQ promoted ROS generation and mitochondrial morphology alterations in mouse testes, suggesting that DQ treatment induced testicular oxidative stress. Subsequent RNA-sequencing further showed that DQ treatment might trigger ferroptosis pathway, attributed to disturbed glutathione metabolism and iron homeostasis in spermatogonia cells in vitro. Consistently, results of western blotting, measurements of MDA and ferrous iron, and ROS staining confirmed that DQ increased oxidative stress and lipid peroxidation, and accelerated ferrous iron accumulation both in vitro and in vivo. Moreover, inhibition of ferroptosis by deferoxamine (DFO) markedly ameliorated DQ-induced cell death and dysfunction. By RNA-sequencing, we found that the expression of HO-1 was significantly upregulated in DQ-treated spermatogonia, while ZnPP (a specific inhibitor of HO-1) blocked spermatogonia ferroptosis by balancing intracellular iron homeostasis. In mice, administration of the ferroptosis inhibitor ferrostatin-1 effectively restored the increase of HO-1 levels in the spermatogonia, prevented spermatogonia death, and alleviated the spermatogenesis disorders induced by DQ. Overall, these findings suggest that HO-1 mediates DQ-induced spermatogonia ferroptosis in mouse testes, and targeting HO-1 may be an effective protective strategy against male reproductive disorders induced by pesticides in agriculture.

ObjectivesDiquat poisoning is an important public health and social security agency. This study aimed to develop a prognostic model and evaluate the prognostic value of plasma diquat concentration in patients with acute oral diquat poisoning, focusing on how its impact changes over time after poisoning.MethodsThis was a retrospective cohort study using electronic healthcare reports from the Second Hospital of Hebei Medical University. The study sample included 80 patients with acute oral Diquat poisoning who were admitted to the hospital between January 2019 and May 2022. Time-to-event analyses were performed to assess the risk of all-cause mortality (30 days and 90 days), controlling for demographics, comorbidities, vital signs, and other laboratory measurements. The prognostic value of plasma DQ concentration on admission was assessed by computing the area under a time-dependent receiver operating characteristic curve (ROC).ResultsAmong the 80 patients, 29 (36.25%) patients died, and 51 (63.75%) patients survived in the hospital. Non-survivors had a median survival time (IQR) of 1.3(1.0) days and the longest survival time of 4.5 days after DQ poisoning. Compared with non-survivors, survivors had significantly lower amounts of ingestion, plasma DQ concentration on admission, lungs injury within 24 h after admission, liver injury within 24 h after admission, kidney injury within 24 h after admission, and CNS injury within 36 h after admission, higher APACHE II score and PSS within 24 h after admission (all p

The transition from paraquat (PQ) to diquat (DQ), both organic dication herbicides, in China has led to significant increases in the number of acute DQ poisoning cases. Case studies have shown that acute DQ poisoning resulted in injury to the central nervous system (CNS), but the mechanism underlying the injury remains to be explored. The present study aimed to investigate how DQ influenced purinergic signaling between astrocytes and microglia and whether extracellular ATP (eATP) was involved in promoting neuroinflammation induced by acute DQ toxicity through the activation of the P2X4/NLRP3 signaling pathway. We constructed a rat model of acute DQ toxicity to observe the pathological changes in hippocampal tissues after DQ exposure and measure the expression levels of IL-1β and TNF-α in the hippocampal tissue. We also established an in vitro co-culture model of C6 astrocytes and BV-2 microglia using transwell chambers, measured the amount of eATP secreted into C6 astrocytes after DQ treatment, and assessed the inflammatory response and changes in the P2X4/NLRP3 signaling pathway in BV-2 microglia. The results showed that the neurons in the hippocampal tissue of rats exhibited loose arrangement, nuclear consolidation, and necrosis after DQ exposure, and IL-1β and TNF-α levels were signification higher in the hippocampal tissue after DQ exposure. DQ exposure to the co-cultured cells induced an increase in ATP secretion from C6 astrocytes as well as a significant increase of P2X4, NLRP3, IL-1β, and IL-18 expression in BV-2 microglia. In contrast, pretreatment of C6 astrocytes with apyrase (an ATP hydrolase) resulted in a significant decrease of P2X4, NLRP3, IL-1β, and IL-18 expression in BV-2 microglia. Furthermore, inhibition of P2X4 expression in BV-2 microglia by transfection with si-P2X4 effectively reversed the increase of NLRP3, IL-1β, and IL-18 in BV-2 microglia induced by DQ when co-cultured with C6 astrocytes. These results indicate that astrocytes can activate the P2X4/NLRP3 signaling pathway in microglia through the DQ-induced extracellular release of ATP to promote neuroinflammation in rat hippocampal tissue. [ABSTRACT FROM AUTHOR]

