[The effect of galvanization on drug pharmacokinetics and pharmacodynamics (the problem of "interstitial" electrophoresis)].
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Animals↗
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Potassium-ion conduction noise in squid axon membrane.
Spectral analysis (1-1000 Hz) of spontaneous fluctuations of potential and current in small areas of squid (Loligo pealei) axon shows two forms of noise: f-1 noise occurs in both excitable and inexcitable axons with an intensity which depends upon the driving force for potassium ions. The other noise has a spectral form corresponding to a relaxation process, i.e. its asymptotic behavior at low frequencies is constant, and at high frequencies it declines with a slope of -2. This latter noise occurs only in excitable axons and was identified in spectra by (1) its disappearance after reduction of K+ current by internal perfusion with solutions containing tetraethylammonium (TEA+), Cs+ or reduced [Ki+] and (2) its insensitivity to block of Na+ conduction and active transport. The transition frequency of relaxation spectra are also voltage and temperature dependent and relate to the kinetics of K+-conduction in the Hodgkin-Huxley formulation. These data strongly suggest that the relaxation noise component arises from the kinetic properties of K+ channels. The f-1 noise is attributed to restricted diffusion in conducting K+ channels and/or leakage pathways. In addition, an induced K+ conduction noise associated with the binding of TEA+ and triethyldecylammonium ion to membrane sites is described. Measurement of the induced noise may provide an alternative means of characterizing the kinetics of interaction of these molecules with the membrane and also suggests that these and other pharmacological agents may not be useful in identifying noise components related to the sodium conduction mechanism which, in these experiments, appears to be much lower in intensity than either the normal K conduction or induced noise components.
Animals↗
Sodium fluxes in internally dialyzed squid axons.
The effects which alterations in the concentrations of internal sodium and high energy phosphate compounds had on the sodium influx and efflux of internally dialyzed squid axons were examined. Nine naturally occurring high energy phosphate compounds were ineffective in supporting significant sodium extrusion. These compounds were: AcP, PEP, G-3-P, ADP, AMP, GTP, CTP, PA, and UTP.(1) the compound d-ATP supported 25-50% of the normal sodium extrusion, while ATP supported 80-100%. The relation between internal ATP and sodium efflux was nonlinear, rising most steeply in the range 1 to 10 microM and more gradually in the range 10 to 10,000 microM. There was no evidence of saturation of efflux even at internal ATP concentrations of 10,000 microM. The relation between internal sodium and sodium efflux was linear in the range 2 to 240 mM. The presence of external strophanthidin (10 microM) changed the sodium efflux to about 8-12 pmoles/cm(2) sec regardless of the initial level of efflux; this changed level was not altered by subsequent dialysis with large concentrations of ATP. Sodium influx was reduced about 50 % by removal of either ATP or Na and about 70 % by removing both ATP and Na from inside the axon.
Adenine Nucleotides↗
Pharmacological assessment of 3-tert-butylsydnone.
The pharmacological effects of the mesoionic derivative, 3-tert-butylsydnone, were investigated. Administration to rats caused clonic convulsions. The CD50 of 3-tert-butylsydnone was 0.471 +/- 0.033 mmole/kg. Trimethadione, but not phenytoin sodium or proadifen hydrochloride, protected the rat from the effects of 3-tert-butylsydnone. After administration of this compound, pentobarbital sodium sleeping time was reduced in the rat, but blood pressure and ECG were unchanged in the dog. Pretreatment of the mouse with 3-tert-butylsydnone did not influence the LD50 of epinephrine hydrochloride. The action of methacholine chloride in the rat was not blocked, and the pupil of the rabbit eye was unaffected. Tests for analgesic and oxytocic activity were negative. Chronic administration of a small dose to the rat for 70 days had no effect on blood glucose, blood urea nitrogen, hemoglobin, or microhematocrit values.
Anesthesia↗
Induction of sister chromatid exchange by various selenium compounds in Chinese hamster cells in the presence and absence of S9 mixture.
