Protective effect of physostigmine and neostigmine against acute toxicity of parathion in rats

The effects of physostigmine and neostigmine on the parathin induced toxicity were examined in adult female rats. Physostigmine (100 μg/kg, ip) or neostigmine (200 μg/kg, ip) inhibited acetylcholinesterase (AChE) and cholinesterase (ChE) activities in blood, brain and lung when the enzyme activity was measured 30 min after the treatment. At the doses of two carbamates equipotent on brain AChE, neostigmine showed greater inhibition on peripheral AChE/ChE. The enzyme activity returned to normal in 120 min following the carbamates except in the lung of rats treated with neostigmine. Carbamates administered 30 min prior to parathion (2 mg/kg) antagonized the inhibition of AChE/ChE by parathion when the enzyme activity was measured 2 hr following parathion. Neostigmine showed greater protective effect on peripheral AChE/ChE. The effect of either carbamate on AChE/ChE was not significant 2 hr beyond the parathion treatment. Carbamates decreased the mortality of rats challenged with a lethal dose of parathion (4 mg/kg, ip) either when treated alone or in combination with atropine (10 mg/kg, ip). Lethal action of paraoxon (1.5 mg/kg, ip), the active metabolite of parathion, was also decreased by the carbamate treatment indicating that the protection was not mediated by competitive inhibition of metabolic conversion of parathion to paraoxon. The results suggest that carbamylation of the active sites may not be the sole underlying mechanism of protection provided by the carbamates.     

The effect of fluoride on the scavenging of organophosphates by human butyrylcholinesterase in buffer solutions and human plasma

Fluoride ion is a reversible inhibitor of human butyrylcholinesterase (HuBChE) that is a viable drug candidate against organophosphates (OPs) toxicity. Since large numbers of communities in many countries are occasionally exposed to relatively high amount of fluoride, its effect on the kinetics of inhibition of HuBChE by OPs was investigated. In saline phosphate, pH 7.4, fluoride in the lower millimolar range significantly slowed the inhibition of HuBChE by paraoxon, DFP, echothiophate, soman, sarin, and VX. The kinetics of the inhibition was found consistent with the formation of a reversible fluoride-HuBChE complex that is at least 25-fold less active towards phosphorylation or phosphonylation than the free enzyme. Heat inactivation experiments indicate that the binding of fluoride to HuBChE probably involves enhanced cross-domain interaction via hydrogen bonds formation that may decrease enzyme activity. In spite of distinct structural differences among the OP used, the dissociation constants of the fluoride-HuBChE reversible complex varied over a narrow range (KF, 0.31-0.70 mM); however, KF in human plasma increased to 2.75-3.40 mM. 19F-NMR spectroscopy revealed that fluoride ion is complexed to plasma components, an observation that explains in part the apparent increase in KF. Results suggest that an estimate of the relative decrease in the rate of OPs sequestration in presence of fluoride can be obtained from the fraction of the free HuBChE (1 + [F]/K(F))(-1). Considering KF values in human plasma, it is concluded that the scavenging efficacy of OPs by HuBChE is not compromised by the normal concentration range of circulating fluoride ions.     

Protective effect of enalapril on vascular reactivity of the rat aorta

Cardiovascular complications are the major cause of morbidity and mortality in patients with diabetes mellitus (DM). Strategies that interrupt the renin-angiotensin system have been shown to reduce the ensuing threatening risk factors. The present study was carried out to investigate the effect of subchronic administration of enalapril on the aortic reactivity of streptozotocin (STZ)-diabetic rats. For this purpose, STZ-diabetic rats received enalapril (10 and 20 mg/kg ip) daily for 2 months. Contractile responses to phenylephrine (PE) and relaxation responses to acetylcholine (Ach) and isosorbide dinitrate (ISD) were obtained from aortic rings. Concentration-response curves from enalapril-treated diabetic (ED) rats to PE were attenuated as compared to vehicle-treated diabetics (VD), especially at a dose of 20 mg/kg for enalapril. In addition, endothelium-dependent relaxation responses induced by Ach was significantly higher in ED rats as compared to diabetic ones. The endothelium-independent relaxation responses for ISD were also found not to be significantly different among the groups. Therefore, subchronic treatment of diabetic rats with enalapril in a dose-dependent manner could prevent the functional changes in vascular reactivity in diabetic rats.     

