OBJECTIVE: To investigate whether auraptene (AUR) exerts a protective effect on acute diquat (DQ)-induced liver injury in mice and explore its underlying mechanisms. METHODS: Forty SPF-grade healthy male C57BL/6 mice were randomly divided into normal control group (Control group), DQ poisoning model group (DQ group), AUR treatment group (DQ+AUR group), and AUR control group (AUR group), with 10 mice in each group. The DQ poisoning model was established via a single intraperitoneal injection of 40 mg/kg DQ aqueous solution (0.5 mL); Control group and AUR group received an equal volume of pure water intraperitoneally. Four hours post-modeling, DQ+AUR group and AUR group were administered 0.5 mg/kg AUR aqueous solution (0.2 mL) by gavage once daily for 7 consecutive days, while Control group and DQ group received pure water. Blood and liver tissues were collected after anesthesia on day 7. Liver ultrastructure was observed by transmission electron microscopy. Serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels were measured via enzyme-linked immunosorbent assay (ELISA). Hepatic glutathione (GSH), superoxide dismutase (SOD), and malondialdehyde (MDA) levels were detected using WST-1, thiobarbituric acid (TBA), and enzymatic reaction methods, respectively. Protein expression of nuclear factor-erythroid 2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), Kelch-like ECH-associated protein 1 (Keap1), and activated caspase-9 in liver tissues was analyzed by Western blotting. RESULTS: Transmission electron microscopy revealed that mitochondria in the Control group exhibited mild swelling, uneven distribution of matrix, and a small number of cristae fractures. In the AUR group, mitochondria showed mild swelling, with no obvious disruption of cristae structure. In the DQ group, mitochondria demonstrated marked swelling and increased volume, matrix dissolution, loss and fragmentation of cristae, and extensive vacuolization. In contrast, the DQ+AUR group showed significantly reduced mitochondrial swelling, volume increase, matrix dissolution, cristae loss and fragmentation, and vacuolization compared to the DQ group. Compared with the DQ group, the DQ+AUR group exhibited significantly lower serum AST levels (U/L: 173.45±23.60 vs. 255.33±41.51), ALT levels (U/L: 51.77±21.63 vs. 100.70±32.35), and hepatic MDA levels (μmol/g: 12.40±2.76 vs. 19.74±4.10), along with higher hepatic GSH levels (mmol/g: 37.65±14.95 vs. 20.58±8.52) and SOD levels (kU/g: 124.10±33.77 vs. 82.81±22.00), the differences were statistically significant (all P < 0.05). Western blotting showed upregulated Nrf2 expression (Nrf2/β-actin: 0.87±0.37 vs. 0.53±0.22) and HO-1 expression (HO-1/β-actin: 1.06±0.22 vs. 0.49±0.08), and downregulated Keap1 expression (Keap1/β-actin: 0.82±0.12 vs. 1.52±0.76) and activated caspase-9 expression (activated caspase-9/β-actin: 1.16±0.28 vs. 1.71±0.30) in the DQ+AUR group compared to the DQ group (all P < 0.05). CONCLUSION AUR attenuates DQ-induced acute liver injury in mice by activating the Keap1/Nrf2 signaling pathway.
Animals ; Male ; Mice ; Mice, Inbred C57BL ; Liver/pathology* ; Chemical and Drug Induced Liver Injury/drug therapy* ; Diquat/poisoning* ; NF-E2-Related Factor 2/metabolism* ; Oxidative Stress ; Apoptosis ; Coumarins