This study was designed to investigate the effect of 3 selenium compounds, namely, sodium selenite, sodium selenide and sodium selenate on induction of sister chromatid exchange (SCE) in the Chinese hamster V79 cell line in the presence and absence of S9 mixture. The results indicated that the most potent SCE inducer in the presence of S9 mixture was sodium selenite and this was followed by sodium selenide, while in the absence of S9 mixture the most effective SCE inducer was sodium selenide which was then followed by sodium selenite. For sodium selenate, the data indicated no increase in SCE rate as compared to the control values both in the presence and absence of S9 mixture. In addition, it was observed that growth inhibition as measured by no sister chromatid differentiation or no metaphases was produced by certain doses of the compounds tested. Based on this, the compound that induced the most growth inhibition both in the presence and absence of S9 mixture was sodium selenide and this was followed by sodium selenite. For sodium selenate no growth inhibition was observed. The different capabilities of the selenium compounds tested to induce SCE were clearly demonstrated in the system employed in this study. It is felt that this effect is an important cytogenetic characteristic of these compounds, yet how this activity relates to the antimutagenic and anticarcinogenic properties of these agents is difficult to discern.
Animals↗
Horseradish peroxidase. XXXIV. Oxidation of compound II to I by periodate and inorganic anion radicals.
The one-electron oxidation of horseradish peroxidase compound II to compound I by sodium periodate was observed. The bimolecular rate constant for the NaIO4--compound II interaction is equal to 9.5 +/- 1 x 10(-3) M-1s-1 at room temperature. Irradiation, using ultraviolet light, of the solution containing compound II and persulfate in the presence of bicarbonate, chloride, or bromide, leads ot the fast accumulation of compound I due to the oxidative action of SO4, CO3, Cl2, and Br2 anion radicals, which are products of the photolysis.
Bicarbonates↗
Double-blind, randomized and parallel comparison between droxicam and diclofenac sodium in patients with coxarthrosis and gonarthrosis.
This double-blind clinical trial compares droxicam, a new non-steroidal anti-inflammatory agent and the reference compound diclofenac sodium. After a 7 day placebo run-in period, 80 patients with gonarthrosis and coxarthrosis were randomized to receive 20mg/day of droxicam and 150mg/day of diclofenac for 6 weeks. Evaluations were carried out at weeks 0 (placebo run-in), 2,3, and 6. Both drugs showed statistically significant improvements in all clinical measurements (index of severity, pain intensity, morning stiffness, maximal forced flexion and extension of the knee) after 6 weeks of treatment. Investigator's and patient's opinions were consistent with these results. The consumption of paracetamol was significantly lower amongst patients treated with droxicam. Withdrawals due to lack of therapeutic efficacy did not occur. A lower incidence of side effects, mostly upper gastrointestinal symptoms, was noticed amongst droxicam-treated patients. However, two patients in the droxicam group were withdrawn at week 3 and two days after week 6 because of epigastric pain and nausea, and cutaneous rash, respectively. Both study drugs are of benefit in reducing pain and improving joint motion and function in patients with coxarthrosis and gonarthrosis.
Adult↗
Bicyclic hydantoins with a bridgehead nitrogen. Comparison of anticonvulsant activities with binding to the neuronal voltage-dependent sodium channel.
The anticonvulsant activity of diphenylhydantoin (DPH or phenytoin) is consistent with its actions on the neuronal voltage-dependent sodium channel. To further elucidate the binding requirements for this site, we synthesized several hydantoin analogs and evaluated these in in vitro sodium channel-binding and/or in vivo whole animal anticonvulsant assays. 5-Pentyl-5-phenylhydantoin (8), the most potent binder to the sodium channel in this study, had the same affinity as DPH (IC50 = 40 microM), revealing that one phenyl ring is sufficient for good interactions. Since our previous studies with monophenyl-substituted bicyclic 2,4-oxazolidinediones suggested that N3-alkylation and the conformational constraint of a 5-alkyl substituent over one face of the oxazolidinedione ring improved activity, we synthesized two examples of analogous bicyclic hydantoins. However, the bicyclic hydantoins were much less potent binders to the neuronal voltage-dependent sodium channel than their monocyclic counterparts. The binding activity for the more potent bicyclic hydantoin, 1,8-diaza-9,10-dioxo-7-phenylbicyclo[5.2.1]decane (4) (IC50 = 427 microM), was comparable to that of the ring-opened, N3-methylated monocyclic hydantoin model, 5-butyl-3-methyl-5-phenylhydantoin (9) (IC50 = 285 microM), and these were 8-11 times less potent than the monocyclic model 8, which contains a free imide NH. Furthermore, 5-butyl-5-phenylhydantoin (7; IC50 = 103 microM) was less potent than 8, suggesting that increased log P may enhance binding. Thus, unlike 2,4-oxazolidinediones, N3-alkylation of hydantoins dramatically decreases sodium channel-binding activity. Bicyclic hydantoin 4 was nevertheless a good anti-MES anticonvulsant in mice (ED50 = 86 mg/kg), although this activity likely results from mechanisms other than interactions at the neuronal voltage-dependent sodium channel. Compound 4 was also relatively neurotoxic (TD50 = 124 mg/kg). These results suggest that the binding of hydantoins to the sodium channel may be enhanced by (a) a free imide NH group and (b) an increased log P. Furthermore, 2,4-oxazolidinediones and hydantoins must either orient differently in the same binding site or interact with different sites on the neuronal voltage-dependent sodium channel.