Purpose: The analysis of water-soluble herbicides, including glyphosate (Glyp), glufosinate (Gluf), paraquat (PQ), and diquat (DQ), is time-consuming and expensive because they cannot be analyzed using general toxicological screening methods. Thus, this study aimed to develop a simple and rapid method to simultaneously analyze these compounds without any derivatization nor ion-pairing reagents. Methods: The analytes were separated using hydrophilic interaction liquid chromatography and detected using tandem mass spectrometry. The developed method was applied to plant and biological samples assuming criminal damage and poisoning cases, respectively. Results: All analytes were separated well and detected with good peak shapes. For plant samples, the herbicides were specifically detected from withered leaves using a simple extraction method. For biological samples, quantitative analysis was successfully validated, and the limit of quantification values of Glyp and Gluf were 0.2 µg/mL, and those of PQ and DQ were 1 ng/mL. Conclusion: The developed method had sufficient performance for practical forensic applications including poisoning cases and malicious uses to damage commercial crops. [ABSTRACT FROM AUTHOR]

The present study aimed to assess the impact of grape seed extract (GSE), onion peel extract (OPE), and rosemary extract (ROE) on Diquat-induced growth restriction and oxidative stress in Lohmann chicks. A total of 200 chicks were randomly assigned to 5 diets: the positive control (PC) group, the negative control (NC) group, GSE group, OPE group, and ROE group. During the first 7 d of trial, compared with NC and PC groups, the GSE group enhanced average daily feed intake (ADFI). From day 8–21, diquat injection resulted in reduced growth performance, increased platelet volume distribution width (PWD), malondialdehyde (MDA) concentration, and activities of alanine aminotransferase (ALT) in chick serum; it also decreased total protein (TP), albumin (ALB), globulin (GLB) concentration, activities of superoxide dismutase (SOD) and glutathione S-transferase (GST) in chick serum; furthermore, it increased MDA concentration while decreasing GST activities in liver. The NC group exhibited lower average daily gain (ADG) than other groups. Compared with NC group, GSE group reduced ALT activities, MDA levels, and red cell distribution width (RDW), and PDW concentration; it also increased SOD, GST activities. The ROE group lowered ALT activities and MDA concentration. The OPE group decreased ALT activities, and MDA levels, RDW, and PDW concentration, and increased SOD activities of chicks. These results suggest that supplementing antioxidants in diets alleviated oxidative stress in chicks challenged by improving antioxidant capacity and liver function. [ABSTRACT FROM AUTHOR]

Objectives: Diquat has replaced paraquat in agricultural areas as a herbicide but has led to extensive poisoning. Unlike paraquat, which targets the lungs, diquat primarily targets the kidneys. Autopsies and animal experiments suggest that interstitial kidney damage is the most critical renal lesion. Diquat is a nonselective chemical widely used for terrestrial and aquatic plants after the ban on paraquat. Although diquat is known to affect the kidneys mainly, no study has reported renal biopsy in patients with diquat poisoning. Methods: We investigated the histopathologic feature in a young man with diquat poisoning who developed acute kidney injury by renal biopsy. Results: Autopsy and animal experiments suggest that interstitial kidney inflammation is the most critical renal lesion. Surprisingly, our results showed that lipid degeneration and acute tubular injury with limited interstitial inflammation were the dominant histologic findings in this patient. Conclusions: Based on a renal biopsy, this was the first study describing the characteristics of the kidney affected by diquat poisoning. Our findings might provide information for managing patients who develop AKI due to diquat poisoning. [ABSTRACT FROM AUTHOR]

Diquat (DQ) is another widely used and harmful herbicide in addition to paraquat (PQ). Due to the lack of specific antidote, the case fatality rate is extremely high. At present, the toxicological mechanism has not been fully elucidated, and it is generally believed that oxidative stress causes cascade reactions, resulting in multiple organ dysfunction caused by damage to various tissues and organs. The early manifestations of DQ poisoning vary, and it is difficult to accurately capture the timing of treatment due to the lack of standardized or accurate evaluation system. How to implement accurate individualized medical treatment to reduce mortality and disability rate remains a medical challenge. Therefore, this review summarizes the pathogenesis and prognosis evaluation of acute DQ poisoning to provide reference for improving clinical treatment, decision-making, and prognosis evaluation. [ABSTRACT FROM AUTHOR]

