Dichlorvos Poisoning Research Articles

Protective Activity of Palm Oil Extracts against Dichlorvos Poisoning in Rats: Biochemical Parameters and Mechanisms of Action

Protective activity on biochemical parameters and possible mechanisms of action of palm oil extracts were investigated in orally Dichlorvos poisoned rats and the efficacy of treatments in the poisoned rats. The safety profile of the extracts was evaluated via acute toxicity studies which was done in two phases. To screen for phytochemicals, present in this extract. This study was carried out in Pharmacy and KIUTH laboratories, Kampala International University, Uganda. Wistar rats of both sexes, weighing 85g and above were used for the study. Selection of rats was done by simple random sampling. At the end of the administration, plasma biochemical parameters were measured as indices of organ toxicity. The red palm oil used in treatment of Dichlorvos poisoned rats caused a reduction in concentration of some of the biochemical parameters of the rats when given simultaneously compared to the kernel oil combinations. Administration of palm oil does not have prophylactic effect against the poison. However, it does seem to have similar protective effects against oxidative stress with ascorbic acid. In summary the administration of palm oil seemed to have limited ameliorative role against Dichlorvos poisoning in rats. Keywords: Dichlorvos, palm oil, palm kernel oil, rats, acute toxicity, oxidative stress.

Application of extracorporeal membrane oxygenation technique in patients with refractory shock caused by dichlorvos poisoning

Dichlorvos poisoning can cause muscarinic (M) -like symptoms, nicotinoid (N) -like symptoms and central nervous system manifestations. When severe poisoning is combined with refractory shock, the mortality rate exceeds 60%. At present, there are more and more studies on ECMO for poisoning, but there is no report on ECMO for treating refractory hypotension caused by dichlorvos poisoning. We analyzed 3 successful cases of veno-arterial extracorporeal membrane oxygenation (VA-ECMO) in the treatment of refractory shock caused by acute severe dichlorvos poisoning to explore the effectiveness of VA-ECMO in patients with severe poisoning.

Gross examination and Toxicological Analysis of Gastrointestinal Tract for Dichlorvos Poisoning Caused by Nuvan Insecticide During Post-Mortem Examination: A Case Series

Background: “Nuvan” is a trading name for Dichlorvos (DDVP) organophosphate insecticide. Nuvan contains76% DDVP and is accessible in India. Nuvan Insecticide is highly misused as orally ingested in suicide attemptsand is one of the leading causes of poisoning deaths in Indian rural areas.Methods: In this case study, we have diagnosed the four poisoning deaths by Nuvan-dichlorvos insecticidethrough Post-Mortem examination and toxicological analysis. The gastro-intestinal tract (GIT) was grosslyexamined. The solvent extraction method is used for withdrawing pesticide content from GIT. Toxicologicalanalyses were performed using thin-layer chromatography (TLC) using a spraying reagentResults: A Fluorescent turquoise blue liquid content was found throughout the stomach to the small intestine.Content had a notable odor of volatile organic compounds (VOCs). The mucosal walls of the stomach were highlycongested and hemorrhagic. Toxicological analyses done for all four cases showed a confirmatory detection ofdichlorvos.Conclusions: The simple gross examination of gastrointestinal viscera during post-mortem is supportingdiagnostic evidence for orally administered Nuvan insecticide. Solvent extraction method is a suitable techniquefor the extraction of pesticides from aqueous biological matrices. Thin Layer Chromatography is a simple andinexpensive technique for chemical confirmation and DDVP was detected.

Acute toxicity profile of chlorpheniramine: Potential use as antidote to dichlorvos poisoning

