Basic &amp Clinical Pharmacology &amp Toxicology (BASIC CLIN PHARMACOL )

Publisher: Nordisk selskab för farmakologi, Blackwell Publishing


Basic and Clinical Pharmacology and Toxicology is an independent journal, publishing original scientific research in all fields of toxicology, basic and clinical pharmacology. This includes experimental animal pharmacology and toxicology and molecular (-genetic), biochemical and cellular pharmacology and toxicology. It also includes all aspects of clinical pharmacology: pharmacokinetics, pharmacodynamics, therapeutic drug monitoring, drug/drug interactions, pharmacogenetics/-genomics, pharmacoepidemiology, pharmacovigilance, pharmacoeconomics, randomized controlled clinical trials and rational pharmacotherapy. For all compounds used in the studies, the chemical constitution and composition should be known, also for natural compounds.

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    Basic and Clinical Pharmacology and Toxicology website
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    Basic & clinical pharmacology & toxicology (Online), Basic and clinical pharmacology and toxicology, BCPT
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    Document, Periodical, Internet resource
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    Internet Resource, Computer File, Journal / Magazine / Newspaper

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Blackwell Publishing

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    • 'Blackwell Publishing' is an imprint of 'Wiley'
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Publications in this journal

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    ABSTRACT: Therapeutic modulation of pain with morphine and other opioids is associated with significant variation in both effects and adverse effects in individual patients. Many factors including gene polymorphisms have been shown to contribute to the interindividual variability in the response to opioids. The aim of this study was to investigate the significance of UGT 2 B 7, OPRM 1 and ABCB 1 polymorphisms for interindividual variability in morphine‐induced analgesia in patients undergoing hysterectomy. The frequency of these polymorphisms was also investigated in forensic autopsies as morphine is also a very commonly abused drug. Blood samples were collected from 40 patients following abdominal hysterectomy, 24 hr after initiation of analgesia through a patient‐controlled analgesia (PCA) pump. Samples were genotyped and analysed for morphine and its metabolites. We also genotyped approximately 200 autopsies found positive for morphine in routine forensic analysis. Patients homozygous for UGT 2 B 7 802C needed significantly lower dose of morphine for pain relief. The same trend was observed for patients homozygous for ABCB 1 1236T and 3435T, as well as to OPRM 1 118A. The dose of morphine in patients included in this study was significantly related to variation in UGT 2 B 7 T802C. Age was significantly related to both dose and concentration of morphine in blood. Regression analysis showed that 30% of differences in variation in morphine dose could be explained by SNPs in these genes. The genotype distribution was similar between the forensic cases and the patients. However, the mean concentration of morphine was higher in forensic cases compared to patients. We conclude that gene polymorphisms contribute significantly to the variation in morphine concentrations observed in individual patients.
    Basic &amp Clinical Pharmacology &amp Toxicology 11/2014; 115(5).
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    ABSTRACT: Drug cytotoxicity detected by high‐content analysis (HCA) of live, cultured, human hepatocytes concurs with human toxic potential. We assessed HCA effectiveness in vivo using human, lymphoma line (HuT‐78) and blood cells from healthy dogs and lymphomatous dogs treated with anticancer drugs: cytarabine, arsenic trioxide (AT), doxorubicin and mitoxantrone. DNA was stained with Hoechst‐33342, calcium with fluo‐4, mitochondria with TMRM and cell permeability with toto‐3. HuT‐78 and canine blood lymphocytes were treated 24 hr with 10 times increasing drug concentrations to determine concentration–response relationships to test agents. These showed hormesis (biphasic response) for TMRM and nuclear area. Fluorescence intensity was decreased with AT and mitoantrone but increased with cytarabine for TMRM, decreased from cell injury or anthracycline interaction for Hoechst‐33342 and decreased with AT and interfered with by doxorubicin for fluo‐4. Nuclear area increased with anthracyclines and AT. Mitochondria, calcium and nuclear area were affected in peripheral blood lymphocytes of lymphomatous dogs receiving chemotherapy: mitochondria were inhibited by acute treatment, but increased 2 weeks after treatment, as were ionized calcium, nuclear area and DNA. We conclude (i) concentration–response relationships are determinable in vitro for human and canine lymphocytes by HCA, (ii) cytotoxicity is detectable in vivo during and after anticancer drug treatment using canine blood lymphocytes: mitochondria are most affected, with smaller changes in calcium and nuclei and (iii) blood cell viability may be a biomarker for anticancer drug toxicity.
    Basic &amp Clinical Pharmacology &amp Toxicology 07/2014; 115(1).