ABSTRACT: This study evaluated the alleviative effect of curcumin (CUR) on the diquat (DQ)-induced cecal injury in broilers. A total of 320 one-day-old Cobb broilers were selected and randomly divided into 4 treatments, namely control, DQ, CUR 100, and CUR150 groups. The control and DQ groups were fed a basal diet, while the CUR 100 and CUR150 groups were fed the basal diet supplemented with 100 and 150 mg/kg CUR, respectively. Each group had 8 replicates, with 10 broilers per replicate. On day 21 of the experiment, 1 broiler was selected from each replicate and intraperitoneally injected 20 mg/kg body weight of DQ for DQ, CUR 100, and CUR 150 groups. Broilers in control group received equivalent volume of saline. Broilers were euthanized 48h postinjection for tissue sampling. The results showed that DQ injection could cause oxidative stress and inflammatory reactions in the cecum, affecting the fatty acid production and flora structure, thus leading to cecum damage. Compared with the DQ group, the activity of superoxide dismutase, the level of interleukin 10, acetic acid, and total volatile fatty, and the abundance of nuclear factor E2-related factor 2, copper and zinc superoxide dismutase and catalase mRNA in the cecal mucosa of broilers in the CUR group increased significantly (P < 0.05). However, the levels of malondialdehyd, reactive oxygen species, tumor necrosis factor-alpha, and the expression of cysteine-aspartic acid protease-3 and tumor necrosis factor-alpha decreased significantly (P < 0.05) in the CUR group. In addition, CUR treatment alleviated the damage to the cecum and restored the flora structure, and Lactobacillus and Lactobacillaceae promoted the alleviative effect of CUR on DQ. In summary, CUR could alleviate the cecal injury caused by DQ-induced oxidative damage and inflammatory reactions by regulating the Nrf2-ARE signaling pathway and intestinal flora, thus protecting the cecum.

Yang Chen,1 Hui-Yi Li,1 Jian-Shu Liu,1 Dao-long Jiang,1 Hao-nan Zheng,2 Xue-Song Dong1 1Department of Emergency, The First Hospital of China Medical University, Shenyang, 110001, People’s Republic of China; 2No.105 Phase, The First Clinical College of China Medical University, Shenyang, 110001, People’s Republic of ChinaCorrespondence: Xue-Song Dong, Department of Emergency, The First Hospital of China Medical University, No. 155 of Nanjing North Street, Heping District, Shenyang, 110001, People’s Republic of China, Tel +86 024-26111099 ; +86 024-83282011, Email dongxunsongdxs0@126.comBackground: We established a diquat-induced human kidney-2 cells (HK-2 cells) apoptosis model in this study to identify differentially expressed microRNAs (miRNAs) and signaling pathways involved in diquat poisoning via gene sequencing and bioinformatics analysis and explored the related therapeutic benefits.Methods: The effects of diquat on the viability and apoptosis of HK-2 cells were explored using the CCK-8 and Annexin V-FITC/PI double staining methods. Total RNAs were extracted using the TRizol method and detected by Illumina HiSeq 2500. Bioinformatics analysis was performed to explore differentially expressed (DE) miRNAs, their enriched biological processes, pathways, and potential target genes. The RT-qPCR method was used to verify the reliability of the results.Results: Diquat led to HK-2 cell injury and apoptosis played an important role, hence an HK-2 cell apoptosis model in diquat poisoning was established. Thirty-six DE miRNAs were screened in diquat-treated HK-2 cells. The enriched biological process terms were mainly cell growth, regulation of apoptotic signaling pathway, extrinsic apoptotic signaling pathway, and Ras protein signal transduction. The enriched cellular components were mainly cell-cell junction, cell-substrate junction, ubiquitin ligase complex, and protein kinase complex. The enriched molecular functions were mainly Ras GTPase binding, ubiquitin-like protein transferase activity, DNA-binding transcription factor binding, ubiquitin-protein transferase activity, nucleoside-triphosphatase regulator activity, transcription coactivator activity, and ubiquitin-like protein ligase binding. Signaling pathways such as MAPK, FoxO, Ras, PIK3-Akt, and Wnt were also enriched.Conclusion: These findings aid in understanding the mechanisms of diquat poisoning and the related pathways, where DE miRNAs serve as targets for gene therapy.Keywords: apoptosis, biological processes, diquat, HK-2 cells, microRNA