Spectroscopic and chromatographic evidences of NADPH in human placental extract used as wound healer

An aqueous extract of human placenta, which is used as wound healer, has been investigated in terms of fluorescence properties. When excited at 340 nm, it results in fluorescence emission having maxima around 436 nm, which is fairly specific for nicotinamide adenine dinucleotide, reduced form (NADH) and nicotinamide adenine dinucleotide phosphate, reduced form (NADPH). The excitation spectra, having emission at 440 nm, show patterns comparable to these nucleotides. Thin layer chromatography and reversed-phase (RP) HPLC confirm presence of only NADPH in the extract. The emission and excitation patterns of NADPH purified after HPLC resemble exactly with the reference compound. Its content has been estimated to be 0.018±0.003 mg/ml based on fluorescence emission with respect to a standard calibration curve (n=6). Biological functionality of NADPH in the extract has been confirmed by glutathione reductase assay (n=5).     

Toxicologic significance of histologic change in the larynx of the rat following inhalation exposure: a critical review

The larynx is a site in the respiratory tract of animals that often shows a response to inhaled substances. In many cases, the most sensitive endpoint in repeated dose inhalation studies is squamous metaplasia (often of minimal severity) of the larynx. The U.S. Environmental Protection Agency has speculated that squamous metaplasia in the rodent larynx might be a pre-neoplastic lesion or a precursor to other serious effects and has proposed to use the effect of squamous metaplasia occurring in subchronic inhalation toxicology studies as a toxicologic endpoint for use in quantitative risk assessment [U.S. Environmental Protection Agency, 2006a. Reregistration Eligibility Decision for MGK-264, U.S. Environmental Protection Agency, 2006b,Reregistration Eligibility Decision for Piperonyl Butoxide, U.S. Environmental Protection Agency, 2006c. Reregistration Eligibility Decision for Pyrethrins]. To reach a conclusion as to its significance, we sought to establish the nature of this effect in the relevant context of rodent inhalation studies.A comprehensive review of the literature shows that laryngeal metaplasia can be produced by a wide range of chemically dissimilar substances, and even by “non-chemical” means such as irritation by aerosols and particles, and dehydration by alcohols or low humidity air. There is no published evidence that this effect is pre-neoplastic and it is clearly and repeatedly characterized as an adaptive response. Moreover, the well-differentiated character of laryngeal squamous metaplasia, the reversibility of incidence and severity of it during recovery periods, combined with no significant clinical observations and the lack of progression over time indicates that this response is adaptive and should not be considered to be indicative of significant human risk. We therefore conclude that squamous metaplasia of the rodent larynx is not a relevant toxicologic endpoint.     

A simplified in vitro preparation of the corpus cavernosum as a tool for investigating erectile pharmacology in the rat

This work describes a simple technique for the assessment of corpus cavernosum function in a species, the rat, representing a convenient model for basic research. We obtained measurable and reproducible responses to different pharmacological agents as well as to electrical field stimulation. In view of the present results we conclude that isolation of the erectile tissue together with the septum may constitute a valuable experimental tool for investigating both local erectile mechanisms and the action of drugs, in the rat corpus cavernosum. Data obtained in the presence of -nitro- -arginine and methylene blue further reinforce the concept that nitric oxide may be involved in the process of erection in the rats as well as in other animal species.     

Pre- and post-treatment effect of physostigmine on soman-inhibited human erythrocyte and muscle acetylcholinesterase in vitro

Standard treatment of organophosphorus (OP) poisoning includes administration of an antimuscarinic (e.g., atropine) and of an oxime-based reactivator. However, successful oxime treatment in soman poisoning is limited due to rapid aging of phosphylated acetylcholinesterase (AChE). Hence, the inability of standard treatment procedures to counteract the effects of soman poisoning resulted in the search for alternative strategies. Recently, results of an in vivo guinea pig study indicated a therapeutic effect of physostigmine given after soman. The present study was performed to investigate a possible pre- and post-treatment effect of physostigmine on soman-inhibited human AChE given at different time intervals before or after perfusion with soman by using a well-established dynamically working in vitro model for real-time analysis of erythrocyte and muscle AChE. The major findings were that prophylactic physostigmine prevented complete inhibition of AChE by soman and resulted in partial spontaneous recovery of the enzyme by decarbamylation. Physostigmine given as post-treatment resulted in a time-dependent reduction of the protection from soman inhibition and recovery of AChE. Hence, these date indicate that physostigmine given after soman does not protect AChE from irreversible inhibition by the OP and that the observed therapeutic effect of physostigmine in nerve agent poisoning in vivo is probably due to other factors.     