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    ABSTRACT: Metformin is an antidiabetic drug recently shown to inhibit cancer cell proliferation and growth, although the involved molecular mechanisms have not been elucidated. In many cancer cells, high expression of thymidine phosphorylase (TP) and Excision repair cross‐complementation 1 (ERCC1) is associated with poor prognosis. We used A549 and H1975 human non‐small cell lung cancer (NSCLC) cell lines to investigate the role of TP and ERCC1 expression in metformin‐induced cytotoxicity. Metformin treatment decreased cellular TP and ERCC1 protein and mRNA levels by down‐regulating phosphorylated MEK1/2‐ERK1/2 protein levels in a dose‐ and time‐dependent manner. The enforced expression of the constitutively active MEK1 (MEK1‐CA) vectors significantly restored cellular TP and ERCC1 protein levels and cell viability. Specific inhibition of TP and ERCC1 expression by siRNA enhanced the metformin‐induced cytotoxicity and growth inhibition. Arachidin‐1, an antioxidant stilbenoid, further decreased TP and ERCC1 expression and augmented metformin's cytotoxic effect, which was abrogated in lung cancer cells transfected with MEK1/2‐CA expression vector. In conclusion, metformin induces cytotoxicity by down‐regulating TP and ERCC1 expression in NSCLC cells.
    Basic &amp Clinical Pharmacology &amp Toxicology 01/2013; 113(1).
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    ABSTRACT: The aim of this study was to investigate the possible protective role of hydrogen‐rich saline solution (HRSS) and WR‐2721 on the testicular damage induced by irradiation. Sprague‐Dawley rats were randomly divided into four groups. Group I served as control group. Rats in group II were exposed to the irradiation. The animals in group III and IV were injected intraperitoneally with HRSS (5 ml/kg) and WR‐2721 (200 mg/kg), respectively, 15 min. before the start of gamma irradiation. Testis weight, testis dimensions, sperm count, sperm motility, apoptosis index and biochemical assays were assessed after a 4‐day initiation of irradiation. Testis weight, testis dimensions, sperm count, sperm motility in group II were significantly lower compared with those in the control group, whereas they were higher in the HRSS and WR‐2721 group. Apoptosis index was significantly increased in group II. Treatment of rats with HRSS and WR‐2721 significantly reduced the apoptosis index. On the other hand, irradiation markedly decreased activities of SOD. Activities of SOD were significantly improved when treated with HRSS and WR‐2721. Significant increase in the MDA level was observed in group II. MDA levels of group III and IV were significantly lowered when compared with group II. HRSS also played a significant role in the recovery of serum testosterone levels. The results from this experimental study suggest that hydrogen has a possible protective effect against radiation‐induced testicular damage.
    Basic &amp Clinical Pharmacology &amp Toxicology 01/2013; 112(3).
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    ABSTRACT: Brefeldin A induces apoptosis in various cancer cells; however, the apoptotic process in cancer cells exposed to brefeldin A remains unclear. In addition, it is unclear whether brefeldin A‐induced apoptosis is mediated by the formation of reactive oxygen species. Furthermore, the effect of brefeldin A on the invasion and migration of human epithelial ovarian cancer cells has not been studied. Therefore, we investigated the effect of brefeldin A on apoptosis, cell adhesion and migration using the human epithelial ovarian carcinoma cell lines OVCAR‐3 and SK‐OV‐3. The results suggest that brefeldin A may induce apoptotic cell death in ovarian carcinoma cell lines by activating the mitochondrial pathway and the caspase‐8‐ and Bid‐dependent pathways. The apoptotic effect of brefeldin A seems to be mediated by formation of reactive oxygen species and depletion of GSH, which results in the activation of apoptotic caspases. Brefeldin A inhibited foetal bovine serum‐induced adhesion and migration of OVCAR‐3 cells. Brefeldin A may prevent the foetal bovine serum‐induced cell adhesion and migration by limiting the focal adhesion kinase‐dependent activation of cytoskeletal‐associated components.
    Basic &amp Clinical Pharmacology &amp Toxicology 01/2013; 113(5).
  • Basic &amp Clinical Pharmacology &amp Toxicology 01/2013; 113:38.
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    ABSTRACT: Glutamate transporter‐1 (GLT‐1) plays a dual role in glutamate transportation: both normally devotion to the clearance of glutamate and during some pathological conditions extruding glutamate to the extracellular space. Therefore, it is uncertain whether increased expression of GLT‐1 will actually be helpful against glutamate excitotoxicity. In this study, GLT‐1 up‐regulation was induced by ceftriaxone, and L‐glutamate was added to induce glutamate toxicity in primary cultured rat cortical cells. The results showed that up‐regulated GLT‐1 induced by 1 μM ceftriaxone for 2 days markedly increased cell viability, decreased apoptotic cell death and alleviated ultrastructural damage induced by 50 μM glutamate 15 min. as well as promoted L‐[3H]‐glutamate uptake in cultured cells. GLT‐1 up‐regulation had no effect on the intracellular free calcium concentration ([Ca2+]i) in the resting situation, while relieved intracellular calcium overloading by reducing the elevation and promoting the recovery of [Ca2+]i following stimulation of 50 μM glutamate for 2 min. Applying 100 μM dihydrokainic acid (GLT‐1 antagonist) 30 sec. before glutamate eliminated the above effect of GLT‐1 up‐regulation on [Ca2+]i. In conclusion, GLT‐1 up‐regulation induced by ceftriaxone plays a positive glutamate transporting role against glutamate toxicity in primary cultured rat cortical cells.
    Basic &amp Clinical Pharmacology &amp Toxicology 01/2013; 112(1).
