Diquat exacerbates oxidative stress and neuroinflammation by blocking the autophagic flux of microglia in the hippocampus.

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.

Thinking Induced by Acute Kidney Injury of Diquat Poisoning: Cases Report.

Diquat poisoning is a fatal condition that is becoming increasingly common. The mortality risk of patients taking lethal doses of diquat is extremely high. It typically leads to rapid dysfunction of multiple organs, including the kidneys, heart, lungs, and brain. Acute kidney injury is usually the first manifestation of this poisoning. However, the optimal treatment strategy for diquat poisoning remains uncertain. Additionally, the mechanism of multiple organ dysfunction syndrome caused by diquat poisoning may resemble the progression of sepsis. In this report, we present 3 cases of diquat poisoning, all of which resulted in death. We emphasize that acute kidney injury is the primary cause of death, and suggest that some strategies used in the treatment of sepsis could be beneficial in managing diquat poisoning-induced acute kidney injury.

Protective effect and mechanism of CoQ10 in mitochondrial dysfunction in diquat-induced renal proximal tubular injury.

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.

Association between toxicity-index of diquat and in-hospital mortality in patients with acute diquat poisoning: a retrospective cohort study.

BACKGROUND: This study investigates the impact of diquat toxicity levels on in-hospital mortality rates among patients with acute diquat poisoning. It aims to clarify the relationship between diquat toxicity scores and the likelihood of death during hospitalization. METHODS: A retrospective cohort study was conducted on 98 individuals with acute diquat poisoning. Data on post-ingestion time, initial diquat plasma concentration, and clinical outcomes were systematically collected for all participants. The toxicity-index of diquat was calculated based on post-ingestion time and initial diquat plasma concentration. Logistic regression analysis was utilized to assess the association between the toxicity-index of diquat and in-hospital mortality rates, adjusting for potential confounding variables such as age, comorbidities, and treatment interventions. RESULTS: The study found that the overall prevalence of in-hospital mortality was 34.7%, with 58.2% in males. The multivariable-adjusted regression coefficient for in-hospital mortality associated with the toxicity-index was 1.09, with a 95% confidence interval (CI) of 1.01-1.17. Subsequent exploratory subgroup analysis indicated that there were no significant interactions (all p values for interaction were >0.05). CONCLUSIONS: The study found that higher diquat toxicity-index values correlate with increased in-hospital mortality in acute diquat poisoning cases, indicating that the toxicity-index could be a useful biomarker for assessing mortality risk.

The toxicity-index of diquat plays a pivotal role in the identification, management, and prognostic prediction of acute diquat poisoning; however, its specific predictive value warrants further investigation.The toxicity-index of diquat serves as a more precise biomarker for differentiating between low-risk and high-risk categories.In comparison to low-risk patients with acute diquat poisoning, the toxicity-index of diquat in high-risk patients were significantly elevated.

Association between initial diquat plasma concentration, severity index and in-hospital mortality in patients with acute diquat poisoning: a retrospective cohort study.

BACKGROUND: Since 2016, diquat has replaced paraquat in China, resulting in increased diquat poisoning cases. However, understanding of diquat poisoning is still limited. This study aimed to investigate the relationship between initial diquat plasma concentration, severity index, and in-hospital mortality in acute diquat poisoning cases. METHODS: This retrospective cohort study, conducted from January 2016 to July 2023 in a tertiary care hospital, used univariate logistic regression to examine the link between the initial diquat plasma concentration, severity index, and in-hospital mortality in acute diquat poisoned patients. A receiver operating characteristic curve assessed the predictive value of these parameters for prognosis. RESULTS: Among the 87 participants, the median age was 32 years, 35 (40.2%) were female. The overall mortality rate was 37.9%. Logistic regression analysis revealed that the initial diquat plasma concentration and severity index were associated with increased in-hospital mortality. These factors also effectively predicted the prognosis of acute diquat poisoning, with an area under the receiver operating characteristic curve of 0.851 and an optimal diquat concentration threshold of 2.25 mg/L (sensitivity 90.9%, specificity 74.1%, P < 0.05) and an area under the receiver operating characteristic curve of 0.845 with an optimal cut-off value for the sevity index of 9.1 mg/L*min (sensitivity 97%, specificity 74.1%, P < 0.05). DISCUSSION: Our results are limited by the retrospective design of this study. However, if validated, these results could impact management strategies, especially in East Asia. Further research is needed due to potential confounding factors. CONCLUSIONS: The findings suggest that a higher initial plasma concentration and severity index in patients with acute diquat poisoning were correlated with higher in-hospital mortality. Prospective validation will confirm the predicative value of these findings.