Copper sulfate is a frequently used copper compound in laboratory settings, with instances of poisoning being uncommon. A study conducted by the American Association of Poison Control Centers' National Poison Data System found that only 140 individuals were exposed to copper compounds over the course of a year, with five cases being intentional (Gummin et al., 2023). Severe poisoning from copper sulfate can result in isolated gastrointestinal injury (Galust et al., 2023), intravascular hemolysis (Adline et al., 2024), rhabdomyolysis (Richards et al., 2020), and other symptoms documented in the literature. However, there have been no reports of long-term uncontrolled hyperglycemia in patients with copper sulfate poisoning. This case study documents the treatment approach for a patient with unexplained, long-term, uncontrolled hyperglycemia, alongside multiple organ dysfunction resulting from intentional ingestion of a large dose of copper sulfate. This case report details the long-term complications in a patient's recovery from acute copper sulfate, highlighting the significance of ongoing monitoring and intervention.
Humans ; Copper Sulfate/poisoning* ; Hyperglycemia/chemically induced* ; Multiple Organ Failure/therapy*

Objective: To observe the effects of transcranial direct current stimulation (tDCS) on nerve injury markers and prognosis in patients with acute severe carbon monoxide poisoning (ASCOP) . Methods: In May 2021, 103 ASCOP patients were treated in the emergency department of Harrison International Peace Hospital of Hebei Medical University from November 2020 to January 2021. The patients were divided into two groups according to whether they received tDCS treatment. The control group (50 cases) were given oxygen therapy (hyperbaric oxygen and oxygen inhalation) , reducing cranial pressure, improving brain circulation and cell metabolism, removing oxygen free radicals and symptomatic support, and the observation group (53 cases) was treated with 2 weeks of tDCS intensive treatment on the basis of conventional treatment. All patients underwent at least 24 h bispectral index (BIS) monitoring, BIS value was recorded at the hour and the 24 h mean value was calculated. Neuron-specific enolase (NSE) and serum S100B calcium-binding protein (S100B) were detected after admission, 3 d, 7 d and discharge. Follow-up for 60 days, the incidence and time of onset of delayed encephalopathy (DEACMP) with acute carbon monoxide poisoning in the two groups were recorded. Results: The NSE and S100B proteins of ASCOP patients were significantly increased at admission, but there was no significant difference between the two groups (P=0.711, 0.326) . The NSE and S100B proteins were further increased at 3 and 7 days after admission. The increase in the observation group was slower than that in the control group, and the difference was statistically significant (P(3 d)=0.045, 0.032, P(7 d)=0.021, 0.000) ; After 14 days, it gradually decreased, but the observation group decreased rapidly compared with the control group, with a statistically significant difference (P=0.009, 0.025) . The 60 day follow-up results showed that the incidence of DEACMP in the observation group was 18.87% (10/53) , compared with 38.00% (19/50) in the control group (P=0.048) ; The time of DEACMP in the observation group[ (16.79±5.28) d] was later than that in the control group[ (22.30±5.42) d], and the difference was statistically significant (P=0.013) . Conclusion: The early administration of tDCS in ASCOP patients can prevent the production of NSE and S100B proteins, which are markers of nerve damage. and can improve the incidence and time of DEACMP.
Humans ; Biomarkers ; Brain Diseases/therapy* ; Carbon Monoxide Poisoning/therapy* ; Oxygen ; Phosphopyruvate Hydratase ; Prognosis ; S100 Calcium Binding Protein beta Subunit ; Transcranial Direct Current Stimulation

The data of a patient with carbamate pesticide poisoning were analyzed. Cardiac arrest, oliguria, acute renal injury and pulmonary infection occurred during treatment. After cardiopulmonary resuscitation, tracheal intubation, CRRT, anti-infection and other symptomatic support treatment, the patient recovered and discharged. The myocardial damage caused by carbamate pesticide poisoning is easy to be ignored, and it often causes cardiac manifestations such as arrhythmia and cardiac insufficiency, and the related markers of cardiac injury, electrocardiogram and echocardiogram are also changed. Therefore, the awareness of cardiac damage caused by carbamate pesticide poisoning should be improved.
Humans ; Pesticides ; Carbamates ; Heart Arrest ; Arrhythmias, Cardiac ; Poisoning/therapy* ; Organophosphate Poisoning