Alkylation↗
Induction of internucleosomal DNA fragmentation by carcinogenic chromate: relationship to DNA damage, genotoxicity, and inhibition of macromolecular synthesis.
Hexavalent chromium (Cr) compounds are respiratory carcinogens in humans and animals. Treatment of Chinese hamster ovary cells with 150 and 300 microM sodium chromate (Na2CrO4) for 2 hr decreased colony-forming efficiency by 46 and 92%, respectively. These treatments induced dose-dependent internucleosomal fragmentation of cellular DNA beyond 24 hr after chromate treatment. This fragmentation pattern is characteristic of apoptosis as a mechanism of cell death. These treatments also induced an immediate inhibition of macromolecular synthesis and delayed progression of cells through S-phase of the cell cycle. Cell growth (as evidenced by DNA synthesis) was inhibited for at least 4 days and transcription remained suppressed for at least 32 hr. Many of the cells that did progress to metaphase exhibited chromosome damage. Chromate caused the dose-dependent formation of DNA single-strand breaks and DNA-protein cross-links, but these were repaired 8 and 24 hr after removal of the treatment, respectively. In contrast, Cr-DNA adducts (up to 1/100 base-pairs) were extremely resistant to repair and were still detectable even 5 days after treatment. Compared with other regions of the genome, DNA-protein cross-links and Cr adducts were preferentially associated with the nuclear matrix DNA of treated cells, which was 4.5-fold enriched in actively transcribed genes. Chromium adducts, formed on DNA in vitro at a similar level to that detected in nuclear matrix DNA, arrested the progression of a DNA polymerase in a sequence-specific manner, possibly through the formation of DNA-DNA cross-links.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
A comparative controlled trial of intralesionally-administered zinc sulphate, hypertonic sodium chloride and pentavalent antimony compound against acute cutaneous leishmaniasis.
A comparative clinical trial between two newly introduced intralesional treatments for acute leishmaniasis and the established treatment of intralesionally-administered pentavalent antimony compounds was performed. Treatments were allocated randomly to a total of 63 patients who received 2% zinc sulphate, 7% sodium chloride solutions or sodium stibogluconate intralesionally. A number of patients were left without treatment as controls. Patients were followed-up for 45 days, the results showing that the three treatments gave comparable cure rates by the end of the follow-up period. However, zinc sulphate gave a high cure rate (94.8%) usually with a single injection.
Acute Disease↗
Some effects of sodium selenite on the cardiovascular system.
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Cardiovascular System↗
[Culture pretreatment of sputum with laurylpyridinium bromide and sodium thiosulphate].
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Bacteria↗
Pegaptanib sodium for the treatment of neovascular age-related macular degeneration.
This article reviews pegaptanib sodium, a compound developed by Eyetech Pharmaceuticals Inc. and Pfizer Inc., for the treatment of neovascular age-related macular degeneration (AMD). Traditional treatment approaches to neovascular AMD have included destructive therapies such as thermal laser photocoagulation and photodynamic therapy; the use of pegaptanib sodium heralds a new treatment approach that is a non-destructive therapy based on the inhibition of vascular endothelial growth factor activity in the eye. This diminishes the neovascular drive in the pathologically hyperpermeable state of the diseased eye. Pegaptanib sodium is one of the first therapeutics belonging to the class of compounds known as aptamers. The chemistry, mechanism of action, pharmacokinetics and rationale for the clinical use of the drug are reviewed. The article highlights and summarises the results of the multi-centre, randomised, sham-controlled clinical trials with pegaptanib sodium to treat subfoveal choroidal neovascularisation in AMD. In addition, the safety profile is reviewed.
Aptamers, Nucleotide↗
Degradation of aldrin in adsorbed system using advanced oxidation processes: comparison of the treatment methods.