Protective effect of recombinant human erythropoietin against cisplatin-induced oxidative stress and nephrotoxicity in rat kidney

Cisplatin (Cisp) is one of the most widely used chemotherapeutic agents for the treatment of several human malignancies. The efficacy of Cisp is dose dependent and at higher doses serious kidney injury may occur. Recombinant human erythropoietin (rhEPO) has recently been shown to exert an important cytoprotective effect in experimental brain injury and ischemic acute renal failure. The aim of the present study was to explore whether rhEPO administration is protective against Cisp-induced oxidative damage and renal injury. Our results showed that Cisp induced a marked oxidative stress and renal failure. Administration of rhEPO (pre-, co- or postadministration with regard to Cisp) decreased oxidative damage induced by Cisp. Recombinant human EPO reduced malondialdehyde and protein carbonyl levels. Recombinant human EPO also prevented glutathione depletion and ameliorated the increased catalase activity induced by Cisp treatment. Furthermore, rhEPO restored creatinine and blood urea nitrogen levels increased by Cisp. We concluded that rhEPO administration especially in pretreatment condition protected rats against Cisp-induced renal oxidative stress and nephrotoxicity.     

川芎嗪对大鼠肝脏缺血再灌注损伤的保护作用

目的：研究川芎嗪对大鼠肝脏缺血再灌注损伤的保护作用及其机制。方法：SD大鼠随机分为5组：空白对照组、假手术组、缺血再灌注组、生理盐水组和川芎嗪组。其中空白对照组大鼠直接处死;假手术组开腹后60 min关闭腹腔;缺血再灌注组阻断70%肝血流60 min,再灌注4 h;生理盐水组予腹腔内注射生理盐水8 ml/kg,30 min后阻断70%肝血流60 min,再灌注4 h;川芎嗪组予腹腔内注射川芎嗪80 mg/kg,30 min后阻断70%肝血流60 min,再灌注4 h。速率法测血清丙氨酸氨基转移酶（alanine aminotransferase,ALT）和天冬氨酸氨基转移酶（aspartate aminotransferase,AST）活性,酶联免疫吸附法（ELISA）测血白介素-1（IL-1）、白介素-10（IL-10）和肿瘤坏死因子-α（TNF-α）水平。苏木素-伊红染色观察肝脏病理改变。结果：川芎嗪组血清ALT、AST、IL-1和TNF-α水平均比缺血再灌注组和生理盐水组明显降低（P〈0.05）,而IL-10则明显高于缺血再灌注组和生理盐水组（P〈0.05）。病理结果显示,川芎嗪组大鼠肝细胞损伤较缺血再灌注组和生理盐水组为轻。结论：川芎嗪对大鼠肝脏缺血再灌注损伤具有保护作用,其机制可能与抑制炎性细胞因子生成及促进抗炎细胞因子表达有关。     

Protective effect of curcumin against cytomegalovirus infection in Balb/c mice

Curcumin has been found to suppress the activity of human cytomegalovirus (HCMV) in vitro, whereas its protective effects against HCMV infection in vivo remain unclear. In this study, we aimed to investigate the protective effects of curcumin against HCMV infection in Balb/c mice. Mice were randomly divided into the control, model, model + ganciclovir (positive control), and model + high-dose, model + middle-dose, and model + low-dose curcumin groups. In the model groups, each mouse was given HCMV by tail injection intravenously. Positive control animals were given ganciclovir. Animals in the curcumin treatment groups were given different concentrations of curcumin. The anti-HCMV activities of ganciclovir and curcumin were assessed by serological examination and pathology. Ganciclovir and curcumin treatment reduced the HCMV IgM level and HCMV DNA load; decreased the serum levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), creatine kinase (CK), and lactate dehydrogenase (LDH) as well as tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) generation in infected mice. These treatments also suppressed malondialdehyde (MDA) content and upregulated superoxide dismutase (SOD) and glutathione (GSH) levels. In addition, both treatments prevented pathological changes of the lung, kidney, liver, and heart tissues in infected mice. Our findings indicate that curcumin protected Balb/c mice against HCMV infection possibly by its anti-inflammatory and antioxidant effects.     