ABSTRACT: This study purposed to investigate the alleviating effect of dietary curcumin supplementation on oxidative stress in the liver of broilers induced by diquat. One-day-old Cobb broilers (400) were selected and randomly divided into 5 groups, with 8 replicates and 10 broilers per replicate. The control group and the diquat group were fed the basal diet, while the curcumin supplementation groups were fed the basal diet supplemented with different amounts of curcumin (50, 100, and 150 mg/kg). On d 21 of the test, 1 broiler was randomly selected from each replicate and intraperitoneally injected with 20 mg/mL of diquat solution at a dose of 1 mL/kg BW or equivalent physiological saline (for the control group). After 48 h of feeding, the selected broilers were slaughtered for analysis. The results show that diquat treatment reduced the antioxidant capacity of the liver, caused oxidative stress, and affected its lipid metabolism. However, diet supplementation using curcumin completely or partially reversed the effect of diquat on the liver of broilers. The blood alanine aminotransferase activity, total bilirubin and total protein levels, and liver Caspase-3 mRNA abundance in broilers were lower or significantly lower in the curcumin supplementation group than in the diquat group (P < 0.05). The curcumin supplementation groups had significantly higher total antioxidant capacity activity but significantly lower malondialdehyde in the liver of broilers than the diquat group (P < 0.05). The blood triglyceride level of broilers was lower or significantly lower in the curcumin supplementation groups than in the diquat group (P < 0.05). The activities of cetyl coenzyme A carboxylase in the liver were significantly lower in the 150 mg/kg curcumin supplementation groups than in the DQ group (P < 0.05). In conclusion, dietary curcumin supplementation could ameliorate the effects of diquat-induced oxidative stress on the antioxidant capacity, tissue morphology, and lipid metabolism of the liver of broilers, thus protecting the liver. The recommended dosage for broiler diets is 100 to 150 mg/kg curcumin.

BACKGROUND: Flexible surface‐enhanced Raman spectroscopy (SERS) substrates such as paper‐based substrates show great potential for rapid detection of residual chemicals on food surfaces. However, controlling the density and distribution of metallic nanoparticles adsorbed on the paper is still challenging. RESULTS: The amount of gold (Au) nanospheres (51 ± 4 nm) attached on the filter paper modified with 3‐aminopropyltriethoxysilane (APTES) was tunable, increasing as the level of APTES (2.5–15.0 g kg−1) applied for paper modification increased. Moreover, the Au nanospheres were relative evenly distributed on the filter paper modified with 2.5–10.0 g kg−1of APTES, which resulted in excellent intra‐ and inter‐reproducibility of SERS signals for pesticides including thiram, diquat dibromide, and paraquat dichloride (relative standard deviation = 2.2–10.1%). The modified paper‐based substrate could be used to detect as low as 0.05–0.2 mg L−1 of pesticides in standard solutions, and as low as 5–20 ng cm−2 of residual pesticides on apple skins with minimum sample pretreatment. CONCLUSION: This paper‐based substrate with tunable feature for the density and distribution of nanoparticles is applicable for rapid SERS detection of residual pesticides in fruits and vegetables. © 2023 Society of Chemical Industry. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Sichuan University (Medical Science Edition) is the property of Editorial Board of Journal of Sichuan University (Medical Sciences) and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