Diagnostic and prognostic value of diquat plasma concentration and complete blood count in patients with acute diquat poisoning based on random forest algorithms.

Currently, the incidence of diquat (DQ) poisoning is increasing, and quickly predicting the prognosis of poisoned patients is crucial for clinical treatment. In this study, a total of 84 DQ poisoning patients were included, with 38 surviving and 46 deceased. The plasma DQ concentration of DQ poisoned patients, determined by liquid chromatography-mass spectrometry (LC-MS) were collected and analyzed with their complete blood count (CBC) indicators. Based on DQ concentration and CBC dataset, the random forest of diagnostic and prognostic models were established. The results showed that the initial DQ plasma concentration was highly correlated with patient prognosis. There was data redundancy in the CBC dataset, continuous measurement of CBC tests could improve the model's predictive accuracy. After feature selection, the predictive accuracy of the CBC dataset significantly increased to 0.81 ± 0.17, with the most important features being white blood cells and neutrophils. The constructed CBC random forest prediction model achieved a high predictive accuracy of 0.95 ± 0.06 when diagnosing DQ poisoning. In conclusion, both DQ concentration and CBC dataset can be used to predict the prognosis of DQ treatment. In the absence of DQ concentration, the random forest model using CBC data can effectively diagnose DQ poisoning and patient's prognosis.

Microhemorrhages in diquat-induced encephalopathy identified using susceptibility-weighted imaging.

INTRODUCTION: Intracerebral 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. CONCLUSION: 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.

Images in acute diquat poisoning, including hepatic portal venous gas and gastrointestinal pneumatosis on computed tomography.

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.

A ratiometric fluorescence method for the detection of diquat by a large Stokes shift fluorescent probe.

Pesticide residues are currently a prominent concern for food safety, and the development of a rapid, convenient, and accurate method for detecting pesticide residues is crucial to ensure the quality of agricultural products. In this study, a small molecule fluorescent probe based on biphenyl disulfonic acid (BDSA) was designed and prepared, and a sensitive, specific, and rapid detection method for diquat (DQ) and paraquat (PQ) was developed. The fluorescent molecule (BDSA-NDA) was synthesized through amide reaction between BDSA and 1,8-naphthalic anhydride, which exhibited cyan fluorescence (480 nm) when excited at 305 nm in aqueous solution with a large Stokes shift (>150 nm). Diquat and paraquat were found to quench the fluorescence of the probe through internal filtration effect (IFE) and photoelectron transfer (PET). Moreover, diquat possessed a large conjugated structure that emitted fluorescence at 340 nm which was assembled into a pair of ratio fluorescence with BDSA-NDA. Under optimized experimental conditions, the developed method achieved detection limits of 0.003 mg/L for diquat and 0.202 mg/L for paraquat. Furthermore, it could identify paraquat doped in diquat formulations. Additionally, when applied to environmental water samples as well as rice and urine, this detection method demonstrated good recovery rates (water: 96.2-100.6 %, rice: 93.5-101.9 %, urine: 96-103.7 %), meeting actual sample detection requirements effectively. This work presents a novel approach for rapidly detecting diquat and paraquat residues which holds practical application value in areas such as pesticide residue analysis in foods, environmental or clinical samples.

Selective Detection of Paraquat in Adulterated and Complex Environmental Samples Using Raman Spectroelectrochemistry.

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.

Erythrocyte membrane biomimetic EGCG nanoparticles attenuate renal injury induced by diquat through the NF-κB/NLRP3 inflammasome pathway.

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-1ß, 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-1ß, 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.

Investigating layer-by-layer films of carbon nanotubes and nickel phthalocyanine towards diquat detection.

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.

Treatments with Diquat Reveal the Relationship between Protein Phosphatases (PP2A) and Oxidative Stress during Mitosis in Arabidopsis thaliana Root Meristems.

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.

Fractionated plasma separation and adsorption integrated with continuous veno-venous hemofiltration in patients with acute bipyridine herbicide poisoning.

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-1ß (MIP-1ß) 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-1ß 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.

Interpretable machine learning for the prediction of death risk in patients with acute diquat poisoning.