Continuous administration of heparin in patients with deep vein thrombosis can increase plasma levels of diamine oxidase

Besides its anticoagulant activity, the sulfated polysaccharide heparin has numerous other biological effects. Especially the antiinflammatory and immunoregulatory properties of heparin may be associated with its ability to release the histamine-degrading enzyme diamine oxidase (DAO) from tissue-bound sites into the circulation. Whereas DAO activity is at the limits of detection in normal human plasma, the application of heparin leads to a significant increase of plasma DAO activity. However, previously, only the effect of bolus injection of unfractionated heparin (UFH) had been studied. To investigate DAO release during continuous heparin infusion, 28 patients with deep vein thrombosis (DVT) undergoing heparin therapy were analyzed. Whereas continuous heparin infusion did not lead to any increase of plasma DAO activity in 12 patients (43%), 6 patients (21%) showed a single elevated and 10 patients (36%) permanently elevated plasma DAO activity. The groups of patients exhibiting different DAO release responses did not differ in age, sex, body weight, concomitant diseases, heparin infusion rates, coagulation indices, location and extension of thrombosis, or clinical outcome. However, the rate of idiopathic DVT was significantly higher in the group of patients releasing DAO. This study shows, for the first time, that continuous heparin infusion can lead to DAO release and that individuals exhibit considerable differences in their release response. Although the significance of heparin-induced DAO release needs further clarification, our results indicate that postheparin plasma DAO activity could be an interesting parameter correlated with idiopathic DVT.     

Protective effect of copper against pancreatic insult in streptozotocin-induced diabetogenic rat

The present study examined the alterations in endogenous oxy-radical scavenging system of pancreatic tissue associated with the dose of 45 mg/kg streptozotocin (STZ) alone or with various combinations. The activities of pancreatic Mn-superoxide dismutase (SOD) and catalase were no apparent changes in the other groups except for the Cu(II) 4 mg/kg pretreated group. The presence of 4 mg/kg of Cu(II) with or without 125 mg/kg of diethylenetriaminepentaacetic acid (DTPA) markedly attenuated the fall in activity of Cu, Zn-SOD by STZ stress. In particular, STZ-induced superoxide generation was dramatically abolished by prior administration of Cu(II) 4 mg/kg. Conclusively, We suggest the possible involvement that copper may enhance the defense mechanism of pancreatic oxidative damage by STZ challenge.     

Protective effect of metoclopramide against organophosphate‐induced apoptosis in the murine skin fibroblast L929

This study was performed to evaluate the protective efficacy of metoclopramide (MCP) against the organophosphates paraoxon (POX)‐ and malathion (MLT)‐induced apoptosis in the murine L929 skin fibroblasts. L929 cells were exposed to either POX (10 nm ) or 1.0 μm MLT in the absence and presence of increased concentrations of MCP. The protective effect of MCP on these organophosphate‐stimulated apoptotic events was evaluated by flow cytometry analysis after staining with annexin‐V/propidium iodide, processing and activation of the executioner caspase‐3, cleavage of the poly‐ADP ribose polymerase, fragmentation of the nucleosomal DNA and disruption of the mitochondrial membrane potential (Δψ). Our results showed that increased doses of MCP alone (≥10 μm ) did not induce apoptosis or activation of caspase‐3. Pretreatment of the cells with MCP attenuated all the apoptotic events triggered by the organophosphate compounds in a dose‐dependent manner reaching ~70–80% protection when they were preincubated at 1 and 5 μm of the drug before the addition of POX and MLT, respectively. Interestingly, MCP did not offer a significant protective effect against the cytotoxicity of tumor necrosis factor‐α, cisplatinum, etoposide or paclitaxel, which stimulate apoptosis by various mechanisms, suggesting that the anti‐apoptotic effect of the drug is specific to organophosphates. The strong and specific anti‐apoptotic activity of subclinical doses of MCP against the cytotoxicity of organophosphate compounds suggests its potential clinical application in treating their poisoning.     