In order to study the clinical characteristics of diquat poisoning patients and evaluate the related factors and molecular mechanism of brain injury in diquat poisoning patients, this study collected 56 patients with diquat poisoning and divided them into a brain injury group of 14 cases and a non-injury group of 42 cases based on their brain injury status during hospitalization, and compared the baseline data and laboratory indicators of patients between the two groups. The study analyzed the relevant factors of brain injury in diquat poisoning patients using logistic regression, and used receiver operating characteristic (ROC) curve analysis to compare the predictive value of the above related factors alone or in combination on the brain injury status of diquat poisoning patients. The grouping comparison results showed that body mass index (BMI), diquat cation poisoning dose, the proportion of mechanical ventilation, and the proportion of continuous renal replacement therapy (CRRT) in the brain injury group were significantly higher than those in the non-injury group (P<0.05). The serum biochemical indicators in the brain injury group such as S100 calcium binding protein B (S100B), alanine aminotransferase (ALT), aspartate aminotransferase (AST), blood urea nitrogen (BUN), serum creatinine (SCR) after admission and the white blood cell (WBC) count, neutrophil count, neutrophil to lymphocyte ratio (NLR) at 24 hours after poisoning were significantly higher than those in the uninjured group (P<0.05). A method of univariate regression followed by multivariate regression analysis was taken to analyse the variables with significant differences in group comparison, and the results of regression showed that the 24-hour NLR after poisoning has certain independent predictive value for the brain injury status of patients with diquat poisoning. The comparison results of ROC curve analysis further indicated that when NLR at 24 hours after poisoning was combined with BMI and the diquat cation poisoning dosage, or NLR at 24 hours after poisoning was combined with BMI and the concentration of diquat in the blood before hemoperfusion, a higher predictive value can be obtained for the brain injury status of diquat poisoning patients. The increase of 24-hour NLR level after diquat poisoning is significantly correlated with the increase of brain injury, which can be used as an independent predictor of the occurrence of brain injury during hospitalization, and when 24-hour NLR is combined with BMI, diquat cation poisoning dose and blood diquat concentration, a higher predictive value of brain injury events can be obtained. [ABSTRACT FROM AUTHOR]

AbstractIntroductionConclusionIntracerebral bleeding that predominantly affects the pons, midbrain, cerebral peduncle, basal ganglia, and thalamus may occur in severe diquat poisoning. We employed magnetic resonance-susceptibility-weighted imaging to highlight the presence of microhemorrhages in a patient with diquat poisoning.Case summary: A 15-year-old female patient presented with kidney and liver damage after ingesting diquat. Three days later, she developed coma. She received seven sessions of hemoperfusion and was discharged with residual cognitive impairment and right limb muscle weakness after 66 days of hospitalization.Images: Cranial computed tomography on day 5 and magnetic resonance imaging on day 8 revealed swelling in the pons, midbrain, and thalamus without evidence of hemorrhage. However, susceptibility-weighted imaging on day 8 demonstrated multiple punctate low signals, suggesting the presence of microhemorrhages.Susceptibility-weighted imaging is a useful technique for detecting microhemorrhages in patients with diquat-induced encephalopathy, as microhemorrhages are often not detectable on computed tomography or conventional magnetic resonance imaging. [ABSTRACT FROM AUTHOR]

Understanding non-target-site resistance (NTSR) to herbicides represents a pressing challenge as NTSR is widespread in many weeds. Using giant duckweed (Spirodela polyrhiza) as a model, we systematically investigated genetic and molecular mechanisms of diquat resistance, which can only be achieved via NTSR. Quantifying the diquat resistance of 138 genotypes, we revealed an 8.5-fold difference in resistance levels between the most resistant and most susceptible genotypes. Further experiments suggested that diquat uptake and antioxidant-related processes jointly contributed to diquat resistance in S. polyrhiza. Using a genome-wide association approach, we identified several candidate genes, including a homolog of dienelactone hydrolase, that are associated with diquat resistance in S. polyrhiza. Together, these results provide new insights into the mechanisms and evolution of NTSR in plants.