Introduction: Pesticide poisoning is a serious public health concern all over the world. Alternative therapies for organophosphorus poisoning are being explored, and this could be very useful especially in emergency situations of antidote shortages. This study therefore set out to determine the effects of chlorpheniramine on the kidney and liver function in dichlorvos poisoning. Methodology: Chlorpheniramine (2mg/kg, 4mg/kg, and 8mg/kg), atropine (0.4mg/kg, 0.8mg/kg, and 1.6mg/kg) and dichlorvos (4mg/kg) were all administered intraperitoneally. Administration was done for 14 days, after which the animals were sacrificed under chloroform anaesthesia and blood samples collected for liver and kidney function tests. Results: Chlorpheniramine and atropine offer some protective effects as they both reduced the raised values of the renal enzymes towards that of the control following dichlorvos poisoning. Chlorpheniramine and atropine counteracted the effect of dichorvos on Na+, K+, Cl- and HC03-, by reducing the values closer to the normal range. However, the combination group significantly (p<0.05) reduced the values and gave normal values of 147mmol/L (Na+), 4.3mmol/L (K+), 127mmol/L (Cl-) and 18.3mmol/L (HC03- respectively) when compared with the control. Chlorpheniramine raised the value closer to the normal range and gave a value of 4.82g/dl, though this increase was not statistically significant. Atropine gave a value of 5.0g/dl which is within the normal range. The combination group (Atropine + Chlorpheniramine) gave a value of 5.6g/dl which is within the normal range and the difference was statistically significant when compared to the negative control (p<0.05). Chlorpheniramine reduced the elevation observed in the liver enzymes caused by dichlorvos poisoning (149.3U/L, 34.33U/L and 142.3U/L respectively). Conclusion: This study concludes that chlorpheniramine has protective property on the liver and kidney against dichlorvos toxicity.

Effect of chlorpheniramine on acute dichlorvos poisoning in wistar rats

Introduction: Pesticide poisoning is a serious public health concern worldwide. According to WHO, about 3 million cases occur every year, resulting in more than 250,000 deaths. In response to the problems of unavailability of antidotes and cost in sub-Saharan Africa, this research set out to investigate chlorpheniramine, a cheap and readily available over the counter (OTC) antihistamine for possible antidotal effects on rats acutely poisoned with dichlorvos. Methodology: The antidotal and protective effect of chlorpheniramine a H1 antihistamine on acute toxicity by dichlorvos, an organophosphorus insecticide in wistar rats was investigated and compared with atropine, the standard antidote. Chlorpheniramine (2mg/kg, 4mg/kg, and 8mg/kg), atropine (0.4mg/kg, 0.8mg/kg, and 1.6mg/kg) and dichlorvos (4mg/kg) were all administered intraperitoneally. Dichlorvos at a dose of 4mg/kg induced acute toxicity in the rats observed as tremor, convulsion, defecation, straub tail, recumbence and gasping. Results: Chlorpheniramine significantly (p<0.05) decreased the occurrence of acute signs of toxicity and also delayed the time of onset of signs of poisoning. Chlorpheniramine also prevented death of the animals with 100% survival rate after 2- 24hours of dichlorvos poisoning. Chlorpheniramine also reduced the toxicity score as compared to the control after acute toxicity testing for 14days. Conclusion: The results suggests that chlorpheniramine possesses antidotal effects against dichlorvos induced toxicity in wistar rats comparable to atropine, the standard antidote and showed an additive positive antidotal effect when administered in combination with atropine.

Investigation of the effects of dichlorvos poisoning on AMPK signaling pathway in chicken brain tissues

Dichlorvos is a common crop insecticide widely used by people which causes extensive and serious environmental pollution. However, it has been shown that organophosphorus poisoning causes energy metabolism and neural disorders. The overall purpose of this study was to investigate the damage to brain tissue and the changes in AMPK signaling pathway-related gene expression after dichlorvos poisoning in chickens. White-feathered broiler chickens, as the research subjects of this experiment, were divided into three groups: control group, low-dose group (77.5% dichlorvos at 1.13 mg/kg dose) and high-dose group (77.5% dichlorvos at 10.2 mg/kg dose). Clinical symptoms were observed after modeling, and an integrative analysis was conducted using HE staining microscopy, immune-histochemical microscopy, electron microscopy and PCR arrays. The results showed that the high-dose group had more obvious dyspnea, salivation, convulsion and other neurological phenomena. Pathological sections showed that nuclear disintegration of neurons was most obvious in the low-dose group, and apoptosis of brain cells was most obvious in the high-dose group, and the mitochondrial structure was destroyed in the two poisoned group, i.e. low-dose group and high-dose group. PCR arrays showed that AMPK signaling pathway was inhibited and the expressions of genes involved in energy metabolism (ACACA and PRKAA1) were significantly changed. Furthermore, genes associated with protein synthesis (EIF4EBP1) were significantly upregulated. FASN and HMGCR expressions were significantly increased. There were significant changes in the expressions of cell cycle-related genes (STK11, TP53 and FOXO3). Organophosphate poisoning can cause a lot of nuclear disintegration of brain neurons, increases cell apoptosis, disrupts the energy metabolism of mitochondrial structure, and inhibits the AMPK signaling pathway. These results provide a certain idea and basis for studying the mechanism of AMPK signaling after organophosphorus poisoning and provide a research basis for the prevention and treatment of organophosphorus poisoning.

