Pharmacology &amp Toxicology Journal Impact Factor & Information

Journal description

Pharmacology & Toxicology is an independent journal, publishing original scientific research in all fields of experimental pharmacology and toxicology, including biochemical, cellular and molecular pharmacology and toxicology. Manuscripts on clinical pharmacology and its aspects, pharmacodynamics and pharmacokinetics, are also accepted.

Current impact factor: 0.00

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5-year impact 0.00
Cited half-life 0.00
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Website Pharmacology & Toxicology website
Other titles Pharmacology and toxicology
ISSN 1600-0773
OCLC 66031455
Material type Periodical
Document type Journal / Magazine / Newspaper

Publications in this journal

  • Pharmacology &amp Toxicology 01/2012;

  • Pharmacology &amp Toxicology 05/2009; 15(4):373 - 383. DOI:10.1111/j.1600-0773.1959.tb00306.x

  • Pharmacology &amp Toxicology 05/2009; 15(4):384 - 394. DOI:10.1111/j.1600-0773.1959.tb00307.x

  • Pharmacology &amp Toxicology 03/2009; 73(1):60 - 62. DOI:10.1111/j.1600-0773.1993.tb01960.x
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    ABSTRACT: The pathophysiologic effects of anatoxin-a(s) from the cyanobacterium Anabaena flos-aquae NRC-525-17 were investigated in anaesthetized adult male Sprague Dawley rats given the toxin by continuous intravenous infusion until death. Rats (n=6) pretreated with atropine sulfate (50 mg/kg) intraperitoneally survived significantly longer (P<0.05) than non-atropinized rats (n = 6), suggesting that the muscarinic effects of anatoxin-a(s) were important in the lethal syndrome. In contrast to rats only given toxin, rats that were pretreated with atropine had a decrease in heart rate and mean blood pressure that followed profound reductions in respiratory tidal and minute volume, suggesting that neuromuscular blockade of the muscles of respiration was the cause of death. Even when survival time of rats was increased by pretreatment with atropine, phrenic nerve amplitude increased, indicating a lack of a depressive effect of anatoxin-a(s) on central mediation of respiration. Rats (n=3) continuously ventilated during toxin infusion survived a dose more than 4 fold greater than a consistently lethal dose of the toxin. Thus, the cardiovascular effects of anatoxin-a(s) alone could not account for the death of rats. Electromyographic activity recorded from the diaphragms of rats (n=5) during continuous toxin administration revealed an increase in muscular electrical activity that became more random and finally decreased prior to death, suggesting a toxin-induced neuromuscular blockade in vivo which ultimately was the cause of death of the anatoxin-a(s) dosed rats.
    Pharmacology &amp Toxicology 03/2009; 67(2):151 - 155. DOI:10.1111/j.1600-0773.1990.tb00802.x
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    ABSTRACT: The distribution of approximately equipotent doses of 14C-labelled clodronate (0.1 mmol/kg), etidronate (0.1 mmol/kg), and amidronate (0.015 mmol/kg), and also an equimolar dose of amidronate (0.1 mmol/kg), was studied in mice by measuring the 14C-activities in various tissues up to 360 days after a single intravenous injection. With the higher dose of amidronate the distribution could be, however, monitored only for 7 days because of the toxicity of the drug. The results indicate that there are major differences in the deposition of the bisphosphonates into soft tissues, while the disappearance from plasma and incorporation into bone are quite similar in terms of percentage of dose per g of tissue. However, the binding capacity of bone for clodronate and etidronate is many times greater than that for amidronate expressed as nmol of the drug per g of tissue. Amidronate deposits in the spleen and liver of mice, when injected in saline, whereas clodronate and etidronate do not. This agrees with the suggestion that amidronate, but not the other two, can interfere with the mononuclear phagocyte system of spleen and liver.