Use of mRNA expression to detect the induction of drug metabolising enzymes in rat and human hepatocytes

It is important to investigate the induction of cytochrome P450 (CYP) enzymes by drugs. The most relevant end point is enzyme activity; however, this requires many cells and is low throughput. We have compared the CYP1A, CYP2B and CYP3A induction response to eight inducers in rat and human hepatocytes using enzyme activities (CYP1A2 (ethoxyresorufin), 2B (benzoxyresorufin for rat and bupropion for human) and CYP3A (testosterone)) and Taqman™ Low Density Array (TLDA) analysis. There was a good correlation between the induction of CYP1A2, CYP2B6 and CYP3A4 enzyme activities and mRNA expression in human hepatocytes. In contrast, BROD activities and mRNA expression in rat hepatocytes correlated poorly. However, bupropion hydroxylation correlated well with Cyp2b1 expression in rat hepatocytes. TLDA analysis of a panel of mRNAs encoding for CYPs, phase 2 enzymes, nuclear receptors and transporters revealed that the main genes induced by the 8 compounds tested were the CYPs. AhR ligands also induced UDP-glucuronosyltransferases and glutathione S-transferases in rat and human hepatocytes. The transporters, MDR1, MDR3 and OATPA were the only transporter genes significantly up-regulated in human hepatocytes. In rat hepatocytes Bsep, Mdr2, Mrp2, Mrp3 and Oatp2 were up-regulated. We could then show a good in vivo:in vitro correlation in the induction response of isolated rat hepatocytes and ex-vivo hepatic microsomes for the drug development candidate, EMD392949. In conclusion, application of TLDA methodology to investigate the potential of compounds to induce enzymes in rat and human hepatocytes increases the throughput and information gained from one assay, without reducing the predictive capacity.     

大蒜新素对脑缺血再灌注大鼠海马的保护作用

目的探讨大蒜新素对脑缺血再灌注海马组织的保护作用与钙转运的关系。方法采用4血管闭塞法制备大鼠全脑缺血再灌注模型,大蒜新素10,20和30mg.kg-1分2次于缺血前30min和再灌注后10min经尾静脉注入,每次注射总量的1/2。再灌注后24h取大鼠海马,甲苯胺蓝染色显微镜下观察海马组织学改变及存活神经元密度;定磷比色法测定Ca2+-转运ATP酶活性;原子吸收法测定钙含量。结果全脑缺血10min再灌注24h时,海马CA1区形态学改变明显,神经元密度明显降低;海马组织Ca2+-转运ATP酶活性降低;组织钙含量显著增加。静脉给予大蒜新素可使缺血再灌注海马组织形态学改变程度明显减轻,存活神经元密度增加,Ca2+-转运ATP酶活性增加,组织钙含量降低。结论大蒜新素对全脑缺血再灌注后海马组织具有明显的保护作用;增加Ca2+-转运ATP酶活性、减少组织钙含量可能是其保护作用的机制之一。     

Protective effect of donepezil in primary-cultured rat cortical neurons exposed to N-methyl-d-aspartate (NMDA) toxicity

Donepezil has a neuroprotective effect against oxygen-glucose deprivation injury and glutamate toxicity in cultured cortical neurons. In this study, we further characterized the neuroprotective properties of donepezil in rat cortical cell cultures using glutamate receptor-specific agonists (N-methyl-d-aspartate (NMDA), alpha-amino-3-hydroxy-5-methylisoxazolepropionate (AMPA) and kainate). Pretreatment with donepezil (1 microM) for 12 h significantly decreased the lactate dehydrogenase (LDH) release in response to NMDA (100 microM) by 43.8%, and reduced the LDH release in response to kainate (100 microM) and AMPA (100 microM) by 11.9% and 7.5% (without statistical significance), respectively. Donepezil appeared to inhibit LDH release in a concentration-dependent manner at 0.1-10 microM. Cortical neurons exposed to NMDA retained a normal morphological appearance in the presence of 10 microM donepezil. In binding assay for glutamate receptors, donepezil at 100 microM only slightly inhibited binding to the glycine and polyamine sites on NMDA receptor complex. On the other hand, 12 h pretreatment with donepezil at 10 and 100 microM significantly decreased the NMDA-induced increase of intracellular calcium concentration ([Ca2+]i). In conclusion, our results show that donepezil has protective activity against NMDA toxicity in cortical neurons, and this neuroprotection seems to be partially mediated by inhibition of the increase of [Ca2+]i.     