An experimental study on investigating the postmortem interval in dichlorvos poisoned rats by GC/MS-based metabolomics.

The estimation of the postmortem interval (PMI) is always a key issue in forensic science. Although many attempts based on metabolomics approaches have been proven to be feasible and accurate for PMI estimation, there have been no reports regarding the determination of the PMI in acute dichlorvos (DDVP) poisoning. In this study, all rats were killed by acute DDVP poisoning at a dose three fold the oral LD50 (240 mg/kg). Gas chromatography-mass spectrometry (GC/MS) was applied to investigate the metabolic profiling of blood samples at various times after death up to 72 h. A total of 39 metabolites were found to be associated with PMI, and the combinations of various numbers of metabolites were used to establish support vector regression (SVR) models to investigate the PMI. The SVR model constructed by 23 metabolites had a minimum mean squared error (MSE) of 5.49 h for the training set. Then, the SVR model was validated by prediction set with an MSE of 10.33 h, suggesting good predictive ability of the model for investigating the PMI. The findings demonstrated the great potential of GC/MS-based metabolomics combined with the SVR model in determining the PMI of DDVP poisoned rats and provided an experimental basis for the application of this approach in investigating the PMI of other toxicants.

Xuebijing injection induces anti-inflammatory-like effects and downregulates the expression of TLR4 and NF-κB in lung injury caused by dichlorvos poisoning

BackgroundThe mechanism in lung injury caused by acute organophosphate pesticide poisoning (AOPP) and an effective treatment remains unclear. We aim to clarify how the inflammatory lung injury caused by AOPP might be modulated by Xuebijing (XBJ) injection. MethodsAOPP-induced lung injury model was induced by dichlorvos (DDVP) subcutaneous administration in rats and XBJ injection was administered by intraperitoneal injection after DDVP challenge. The effects of XBJ injection were assessed by lung histopathological analysis and lung injury scores, lung wet-to-dry weight ratios (WDR) and oxygenation, differential immune cell count in bronchoalveolar lavage fluid (BALF), IL-6 and TNF-α levels in blood, the levels of TLR4 and NF-κB proteins in lung tissue and blood acetylcholinesterase (AChE) activity. ResultsDDVP administration resulted in damage of lung histopathology and lower PaO2/FiO2 ratios (P < 0.05), which were notably attenuated by XBJ injection (P < 0.05). Total cell, macrophage, and neutrophils count in BALF and TNF-α and IL-6 levels in blood were significantly increased after DDVP exposure (P < 0.05), which were notably ameliorated by XBJ injection (P < 0.05). TLR4 and NF-κB protein in lung tissue expression after DDVP challenge were markedly increased (P < 0.05), and they were substantially downregulated by XBJ injection (P < 0.05). In addition, blood AChE activity was significantly decreased by DDVP administration (P < 0.05), however, there was no significant improvement after XBJ injection. ConclusionXBJ injection prevents DDVP poisoning induced lung injury by attenuating the inflammatory response. The protective effect appears to be mediated through downregulation of the TLR4 and NF-κB expression.

The protective effect of rabbit serum paraoxonase-1 on the renal injury induced by dichlorvos in rats