Objective: To investigate the clinical significance of blood purification on changes in serum toxicant concentration and prognosis of acute benzene-based thinner poisoning. Methods: A total of 44 patients with acute benzene-based thinner poisoning admitted to the emergency department of Characteristic Medical Center of Armed Police from August 2013 to August 2020 were collected and divided into a blood purification group (24 cases) and a conventional treatment group (20 cases) , the general data, toxicant concentrations and prognosis of the two groups of patients were analyzed, and logistic regression analysis was performed on the influencing factors of the prognosis to explore the clinical effect of blood purification. Results: The concentration of poisons in the blood purification group at 24 hours after treatment was significantly lower than that in the conventional treatment group (t=6.76, P<0.001) , and the reduction in the concentration of poisons was significantly higher than that in the conventional treatment group (t=3.33, P=0.002) . The overall improvement rate in the blood purification group was 91.7% (22/24) , which was higher than that in the conventional treatment group (60.0%, 12/20) . Logisitic regression analysis showed that blood purification treatment method was the main factor affecting the prognosis of patients (OR=7.605×10(-5), 95%CI: 6.604×10(-8)-0.087, P=0.008) , and the toxic dose was a synergistic effect on the prognosis of patients factor (OR=1.038, 95%CI: 1.008-1.068, P=0.011) . Conclusion: Early blood purification treatment in patients with acute benzene-based thinner poisoning can rapidly reduce blood toxin concentration, avoid disease progression, and ultimately improve patient prognosis.
Benzene ; Hazardous Substances ; Humans ; Poisoning/therapy* ; Prognosis ; Retrospective Studies

Objective: To explore the clinical characterist ics and risk factors of hemorrhage complicated by hemoperfusion therapy in patients with acute poisoning. Methods: In January 2021, the clinical data of 196 patients with acute poisoning who received hemoperfusion therapy in the Second Affiliated Hospital of Air Force Military Medical University from January 2018 to December 2020 were analyzed, and the patients were divided into bleeding group and non-bleeding group according to whether the patients were complicated with bleeding. Multivariate logistic regression was used to analyze the independent risk factors for hemorrhage in patients treated with hemoperfusion. Results: A total of 21 patients in the bleeding group and 175 patients in the non-bleeding group were included. There was no significant difference in general data such as gender, age, and body mass index between the two groups (P>0.05) . Organophosphorus pesticides (χ(2)= 4.56, P=0.030) , HA230 perfusion device (χ(2)=4.12, P=0.042) , platelet count (t=-2.33, P=0.009) and activated partial thromboplastin time (t=14.53, P<0.001) at 2 h of perfusion were the influencing factors of hemorrhage in patients with acute poisoning treated with hemoperfusion. Among them, organophosphorus pesticides, 2 h perfusion activated partial thromboplastin time ≥35 s and other factors were independent risk factors forcomplicated bleeding (P<0.05) . Conclusion: Patients with acute poisoning, especially organophosphorus pesticide poisoning, are at greater risk of bleeding during hemoperfusion therapy. Monitoring of changes in activated partial thromboplastin time should be strengthened and the dose of anticoagulants should be adjusted in time to reduce the risk of bleeding.
Hemoperfusion ; Hemorrhage/therapy* ; Humans ; Organophosphorus Compounds ; Pesticides ; Poisoning/therapy* ; Risk Factors

The Second Affiliated Hospital of Shandong First Medical University treated a patient with oral sulfur mixture poisoning on January 14, 2020. The patient presented with cyanosis and disturbance of consciousness as the first manifestations, accompanied by metabolic acidosis, shock, hypercalcemia and severe liver function and myocardial damage. The patient was given active treatment, including gastric lavage, blood purification, methylene blue application, correction of shock, organ support and other therapies. However the treatment was poor. Finally, the patient's family chose to give up and requested to be discharged from the hospital, and the patient died on the same day after follow-up.
Calcium Compounds ; Humans ; Poisoning/therapy* ; Sulfides