The aim of this study was to develop and validate predictive models for assessing the risk of death in patients with acute diquat (DQ) poisoning using innovative machine learning techniques. Additionally, predictive models were evaluated through the application of SHapley Additive ExPlanations (SHAP). A total of 201 consecutive patients from the emergency departments of the First Hospital and Shengjing Hospital of China Medical University admitted for deliberate oral intake of DQ from February 2018 to August 2023 were analysed. The initial clinical data of the patients with acute DQ poisoning were collected. Machine learning methods such as logistic regression, random forest, support vector machine (SVM), and gradient boosting were applied to build the prediction models. The whole sample was split into a training set and a test set at a ratio of 8:2. The performances of these models were assessed in terms of discrimination, calibration, and clinical decision curve analysis (DCA). We also used the SHAP interpretation tool to provide an intuitive explanation of the risk of death in patients with DQ poisoning. Logistic regression, random forest, SVM, and gradient boosting models were established, and the areas under the receiver operating characteristic curves (AUCs) were 0.91, 0.98, 0.96 and 0.94, respectively. The net benefits were similar across all four models. The four machine learning models can be reliable tools for predicting death risk in patients with acute DQ poisoning. Their combination with SHAP provides explanations for individualized risk prediction, increasing the model transparency.

Diquat causes mouse testis injury through inducing heme oxygenase-1-mediated ferroptosis in spermatogonia.

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.

Prognostic value of plasma diquat concentration in patients with acute oral diquat poisoning: a retrospective study.

Objectives: Diquat 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. Methods: This 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). Results: Among 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 < 0.05). Plasma Diquat concentration at admission (HR = Exp (0.032-0.059 × ln (t))) and PSS within 24 h after admission (HR: 4.470, 95%CI: 1.604 ~ 12.452, p = 0.004) were independent prognostic factors in the time-dependent Cox regression model. Conclusion: Plasma DQ concentration at admission and PSS within 24 h after admission are independent prognostic factors for the in-hospital case fatality rate in patients with acute oral DQ poisoning. The prognostic value of plasma DQ concentration decreased with time.

Vascular endothelium, a promising target for effectively treating fulminant diquat intoxication?

Following the withdrawal of paraquat, diquat (DQ) has emerged as the predominant herbicide. When people come into contact with or ingest DQ, may lead to poisoning and potentially fatal outcomes. Reports suggest that the mortality of DQ poisoning can be as high as 50%. DQ poisoning can be categorized as mild, moderate to severe or fulminant. In cases of fulminant poisoning, victims often succumb to multiple organ failure within 48 h. This presents a significant challenge in the clinical management. Scholars have discovered that oxidative stress, inflammatory injury, and cell apoptosis play crucial roles in the DQ poisoning. However, the underlying connection of the extensive organ damage remains unknown. The abnormal function and activity of endothelial cells (EC) should play a crucial role in tissue damage caused by DQ due to rich microcirculation and high sensitivity to perfusion in the vulnerable organs. However, reports on DQ-induced EC injury is rare. We made a preliminary discovery-the presence of severe vascular endothelial damage in the kidneys and lungs affected by DQ. Therefore, we hypothesize that DQ poisoning may be attributed to EC damage, ultimately resulting in multiple organ failure.

A SERS-based point-of-care testing approach for efficient determination of diquat and paraquat residues using a flexible silver flower-coated melamine sponge.

Diquat (DQ) and paraquat (PQ) residues in food are potential hazards to consumers' health. Point-of-care testing (POCT) of them remains challenging. Based on surface-enhanced Raman spectroscopy (SERS) technology, we developed a POCT strategy for DQ and PQ on apple surface and in apple juice. A point-of-use composite was fabricated using a piece of porous melamine sponge (MS) modified with silver nanoflowers (AgNFs), combining the specificity of the SERS fingerprint and the excellent adsorption capacity of MS. Using this dual-functional AgNFs@MS, the on-site determination of the DQ and PQ residues was completed within 3 min without pretreatment. Clear trends were observed between SERS intensity and logarithmic concentrations, with r values from 0.962 to 0.984. The limit of detection of DQ and PQ were 0.14-0.70 ppb in apple juice and on apple surface. This study provides a new point-of-use alternative for rapidly detecting DQ and PQ residues in nonlaboratory settings.

High expression of 3-hydroxy-3-methylglutaryl-CoA synthase 2 (HMGCS2) associated with Diquat-induced damage.

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.