    Pharmacology &amp Toxicology 03/2009; 66(4):294 - 298. DOI:10.1111/j.1600-0773.1990.tb00750.x
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    ABSTRACT: The antidotal efficacies of chelators during acute cadmium intoxication has previously been examined in experiments where both a soluble cadmium salt and the chelator were administered parenterally. In the present study, PA, DMSA and related compounds were studied as oral antidotes during oral CdCl2 intoxication. According to the antagonistic effects noted on mortality, peristaltic toxicity and intestinal cadmium uptake, the relative efficacies of the compounds tested were: DMSA > PAD > DMPS > MSA > PA > NAPA. None of the chelators induced major changes in the organ distribution of absorbed cadmium, in particular no increased cerebral deposition of cadmium. This study indicates that, in oral cadmium intoxication in humans, orally administered DMSA would be likely to offer protection against the local toxicity of cadmium in the gastrointestinal tract as well as to reduce the risk of systemic toxicity of absorbed cadmium.
    Pharmacology &amp Toxicology 03/2009; 63(5):386 - 389. DOI:10.1111/j.1600-0773.1988.tb00973.x
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    ABSTRACT: N-nitrosooxprenolol (NO-oxprenolol) might be formed in the stomach of patients taking the β-adrenergic blocking drug, oxprenolol. This nitroso derivative has previously been shown to induce DNA damage and repair in both rat and human cultured hepatocytes. The results of the present study show that in the presence of co-cultured rat hepatocytes, 0.03 mM NO-oxprenolol produced a significant increase in the frequency of 6-thioguanine-resistant but not of ouabain-resistant mutants. No mutagenic activity was detected in the absence of metabolic activation. In mice, NO-oxprenolol (1 g/kg) increased the incidence of micronucleated cells in the liver but not in the bone marrow and the spleen. These results suggest that NO-oxprenolol, consistent with its chemical nature of nitrosamine, is biotransformed into short-lived reactive species.
    Pharmacology &amp Toxicology 03/2009; 71(2):154 - 158. DOI:10.1111/j.1600-0773.1992.tb00536.x
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    ABSTRACT: This investigation was aimed to study the effect of magnesium on 1–methyl–4–phenyl–1,2,3,6–tetrahydropyridine (MPTP)–induced neurotoxicity in mice. Four groups of mice were given magnesium sulfate (MgSO4.7H2O) in drinking water at four different concentrations of 0.0 g/l (control), 2.5 g/l (low), 5.0 g/l (medium) and 10.0 g/l (high) respectively for a period of 16 weeks; these animals also received MPTP (30 mg/kg, intraperitoneally daily) during the last five days of Mg treatment. Other four groups of mice were given similar dose regimen of MgSO4 but received injections of saline instead of MPTP. Seventy–two hr after the last dose of MPTP, neurobehavioural studies including locomotor activity, pole climbing test and heat nociception test were performed and striata were collected for the analysis of dopamine. The results of this study show that treatment of mice with MgSO4 or MPTP individually has no effect on their behaviour. Concomitant administration of low dose of MgSO4 (2.5 g/l) along with MPTP produced increase in motor activity and latency to heat stimuli; whereas medium and high doses of MgSO4 in combination with MPTP produced opposite (as compared to low dose) effects resulting in a decrease in motor activity and latency to heal stimuli and increase in pole climbing time. However, MgSO4 dose–dependently exacerbated MPTP–induced depletion of striatal dopamine. The mortality was drastically increased (30–55%) in the animals receiving combined treatments of MPTP and MgSO4 as compared to the mice treated with MPTP alone (12%). This study clearly points towards the ability of MgSO4 to modify MPTP–induced neurotoxicity.
    Pharmacology &amp Toxicology 03/2009; 82(5):218 - 222. DOI:10.1111/j.1600-0773.1998.tb01428.x