Objective: To explore the expulsion effect of sodium dimercaptopropanesulfonate (DMPS) on mercury in different organs of mercury poisoning and the therapeutic effect of glutathione (GSH) combined with antioxidant therapy on mercury poisoning. Methods: In February 2019, 50 SPF male SD rats were randomly divided into 5 groups, 10 rats in each group: A (saline negative control group) , B (HgCL2 positive control group) , treatment group (C: intramuscular injection of DMPS 15 mg/kg treatment, D: intramuscular injection of DMPS30 mg/kg treatment, E: intramuscular injection of DMPS 15 mg/kg and intraperitoneal injection of GSH200 mg/kg treatment) . Rats in group B, C, D and E were subcutaneously injected with mercury chloride solution (1 mg/kg) to establish a rat model of subacute mercury poisoning kidney injury. Rats in group A were subcutaneously injected with normal saline. After the establishment of the model, rats in the treatment group were injected with DMPS and GSH. Rats in group A and group B were injected with normal saline. At 21 d (treatment 7 d) and 28 d (treatment 14 d) after exposure, urine and blood samples of 5 rats in each group were collected. Blood biochemistry, urine mercury, urine microalbumin and mercury content in renal cortex, cerebral cortex and cerebellum were detected. Results: After exposure to mercury, the contents of mercury in renal cortex, cerebrum and cerebellum of rats in group B, C, D and E increased, and urine microalbumin increased. Pathology showed renal tubular injury and renal interstitial inflammation. Compared with group B, urinary mercury and renal cortex mercury in group C, D and E decreased rapidly after DMPS treatment, and there was no significant decrease in mercury levels in cerebellum and cerebral cortex of rats, accompanied by transient increase in urinary albumin after DMPS treatment (P<0.05) ; the renal interstitial inflammation in group E was improved after GSH treatment. There was a positive correlation between urinary mercury and the contents of mercury in renal cortex, cerebral cortex and cerebellum (r=0.61, 0.47, 0.48, P<0.05) . Conclusion: DMPS mercury expulsion treatment can significantly reduce the level of metal mercury in the kidney, and there is no significant change in the level of metal mercury in the cortex and cerebellum.
Animals ; Brain/drug effects* ; Glutathione ; Inflammation ; Kidney/drug effects* ; Kidney Diseases/chemically induced* ; Male ; Mercuric Chloride/therapeutic use* ; Mercury/urine* ; Mercury Poisoning/drug therapy* ; Rats ; Rats, Sprague-Dawley ; Saline Solution/therapeutic use* ; Unithiol/therapeutic use*

Acute methanol poisoning harms the optic nerve and central nervous system, can cause irreversible damage, even coma or death in severe cases. This article reported four cases of methanol poisoning. 3 patients mistakenly ingested industrial alcohol containing methanol, the most serious patient suffered from coma, vision loss and other symptoms, the blood methanol concentration was 869.3 μg/ml. Another patient was poisoning caused by inhalation of methanol, with symptoms such as total blindness in the right eye and decreased visual acuity in the left eye. After active supportive treatment, 2 patients had partial recovery of visual acuity, and 2 patients had no sequelae. This article discussed the clinical features, treatment and prognosis of optic nerve damage caused by methanol poisoning, in order to raise awareness of this disease.
Coma ; Follow-Up Studies ; Humans ; Methanol ; Optic Nerve ; Optic Nerve Injuries ; Poisoning/therapy*

Acute carbon monoxide poisoning can cause multiple organ damage due to hypoxia. In severe cases, it can be life-threatening and has a high fatality rate. Intestinal obstruction and thrombosis are rare complications of carbon monoxide poisoning. A case of carbon monoxide poisoning was reported. In addition to the central nervous system lesion, intestinal obstruction and lower limb thrombosis were also found. In the treatment of carbon monoxide poisoning patients, the clinician was able to treat the common complications, attention should be paid to gastrointestinal tract, thrombotic disease and other rare complications, so as to avoid missed diagnosis.
Carbon Monoxide Poisoning/therapy* ; Humans ; Intestinal Obstruction/etiology* ; Thrombosis/etiology*