Aims: To preliminarily explore, whether glucocorticoids have a therapeutic effect on diquat-induced acute kidney injury in rats. Method: 150 Wistar rats were randomly divided into six groups: exposure model group (DQ group), dexamethasone control group (GC group), blank control group (Ctrl group), dexamethasone 2.1 mg/kg dose group (DQ+L-GC group), dexamethasone 4.2 mg/kg dose group (DQ+M-GC group), and dexamethasone 8.4 mg/kg dose group (DQ+H-GC group), with 25 rats in each group. Each group was further divided into five subgroups, 24 h, 3 d, 7 d, 14 d, and 21 d after exposure, according to the feeding time and the course of treatment, with five animals in each subgroup. The rats in DQ, DQ+L-GC, DQ+M-GC, and DQ+H-GC groups were administered 115.5 mg/kg diquat by gavage, respectively. Moreover, 30 min after gavage, rats in DQ+L-GC group, DQ+M-GC group, DQ+H-GC group and GC group were intragastric administered dexamethasone 2.1 mg/kg, 4.2 mg/kg, 8.4 mg/kg and 8.4 mg/kg, respectively. After 7 days, the intraperitoneal injection of dexamethasone was changed to 6.3 mg/kg prednisone by intragastric administration. Subsequently, 7 days later, it was changed to 3.15 mg/kg prednisone by intragastric administration until the end of the experiment on 21 days. After the start of the experiment, changes in the conditions of the rats in each group were observed at a fixed time every day, changes in the body weight of the rats were monitored at the same time, and the death of the rats was recorded at 24 h, 3 d, 7 d, 14 d, and 21 d after exposure. The rats were sacrificed by an intraperitoneal injection of 100 mg/kg sodium pentobarbital overdose. Blood was collected by puncture of the inferior vena cava, used to determine Cr and BUN. The upper segment of the left kidney was collected for histopathological examination. Elisa was used to detect neutrophil gelatinase-associated lipocalin (NGAL) and kidney injury molecule-1 (KIM-1) in the lower segment of left kidney. TLR4, Myd88, and NF-κB were detected in the right kidney. Results: (1) After exposure, most rats in DQ group, DQ+L-GC group, DQ+M-GC group and DQ+H-GC group showed shortness of breath, oliguria, diarrhea, yellow hair and other symptoms. No symptoms and related signs were observed in Ctrl group and GC group.(2) The weight of rats in the Ctrl group and the GC group increased slowly during the test. the body weight of the rats in the DQ, DQ+L-GC, DQ+M-GC, and DQ+H-GC groups continued to decrease after self-infection. Body weight dropped to the lowest point at approximately 7 d, and gradually increased from 7 d to 21 d.(3) A small amount of capillary congestion in the medulla was observed after 7 days in the GC group. The DQ group showed tubular atrophy, edema of the epithelial cells, and over time, the tubules were seen dilated and became irregular in shape; large amount of capillary congestion was also observed in the renal cortex and medulla. The renal injury in the DQ+L-GC group was less than that in the DQ group. DQ+H-GC group had no obvious injury before 7 d, but more renal tubules were seen in the DQ+H-GC group from 7 d to 14 d.(4) Compared with the DQ group, there was no difference before 14 d, and at 14 d-21 d, DQ+L-GC group, DQ+M-GC group, DQ+H-GC group all had different degrees of decline. NGAL content: Compared with the DQ group, the content of NGAL and KIM-1 in kidney tissue of the DQ+L-GC, DQ+M-GC, and DQ+H-GC groups decreased compared with the DQ group at each time node.(5) Compared with the Ctrl group, the expression of TNF-α, TLR4, MyD88, NF-κB in the DQ, DQ+L-GC, DQ+M-GC, and DQ+H-GC groups at each time node increased in the renal tissue. The content of TNF-α, TLR4, MyD88, NF-κB in kidney tissue of the DQ+L-GC, DQ+M-GC, and DQ+H-GC groups at each time node was lower than that in the DQ group. Conclusion: (1) Diquat can cause kidney damage in rats, mainly manifested as renal tubular atrophy, epithelial cell edema, capillary congestion and dilation, and the renal function damage indicators have been improved to varying degrees.(2) Glucocorticoids have therapeutic effects on acute kidney injury in rats exposed to diquat. During the treatment, the efficacy of glucocorticoids did not increase with increasing doses after reaching a dose of 4.2 mg/kg.(3) TLR4 receptor-mediated TLR4/Myd88/NF-κB signaling pathway is involved in the inflammatory response of acute kidney injury in diquat poisoning rats. Glucocorticoids can inhibit the inflammatory response, thereby affecting the expression of TLR4/Myd88/NF-κB signaling pathway-related proteins.

Diquat (DQ), chemically known as 1,1 '-ethylene-2,2' -bipyridine, is a nonselective herbicide for leaf removal and drying. It has toxic effects on central nervous system cells, and toxic neurological lesions include axonal degeneration and pontine myelolysis. At the same time, DQ can also affect the activity of dopaminergic nerve cells through oxidative stress, causing degeneration and reducing dopamine uptake. With the increasing application of DQ in agricultural production, the clinical reports of neurotoxicity caused by acute DQ poisoning are also increasing. At present, DQ rapid-phase-related toxic encephalopathy mainly involves the pons, midbrain, basal ganglia, thalamus and other brain regions. However, this case is unusual in that the lesion mainly involved the splenium of the corpus callosum. It is also the first time to be reported. [ABSTRACT FROM AUTHOR]