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    ABSTRACT: Facilitation of spinal GABAergic inhibition with benzodiazepines (BZDs) reverses pain sensitization in animals; however, the use of BZDs in man is limited by their sedative effect. The antihyperalgesic effects of GABAA agonists are mediated by GABAA receptors containing α2 subunits, whereas sedation is linked to α1 subunit‐containing receptors. α2 and α3 selective GABAA receptor modulators have been tested in animals but are not yet available for use in human beings. Clobazam is a 1,5‐BZD, which exhibits less cognitive side effects than other benzodiazepines. Here, we studied its antihyperalgesic effects in a mouse model of neuropathic pain. Clobazam showed a dose‐dependent antihyperalgesic effect in the chronic constriction injury (CCI) model of neuropathic pain, peaking at 1 hr after administration and lasting for 4 hr with no relevant sedation at a dose of 3 mg/kg. At higher doses, the antihyperalgesic effect was stronger, but sedation became significant. The blood and brain kinetics of clobazam were linear over the range of doses tested with a short half‐life of the parent compound and a ready penetration of the blood–brain barrier. Clobazam blood concentrations decreased rapidly, falling below the limit of detection at 120 min. after drug application. Its main metabolite, N‐desmethyl‐clobazam, showed more delayed and prolonged pharmacokinetics, partly explaining why antihyperalgesia persisted when clobazam was no longer detectable in the blood. Considering its therapeutic margin and its pharmacokinetic properties, clobazam would be a valuable compound to assess the role of the GABAergic pathway in pain transmission in human beings.
    Basic &amp Clinical Pharmacology &amp Toxicology 01/2013; 112(3).
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    ABSTRACT: Curcumin is a well‐known component of traditional turmeric (Curcuma longa), which has been reported to prevent obesity and diabetes. However, the effect of curcumin on hepatic lipid metabolism remains unclear. The aim of this study was to examine the effects of curcumin on hepatic steatosis in high‐fat/cholesterol diet (HFD)‐induced obese mice. Male C57BL/6J mice were fed a normal diet (ND), HFD or HFD with 0.15% curcumin (HFD+C) for 11 weeks. We found that curcumin significantly lowered the body‐weight and adipose tissue weight of mice in the HFD+C group compared with the findings for the HFD group (p p Document Type: Research Article DOI: Publication date: September 1, 2013 More about this publication? Formerly Pharmacology & Toxicology $(document).ready(function() { var shortdescription = $(".originaldescription").text().replace(/\\&/g, '&').replace(/\\, '<').replace(/\\>/g, '>').replace(/\\t/g, ' ').replace(/\\n/g, ''); if (shortdescription.length > 350){ shortdescription = "" + shortdescription.substring(0,250) + "... more"; } $(".descriptionitem").prepend(shortdescription); $(".shortdescription a").click(function() { $(".shortdescription").hide(); $(".originaldescription").slideDown(); return false; }); }); Related content In this: publication By this: publisher In this Subject: Ecology , Pharmacology , Toxicology By this author: Um, Min Young ; Hwang, Kwang Hyun ; Ahn, Jiyun ; Ha, Tae Youl GA_googleFillSlot("Horizontal_banner_bottom");
    Basic &amp Clinical Pharmacology &amp Toxicology 01/2013; 113(3).
  • Basic &amp Clinical Pharmacology &amp Toxicology 11/2012; 111(S1):25.
  • Basic &amp Clinical Pharmacology &amp Toxicology 11/2012; 111(S1):26.
  • Basic &amp Clinical Pharmacology &amp Toxicology 11/2012; 111(S1):25.
  • Basic &amp Clinical Pharmacology &amp Toxicology 06/2011; 109(SI Suppl 1-ISSN: 1742-7835):105.
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    Basic &amp Clinical Pharmacology &amp Toxicology 01/2011; 108(5).
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    ABSTRACT: Popolis (bee glue) is a resinous or sometimes wax-like bee hive product that has been used by man since ancient times for its pharmaceutical properties. The antibacterial and antifungal activities are the most popular and among the most extensively investigated biological actions of propolis. ermatophytosis refers to the disease of the skin, hair and nail which caused by dermatophytes. Topical or systemic treatments have been empirically administered, although such drugs are widely used, some of them have been reported as ineffective and even toxic to the host and sometimes it takes time to be cured. Recently, propolis has been attracted the attention of researchers due to its various biological activities and therapeutic properties. The aim of this study was making topical cream from propolis for treatment of dermatophytic infections. Material and methods: For making of different formulations, we used from a base formulation, and then with adding the other materials and some variations established in the base formulation, finally 25 formulations were provided. All of formulations were examined in terms of consistency, stability, PH average, appearance, microbial studies and some other features of cream and the best formulation with the best efficacy was selected. Results: The selected formulation had a very good effect for treatment of experimental dermatophytosis in rabbits in comparison with synthetic products such as some azoles. Conclusion: The natural products are very effective for treatment of many fungal infections and also in comparison with synthetic drugs are more inexpensive and have lower side effects.
    Basic &amp Clinical Pharmacology &amp Toxicology 07/2010; 107(1).