Objective To assess the protective effect of rabbit serum paraoxonase-1 (PON-1) on renal injury induced by dichlorvos in rats. Methods Totally 30 healthy S-D rats were randomly divided into 5 groups : control group ( group A, n=6), exposure group ( group B, n=6), PON-1 pretreatment group (group C, n=6), traditional atropine, pralidoxime treatment group(group D, n=6) and combination therapy group (group E, n=6). The rats of group A were given normal saline in equal volume of dichlorvos injected into abdominal cavity to make a false model of dichlorvos poisoning. In rats of groups B, C, D and E, 9 mg/kg dichlorvos was administered. In rats of groups C and E, PON-1 4 500 units/kg was injected into vein of the tails half an hour before dichlorvos administration. After dichlorvos exposure, rats in group D and E were treated with 45 mg/kg iodoprofen and 10 mg/kg atropine by intraperitoneal injection. The activity of blood urea nitrogen (BUN) was assayed with urease. Serum creatinine (Cr) were measured by picric acid colorimetry. Serum Cys-C, KIM-1 and NAG in urine were determined by ELISA. Ultrastructural changes in renal tissues of rats were examined by light microscopy. The differences in laboratory findings between groups were compared. Results The creatinine level in group B was significantly higher than that in other groups (P<0.05). The levels of Cys-C, KIM-1 and NAG in group B and group D were significantly higher than those in group A (P<0.01). But there were no significant differences in above biomarkers among group C, group E and group A. There were no significant differences in above biomarkers between group B and group D. In group B, inflammatory cells infiltrated extensively in renal tissues and, the renal cells were congested and edematous, the lumen was obliterated and the border of the brush disappeared. The tubular structures were not clearly distinct found in group B, but edema and inflammatory cell infiltration with lesser degree were found in group D than those in dichlorvos exposure groups. The clearly distinct structure of the tube without completely occluded lumen in group D, and the most serious lesions were found in distal convoluted tubules. In group C, and group E, there were only mild congestion and edema without significant cell degeneration and necrosis. In group A, the structure of renal tubular epithelium was clearly distinct with brush-shaped margin, and without tubular or necrotic cell debris in the lumen. Conclusion The rabbit serum PON-1 can protect the renal tissue of rats after dichlorvos exposure. Key words: Dichlorvos; Paraoxonase -1; Renal injury; Protective effect; Rats

The protective effect of regulation of paraoxonase 1 gene on liver oxidative stress injury induced by dichlorvos poisoning in mice

To investigate the protective effect of paraoxonase 1 (PON1) gene against liver oxidative stress injury in mice due to dichlorvos poisoning. Experiment 1: 12 male Balb/c mice were randomly divided into three groups, with 4 mice in each group: control group, green fluorescent protein lentivirus control group (Lv-GFP group), and recombinant PON1 lentivirus group (Lv-PON1 group). 2 × 10⁷ TU of Lv-GFP or Lv-PON1 was transfected via tail vein, while normal saline was given to those in control group. Blood was collected on 0, 1, 3, 5, 7, 9 days via fundus venous plexus for the assay of serum PON1 activity. PON1 mRNA and protein expression levels were respectively determined by reverse transcription-polymerase chain reaction (RT-PCR) and Western Blot on the 3rd post-lentivirus transfection day. Experiment 2: according to the random number table method, another 96 male Balb/c mice were divided into four groups of 24 mice in each control group, dichlorvos group, Lv-GFP intervention group, and Lv-PON1 intervention group. Lv-GFP or Lv-PON1 was transfected via tail vein followed by intraperitoneal injection of dichlorvos 9 mg/kg, while those in control group were given normal saline. Six mice in each group were sacrificed respectively at 6, 12, 24, 48 hours, and liver tissue was collected. PON1 mRNA and nuclear factor E2-related factor 2 (Nrf2) mRNA expression levels were determined by RT-PCR, and PON1 protein level was determined by Western Blot. The content of malondialdehyde (MDA) and glutathione (GSH) in the liver tissue were determined by chemical colorimetry. The activity of superoxide dismutase (SOD) and catalase (CAT) were measured by double antibody sandwich enzyme linked immunosorbent assay (ELISA). Experiment 1: after Lv-PON1 was transfected to normal mice, PON1 activity in serum gradually increased and maintained a high level on 3rd day, while that of the control group and Lv-GFP group showed a normal low level. On the 3rd post-lentivirus transfection day, PON1 mRNA and PON1 protein expressions in liver were significantly higher than those of control group and Lv-GFP group. Experiment 2: compared with control group, the mice in dichlorvos group showed significant decreases in PON1 mRNA, PON1 protein, Nrf2 mRNA as well as GSH, SOD, CAT levels at 6 hours [PON1 mRNA (gray value): 0.237 ± 0.075 vs. 0.674 ± 0.011, PON1 protein (gray value): 0.602 ± 0.086 vs. 0.998 ± 0.124, Nrf2 mRNA (gray value): 0.089 ± 0.012 vs. 0.126 ± 0.010, GSH (mg/g): 3.84 ± 0.33 vs. 5.52 ± 0.40, SOD (μg/g): 0.383 ± 0.040 vs. 0.564 ± 0.052, CAT (ng/g): 7.32 ± 1.28 vs. 12.46 ± 1.54, all P < 0.05 ], and remarkable increase in MDA content (nmol/g: 7.78 ± 0.41 vs. 2.34 ± 0.25, P < 0.05). With the extension of time, PON1 mRNA, PON1 protein, Nrf2 mRNA and GSH, SOD, CAT levels gradually increased, MDA content gradually decreased, Nrf2 mRNA expression level had risen to the level of control group at 24 hours (0.133 ± 0.019 vs. 0.126 ± 0.009, P > 0.05), and it was higher than that of the control group at 48 hours ( 0.206 ± 0.028 vs. 0.124 ± 0.010, P < 0.05). Compared with that of the dichlorvos group, Lv-PON1 intervention group showed a significant increase in PON1 mRNA, PON1 protein, Nrf2 mRNA and GSH, SOD, CAT levels [PON1 mRNA (gray value): 0.726 ± 0.021 vs. 0.237 ± 0.075, PON1 protein (gray value): 0.739 ± 0.050 vs. 0.602 ± 0.086, Nrf2 mRNA (gray value): 0.158 ± 0.007 vs. 0.089 ± 0.012, GSH (mg/g): 4.30 ± 0.22 vs. 3.84 ± 0.33, SOD ( μg/g): 0.454 ± 0.062 vs. 0.383 ± 0.040, CAT (ng/g): 8.98 ± 1.02 vs. 7.32 ± 1.28, all P < 0.05 ], and a decrease in MDA content (nmol/g: 6.56 ± 0.44 vs. 7.78 ± 0.41, P < 0.05). Regulation of PON1 gene can reduce MDA content, enhance SOD and CAT activities, increase GSH content, and it may also up-regulate Nrf2 mRNA expression to play a protective effect against oxidative stress of liver injury induced by dichlorvos poisoning.