  • Pharmacology &amp Toxicology 03/2009; 72(s1):176 - 179. DOI:10.1111/j.1600-0773.1993.tb01688.x
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    Pharmacology &amp Toxicology 03/2009; 80(6):255 - 261. DOI:10.1111/j.1600-0773.1997.tb01970.x

  • Pharmacology &amp Toxicology 03/2009; 66(s3):144 - 148. DOI:10.1111/j.1600-0773.1990.tb02082.x
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    ABSTRACT: In order to study the effects of nicotine on liver, groups of rats were given nicotine doses that simulated those seen in chronic smoking (54 and 108 μmol/l of nicotine) for 10 days. A subgroup was also given a single subcutaneous injection of 6 g/kg of carbon tetrachloride (CCl4) shortly before the animals of the group were killed. Histology demonstrated a significant hepatotoxic effect in the group receiving 108 μmol/l of nicotine when compared with the control group in the form of fatty change, focal or confluent necrosis and dark-cell change. The effects in pregnant rats were less severe. Carbon tetrachloride alone induced significant fatty change and focal necrosis in non-pregnant rats but not in pregnant rats. Nicotine also aggravated the CCl4 induced pathological changes in livers of both non-pregnant and pregnant animals. Thus nicotine alone, when given at a concentration of 108 μmol/l, exerted hepatotoxic effects; the alkaloid also aggravated the hepatotoxicity of CCl4. Pregnant rats were more resistant to the hepatotoxic effects produced by nicotine and CCl4.
    Pharmacology &amp Toxicology 03/2009; 77(3):225 - 230. DOI:10.1111/j.1600-0773.1995.tb01017.x
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    ABSTRACT: Felodipine, a potent dihydropyridine calcium antagonist with a pronounced vascular selectivity, was given intravenously (0.006-0.025 μmol kg−1) to anaesthetized, open-chest dogs with denervated hearts. The result was a dose-dependent decrease in mean arterial pressure (MAP) and total peripheral resistance (TPR), while heart rate (HR), stroke volume (SV) and left ventricular end-diastolic pressure remained relatively unchanged. Cardiac tension work (TTI) and oxygen consumption (MVO2) were reduced, probably due to the decrease in afterload. The relative reduction of the coronary vascular resistance (CVR) was greater than that of TPR. The hypotensive effect of verapamil (0.05-0.20 μmol kg−1) was small and MAP decreased mainly via a decrease in HR and SV. Higher doses of verapamil which induced vasodilatation could not be given without the development of complete atrio-ventricular dissociation. Hydralazine (11-45 μmol kg−1) decreased TPR and CVR in parallel but the decrease in MAP was partly counteracted by a powerful increase in HR, SV and cardiac inotropy which was associated with elevated catecholamine levels in plasma. When MAP and HR were maintained constant by means of aortic balloon inflation and atrial pacing, felodipine markedly increased coronary blood flow and coronary sinus oxygen saturation while SV, TTI, inotropy and MVO2 remained relatively unchanged. It is concluded that felodipine markedly dilates peripheral resistance vessels, and in particular those in the coronary vascular bed, without any cardiodepressant effects.
    Pharmacology &amp Toxicology 03/2009; 68(4):310 - 315. DOI:10.1111/j.1600-0773.1991.tb01244.x
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    ABSTRACT: The possible role of vasodilatory prostanoids in the antihypertensive action of captopril was investigated in spontaneously hypertensive rats (SHR). Captopril (100 mg/kg/day for 5 days) decreased systolic blood pressure and increased water consumption, urine excretion and plasma renin activity (PRA). It also enhanced the urinary excretion of the prostacyclin metabolite 6-keto-PGF1α, but did not change the excretion of PGE2. Indomethacin (3 mg/kg/day), given both alone and in combination with captopril, reduced markedly the urinary excretions of 6-keto-PGF1α and PGE2 but did not alter PRA, compared with corresponding groups without indomethacin. The suppression of prostanoid synthesis caused by indomethacin did not affect the antihypertensive effect of captopril or the basal blood pressure in SHR. Neither did indomethacin influence drinking or urine excretion in SHR not receiving captopril, but it reduced the dipsogenic and diuretic effects of captopril. The results suggest that captopril augments the production of vasodilatory prostacyclin. Yet prostanoids have no significant role in the antihypertensive mechanism of captopril in SHR.
    Pharmacology &amp Toxicology 03/2009; 61(3):195 - 198. DOI:10.1111/j.1600-0773.1987.tb01802.x
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    ABSTRACT: Vasoactive agonists like adenosine-5′-triphosphate (ATP) increase intracellular Ca2+ ([Ca2+]i) in vascular endothelial cells with an initial peak due to inositol 1,4,5-triphosphate-mediated Ca2+ release from intracellular stores followed by a sustained plateau that is dependent on the presence of extracellular Ca2+, thus leading to an increased synthesis and release of prostacyclin and nitric oxide. We studied the effects of nucleotides on membrane potential and [Ca2+]i in confluent human microvascular cardiac endothelial cells obtained from patients with dilated cardiomyopathy. The whole-cell configuration of the patch-clamp technique and a confocal laser scanning microscope employing fluo-3 as a Ca2+ indicator were used. Both uridine-5′-triphosphate (UTP) and 2-methylthioadenosine-5′-triphosphate (2MeSATP) induced depolarizations in human microvascular cardiac endothelial cells and increased [Ca2+]i with a rank order of potency 2MeSATP>ATP=UPP (EC50 values (in μM) were 0.084 2MeSATP, 0.67 ATP and 1.1 UTP). This suggests that both P2u and P2y purinoceptors are present on human microvascular cardiac endothelial cells. Maximal [Ca2+]i responses of confluent human microvascular cardiac endothelial cell monolayers to UTP were lower when compared to 2MeSATP. Nucleotide-induced increases in [Ca2+]i consisted of a transient peak, which was also observed in the absence of extracellular Ca2+, and a sustained [Ca2+]i plateau. This plateau, which was not observed in all monolayers studied, was not markedly influenced by increasing extracellular [K+]. Previous incubation with thapsigargin abolished ATP-induced increases of [Ca2+]i. It is concluded that human microvascular cardiac endothelial cells express both P2y and P2u purinoceptors. P2 purinoceptor agonists release Ca2+ from intracellular thapsigargin-sensitive stores and stimulate capacitative Ca2+ influx pathways. K+ efflux through Ca2+-dependent K+ (Kca) channels does not play a major role in the regulation of nucleotide-induced Ca2+ influx in human microvascular cardiac endothelial cells, which might be related to an impaired function of the cells.
    Pharmacology &amp Toxicology 03/2009; 85(3):7 - 15. DOI:10.1111/j.1600-0773.1999.tb01056.x

  • Pharmacology &amp Toxicology 03/2009; 61(s3):1 - 55. DOI:10.1111/j.1600-0773.1987.tb01921.x