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Herbicides are used in agriculture to control harmful crop weeds, prevent algae proliferation, and enhance macrophyte growth. Herbicide contamination of water bodies might exert toxic effects on fish in different development stages. Sperm, embryos, and adults of Astyanax altiparanae were used as a model to examine the detrimental effects of the following herbicide formulations: Roundup Transorb® (glyphosate), Arsenal® NA (imazapyr), and Reglone® (diquat). The lethal concentration 50 (LC50) values for adults using glyphosate and imazapyr were 3.14 mg/L and 4.59 mg/L, respectively, while the LC50 was higher than 28 mg/L for diquat. For the initial stages of embryo development, LC50 values were 16.52 mg/L glyphosate, 9.33 mg/L imazapyr, and 1084 mg/L diquat. Inhibition of sperm motility was noted at 252 mg/L glyphosate, 137 mg/L imazapyr, and 11,300 mg/L diquat, with an average sperm viability of 12.5%, 73.2%, and 89.3%, respectively, compared to 87.5% detected to control. A.altiparanae exhibited different sensitivities to the herbicide formulations investigated in the developmental stages evaluated. Roundup Transorb® exposure was more toxic for adults, while Arsenal® NA was most harmful for early embryonic development and inhibited sperm motility. Reglone® demonstrated low toxicity for A.altiparanae compared to Roundup Transorb® and Arsenal® NA. A.altiparanae may be considered an emerging fish model for toxicological studies for the neotropical region due to its wide distribution and biological characteristics. [ABSTRACT FROM AUTHOR]

Invasive knotweeds (Reynoutria spp.) pose an ongoing challenge for weed management programs worldwide, requiring years of persistent treatment. In this study, we tested efficacy of diquat applied as foliar spray early in the growing season for short‐term suppression, and for potential to boost long‐term control when applied sequentially with a mid‐season treatment of imazapyr. We evaluated responses of knotweeds (R. japonica, R. × bohemica, and R. sachelinensis) treated with one of three diquat concentrations (0.25%, 0.50%, or 1.0%, v/v), using multiple metrics to capture changes in aboveground plant density and abundance. Canopy cover and biomass were significantly reduced by all diquat concentrations and resembled pre‐treatment conditions at 8WAT, reflecting the shift toward reduced stem heights in treated compared with untreated plots. Stem counts at 8WAT, however, did not differ in response to diquat treatments. Sequentially applied early‐season diquat and mid‐season imazapyr treatments reduced canopy cover (66%–82%), biomass (65%–91%), and stem density (57%–79%) when evaluated 1 year after treatment; reductions were greatest in plots treated with medium and high diquat concentrations, suggesting that diquat treatments may have an additive effect. Overall, our study establishes rates of diquat to reduce biomass of invasive knotweed, and supports additional testing to assess improvement in long‐term control when used sequentially with a systemic herbicide. [ABSTRACT FROM AUTHOR]

This study was conducted to demonstrate that dietary puerarin supplementation alleviates oxidative stress in the small intestine of diquat-challenged piglets. The results showed that puerarin administration markedly alleviated diquat-induced intestinal injury, which was indicated by the improvement of intestinal morphology, cell proliferation and barrier function. One of the potential mechanisms responsible for this was the decrease in oxidative stress, as evidenced by the increase in activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and total antioxidant capacity (T-AOC) in the small intestine. Puerarin increased the protein expression levels of NF-E2-related factor 2 (Nrf2) and its downstream enzymes, including heme oxygenase 1 (HO-1), glutamate-cysteine ligase catalytic and its modifier subunit (GCLc and GCLm) in the jejunal mucosa of diquat-induced piglets. Puerarin administration improved intestinal morphology, cell proliferation, and barrier function, and increased Nrf2 and its downstream enzymes. These findings indicate that the dietary supplementation of puerarin attenuates the oxidative stress involving Nrf2 signaling pathways in diquat-challenged piglets.

This study was undertaken to determine the protective effect of chitosan against oxidative injury in pancreas of weaned piglets. A 2 × 2 factorial experiment was conducted. Twenty-four weaned piglets were randomly divided into one of two dietary treatments (0 or 0.5 g/kg chitosan). After 2 weeks of feeding, half of the piglets on each dietary treatment were given an intraperitoneal injection of diquat or saline. Piglets were killed and samples were collected to assess enzyme activity, redox parameters and nutrient apparent digestibility. The results show that diquat decreased growth performance and induced pancreatic injury, markedly increased pancreas weight, the pancreatic MDA content, activities of pancreatic lipase, serum amylase and lipase, but decreased antioxidant enzyme activity of pancreas. However, chitosan improved growth performance, decreased the relative pancreas weight, activities of serum amylase and lipase, pancreatic lipase activity and crude fat apparent digestibility, but increased the pancreatic T-AOC and activities of antioxidant enzyme, pancreatic trypsin activity, and crude protein apparent digestibility. Furthermore, in the weaned piglets challenged with diquat, chitosan inclusion alleviated the activities of serum amylase and lipase, and pancreatic MDA concentration. The results of the present study indicated that chitosan could be a safe and potent new additive for alleviating pancreatic oxidative injury.