Pharmacokinetics of OpdA, an organophosphorus hydrolase, in the African green monkey

Organophosphorus (OP) pesticides are a broad class of acetylcholinesterase inhibitors that are responsible for tremendous morbidity and mortality worldwide, contributing to an estimated 300,000 deaths annually. Current pharmacotherapy for acute OP poisoning includes the use of atropine, an oxime, and benzodiazepines. However, even with such therapy, the mortality from these agents are as high as 40%.Enzymatic hydrolysis of OPs is an attractive new potential therapy for acute OP poisoning. A number of bacterial OP hydrolases have been isolated. A promising OP hydrolase is an enzyme isolated from Agrobacterium radiobacter, named OpdA. OpdA has been shown to decrease lethality in rodent models of parathion and dichlorvos poisoning. However, pharmacokinetic data have not been obtained. In this study, we examined the pharmacokinetics of OpdA in an African Green Monkey model.At a dose of 1.2mg/kg the half-life of OpdA was approximately 40min, with a mean residence time of 57min. As expected, the half-life did not change with the dose of OpdA given: at doses of 0.15 and 0.45mg/kg, the half-life of OpdA was 43.1 and 38.9min, respectively. In animals subjected to 5 daily doses of OpdA, the residual activity that was measured 24h after each OpdA dose increased 5-fold for the 0.45mg/kg dose and 11-fold for the 1.2mg/kg dose.OpdA exhibits pharmacokinetics favorable for the further development as a therapy for acute OP poisoning, particularly for hydrophilic OP pesticides. Future work to increase the half-life of OpdA may be beneficial.

Acute dichlorvos poisoning induces hemorheological abnormalities in rabbits via oxidative stress

Dichlorvos is an important insecticide used largely. Some studies have demonstrated that organophosphate pesticide has effects on erythrocyte membrane structures, which is critical to erythrocyte function and hemorheology. The aim of the present study was to explore the effect of oxidative stress on hemorheological changes during dichlorvos poisoning in rabbits. Data indicated that after dichlorvos exposure the hematocrit adjusted viscosity at high shear rate increased and erythrocyte membrane fluidity decreased. Data obtained from plasma showed that lipid peroxidative substance-malonaldehyde was elevated and superoxide dismutase was reduced. In summary, oxidative stress does occur in dichlorvos poisoning and may lead to hemorheological alterations. The changes of hemorheology may be responsible for the pathophysiology of the dichlorvos poisoning.