Protective effect of pyruvate against ethanol-induced apoptotic neurodegeneration in the developing rat brain

Exposure to alcohol during the early stages of brain development can lead to neurological disorders in the CNS. Apoptotic neurodegeneration due to ethanol exposure is a main feature of alcoholism. Exposure of developing animals to alcohol (during the growth spurt period in particular) elicits apoptotic neuronal death and causes fetal alcohol effects (FAE) or fetal alcohol syndrome (FAS). A single episode of ethanol intoxication (at 5 g/kg) in a seven-day-old developing rat can activate the apoptotic cascade, leading to widespread neuronal death in the brain. In the present study, we investigated the potential protective effect of pyruvate against ethanol-induced neuroapoptosis. After 4 h, a single dose of ethanol induced upregulation of Bax, release of mitochondrial cytochrome-c into the cytosol, activation of caspase-3 and cleavage of poly (ADP-ribose) polymerase (PARP-1), all of which promote apoptosis. These effects were all reversed by co-treatment with pyruvate at a well-tolerated dosage (1000 mg/kg). Histopathology performed at 24 and 48 h with Fluoro-Jade-B and cresyl violet stains showed that pyruvate significantly reduced the number of dead cells in the cerebral cortex, hippocampus and thalamus. Immunohistochemical analysis at 24 h confirmed that ethanol-induced cell death is both apoptotic and inhibited by pyruvate. These findings suggest that pyruvate treatment attenuates ethanol-induced neuronal cell loss in the developing rat brain and holds promise as a safe therapeutic and neuroprotective agent in the treatment of neurodegenerative disorders in newborns and infants.     

Gamma scintigraphic evaluation of the fate of hydroxypropyl methylcellulose capsules in the human gastrointestinal tract

The fate (movement and disintegration) of hard novel hydroxypropyl methylcellulose (HPMC) two-piece capsules in the human gastrointestinal tract was investigated using a gamma scintigraphic imaging method. Two different prolonged-release formulations without an active ingredient were used. The capsules contained different viscosity grades of HPMC powder (HPMC K100 and HPMC K4M). The aim was to determine the main reason why the pharmacokinetic profiles of model drugs change when the diluent was changed to a higher viscosity grade. The results were compared with our previous pharmacokinetic studies with corresponding capsules containing metoclopramide hydrochloride or ibuprofen as a model drug. The first observation was that the HPMC capsules had a tendency to attach to the oesophagus. Therefore, it is recommended that the HPMC capsules as well as gelatine capsules be taken with a sufficient amount of water (150–200 ml) in an upright position and maintaining the upright position for several minutes. The viscosity grade of the HPMC did not affect the transit times of the capsules in the GI tract. The major differences between the two formulations were the complete disintegration times of the capsules and the spreading of the capsules to the large intestine. Most of the HPMC K100-based capsules were completely disintegrated during the 8 h study, whereas the HPMC K4M-based capsules still exhibited plug formations in the large intestine. Also the HPMC K100-based capsules spread better to the ascending colon than the HPMC K4M-based capsules. The faster disintegration of the HPMC K100-based capsules explains the differences in the pharmacokinetic profiles of the model drugs between the HPMC K100- and K4M-based capsules in our previous studies. The main absorption site of the drugs from the capsules studied here is probably the large intestine when taken in a fasting state.     

Protective effect of proteins derived from Calotropis procera latex against acute inflammation in rat

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尿多酸肽对人胃癌细胞SGC7901增殖的体外抑制作用

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