A series of new organic donor–π–acceptor dyes incorporating a diquat moiety as a novel electron‐acceptor unit have been synthesized and characterized. The analytical data were supported by DFT calculations. These dyes were explored in the aerobic thiocyanation of indoles and pyrroles. Here they showed a high photocatalytic activity under visible light, giving isolated yields of up to 97 %. In addition, the photocatalytic activity of standalone diquat and methyl viologen through formation of an electron donor acceptor complex is presented. [ABSTRACT FROM AUTHOR]

The aim of this study was to investigate the protective effects of glutathione (GSH) against oxidative stress and intestinal barrier disruption caused by diquat (an oxidative stress inducer) in weaned piglets. Twenty-four piglets were randomly assigned to four treatments with six pigs per treatment for an 18-d trial. Treatments were basal diet, basal diet + diquat challenge, 50 mg/kg GSH diets + diquat challenge and 100 mg/kg GSH diets + diquat challenge. On day 15, piglets in basal diet group and diquat-challenged groups were intraperitoneally injected with sterile saline and diquat at 10 mg/kg body weight, respectively. The results showed that GSH supplementation improved growth performance of diquat-injected piglets from days 15 to 18 (p < 0.05), especially at a dose of 100 mg/kg GSH. Meanwhile, diquat also caused oxidative stress and intestinal barrier damage in piglets. However, GSH supplementation enhanced the antioxidant capacity of serum and jejunum, as evidenced by the increase in GSH content and total superoxide dismutase activities and the decrease in 8-hydroxy-2'-deoxyguanosine concentrations (p < 0.05). GSH also up-regulated the mRNA expressions of intestinal tight junction protein (zonula occludens 1, ZO1; occludin, OCLN; claudin-1, CLDN1) and mitochondrial biogenesis and function (peroxisome proliferator-activated receptor-gamma coactivator-1 alpha, PGC1α; mitochondrial transcription factor A, TFAM; cytochrome c, CYCS), compared with diquat-challenged piglets in basal diet (p < 0.05). Thus, the study demonstrates that GSH protects piglets from oxidative stress caused by diquat and 100 mg/kg GSH has a better protective role. [ABSTRACT FROM AUTHOR]

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O Paraquat é um herbicida não seletivo altamente tóxico, sendo responsável por altas taxas de letalidade acidentais ou provocadas, devido, principalmente, à insuficiência respiratória. Apesar de a intoxicação por via oral ser a principal e mais grave, o contato prolongado com a substância em uma grande área corporal pode gerar uma toxicidade similar e levar ao óbito – fato pouco elucidado na literatura. Este é o relato de caso de um homem de 22 anos, que foi admitido em um hospital devido a queixas de mal-estar, náuseas, febre, cefaleia, dor abdominal, diarreia, queimaduras e dispneia. A suspeita diagnóstica inicial foi de hantavirose, leptospirose, dengue e tromboembolismo pulmonar e, posteriormente, foi comprovado intoxicação exógena com agrotóxico por via inalatória e cutânea. Exames de imagem revelaram fibrose pulmonar difusa e ele também apresentou alterações renais, hepáticas e coagulatórias. Como não há antídoto específico, foi empregado tratamento sintomático e suportivo, com uso de carvão ativado, antibióticos, corticoides, antioxidantes e hemodiálise. No entanto, o paciente teve uma piora progressiva do quadro, vindo a óbito devido à síndrome da angústia respiratória aguda e fibrose pulmonar. O Paraquat, embora proibido no Brasil em 2020, continua sendo utilizado de forma ilegal. Além disso, seu substituto, o Diquat, possui toxicidade semelhante. Assim, é fundamental que os profissionais da saúde reconheçam o diagnóstico da intoxicação por tais substâncias e suas diferentes vias de exposição. Também são necessárias novas medidas de fiscalização das substâncias e maior investimento em educação em saúde para evitar exposições acidentais, assim como relatado.