Intramuscular ophthalmic homatropine vs. atropine to prevent lethality in rates with dichlorvos poisoning

Most hospitals lack a sufficient supply of atropine to treat, simultaneously, patients poisoned with multiple organophosphorous compound (OC) or nerve agent. The presence of a ubiquitous alternate antidote would prove useful if mass poisoning occurred. Our objective was to evaluate the effect of ophthalmic homatropine (Isopto Homatropine 5%) on survivability in a rat model of significant, acute OC poisoning. Sprague-Dawley rats were randomized to one of five pre-treatment groups (N = 10 per group). Prior to experimentation, animals were pre-treated with intramuscular (IM) injections of either atropine 5 mg/kg, atropine 10 mg/kg, homatropine 10 mg/kg, or homatropine 20 mg/kg. The control group received 0.3 mL normal saline IM. Five minutes later, 25 mg/kg of dichlorvos was subcutaneously administered. Mortality rates were compared using Fisher's Exact test. Kaplan-Meier survival curves with Logrank analysis was also performed. If alive at 120 minutes, survival was assumed, and the study was terminated. All rats pre-treated with normal saline, atropine 5 mg/kg, and homatropine 10 mg/kg died. Survival in the homatropine (20 mg/kg) and atropine (10 mg/kg) groups was 30% and 40% respectively. Times to death ranged between 4 and 12 minutes. Overall comparison of time to death revealed a statistically significant improvement for groups pre-treated with homatropine (20 mg/kg) and atropine (10 mg/kg). Pre-treatment with homatropine (20 mg/kg) was comparable with atropine (10 mg/kg) in preventing lethality in this rat model of acute OC poisoning.

Multiple Centrally Acting Antidotes Protect against Severe Organophosphate Toxicity

Accumulation of acetylcholine in the central nervous system is believed to account for the rapid lethality of organophosphate pesticides and chemical nerve agents. Diazepam is known to supplement atropine therapy, but its specific mechanism of action is uncertain. To test four centrally acting agents for early antidotal efficacy in severe dichlorvos poisoning in the murine model. The up-and-down method was used to dose four candidate antidotes: diazepam, xylazine, morphine, and ketamine. Antidotes were administered subcutaneously to unsedated adult Sprague-Dawley rats who were pretreated with 3 mg/kg intraperitoneal glycopyrrolate. All animals received 20 mg/kg of dichlorvos subcutaneously 5 minutes later. A blinded observer adjudicated the outcomes of 10-minute mortality and survival time. All animals pretreated with either no antidote (8/8 deaths) or glycopyrrolate alone (8/8) died within 10 minutes of dichlorvos injection. Pretreatment with diazepam (3/9 deaths), or xylazine (3/9), decreased lethality substantially (Fisher p = 0.007; median effective doses, 0.12 mg/kg and 3.0 mg/kg, respectively). Intermediate doses of morphine (3.1 to 5.5 mg/kg) resulted in survival, but higher doses did not, presumably because of excessive respiratory depression (7/11 deaths; p = 0.09). Ketamine (7/8 deaths) was ineffective as an antidote. Survival times also were prolonged in the diazepam and xylazine groups (log-rank p < 0.001) and, to a lesser degree, the morphine group (p = 0.07). Doses of diazepam, xylazine, and morphine below those used for deep sedation protect against severe dichlorvos poisoning, implying that several distinct central mechanisms are each sufficient to avert lethality. These findings suggest new possibilities for prophylaxis or therapy.

Therapeutic efficacy of pralidoxime chloride on acute dichlorvos poisoning

To study the therapeutic efficacy and mechanism of oxime drug, pralidoxime chloride (PAM-Cl), on acute dichlorvos (DDV) poisoning. The toxic signs and survival rate were recorded and ChE activity in blood was determined in treatment group with PAM-Cl and non-treatment group after DDV was given to rats and mice by gastrogavage; the therapeutic efficacy and reactivation of DDV-inhibited ChE by PAM-Cl were observed on the patients with acute DDV poisoning. (1) The alleviated and delayed toxic signs as well as higher survival rate were found in PAM-Cl treatment group compared with non-treatment group. (2) After the rats were exposed to DDV, the ChE activities of whole blood in different time within 24 h were statistically significantly higher in PAM-Cl treatment group than in non-treatment group (P < 0.05). (3) After PAM-Cl treatment, muscular fasciculation and other nicotinic signs in poisoned patients were disappeared and the inhibited blood ChE activities were gradually reactivated to normal level. PAM-Cl has therapeutic efficacy against acute toxicity of DDV through its reactivation of inhibited ChE.