In this study, Fenton, UV/Fenton, UV/H2O2, UV/Fe2+ advanced oxidation processes have been applied for degradation of aldrin adsorbed on Na-montmorillonitte and activated carbon. Aldrin adsorbed on Na-montmorillonitte was degraded more efficiently than that of on activated carbon. For example, in UV/Fenton technique 95% of aldrin was removed from Na-montmorillonitte while 50% degradation was observed on activated carbon. Degradation of aldrin adsorbed on Na-montmorillonitte has also been achieved effectively using UV/Fe2+ technique despite the absence of H2O2. All AOPs but Fenton have been observed nearly equally effective for degradation of aldrin on Na-montmorillonitte sorbent. Fenton reaction exhibited least activity in degradation aldrin adsorbed on Na-montmorillonitte. The experiments with activated carbon sorbent indicated that phenyl groups in activated carbon structure and aldrin molecules exhibited competitive behavior on reaction with OH* radicals. The results of infrared spectroscopy support this assumption. The degradation efficiency of aldrin using activated carbon sorbent was determined in the following order: UV/Fenton > UV/H2O2 > Fenton > UV/Fe2+.
Adsorption↗
Carbohydrate utilization by tilapia (Oreochromis niloticus x O. aureus) as influenced by different chromium sources.
An experiment was conducted to study the influence of three different forms of chromium (CrCl3.6H2O, Na2CrO4.4H2O and Cr2O3) on the utilization of two carbohydrates (glucose and cornstarch) by juvenile hybrid tilapia (Oreochromis niloticus x O. aureus). Average initial body weight of the fish was 1.13 +/- 0.02 g. Fish were fed 5% body wt/d. Significantly (P < 0.05) greater body weight gain, food intake, protein retention, energy retention and body lipid concentration were observed in fish fed the starch diet than in those fed the glucose diet. Fish fed the glucose diet supplemented with any type of chromium had significantly greater weight gain than those fed the glucose diet without chromium supplementation. Fish fed the glucose diet supplemented with Cr2O3 had greater weight gain, food intake, protein retention, energy retention and body lipid concentration than those fed the unsupplemented glucose diet or the glucose diet supplemented with CrCl3.6H2O or Na2CrO4.4H2O. Delayed plasma glucose peak time was observed in tilapia fed the glucose diet supplemented with any type of chromium. Chromium supplementation generally lowered the glucose-6-phosphatase activity in tilapia. Phosphofructokinase activity was significantly higher in fish fed the glucose diet supplemented with Cr2O3 than in the other glucose-fed groups. These data suggest that chromium supplementation improved glucose utilization by tilapia and that Cr2O3 supplementation was markedly more effective than other chromium forms.
Animals↗
Tityustoxin effect on nerve compound action potentials requires extracellular sodium.
Previous studies have demonstrated that Li(+) ions can substitute for Na(+) in a variety of functional systems. Using the single sucrose-gap recording technique, we measured the nerve compound action potential to study the effects of tityustoxin (an alpha-scorpion toxin that selectively inhibits fast Na(+) channel inactivation) upon removal of extracellular Na(+). Our results suggest that tityustoxin requires the presence of extracellular Na(+) to produce its typical pharmacological effect on Na(+) channel inactivation kinetics, but not to bind to its site.
Action Potentials↗
Requirement of thiols for activation of coronary arterial guanylate cyclase by glyceryl trinitrate and sodium nitrite: possible involvement of S-nitrosothiols.
Glyceryl trinitrate specifically required cysteine, whereas NaNO2 at concentrations less than 10 mM required one of several thiols or ascorbate, to activate soluble guanylate cyclase from bovine coronary artery. However, guanylate cyclase activation by nitroprusside or nitric oxide did not require the addition of thiols or ascorbate. Whereas various thiols enhanced activation by nitroprusside, none of the thiols tested enhanced activation by nitric oxide. S-Nitrosocysteine, which is formed when cysteine reacts with either NO-2 or nitric oxide, was a potent activator of guanylate cyclase. Similarly, micromolar concentrations of the S-nitroso derivatives of penicillamine, GSH and dithiothreitol, prepared by reacting the thiol with nitric oxide, activated guanylate cyclase. Guanylate cyclase activation by S-nitrosothiols resembled that by nitric oxide and nitroprusside in that activation was inhibited by methemoglobin, ferricyanide and methylene blue. Similarly, guanylate cyclase activation by glyceryl trinitrae plus cysteine, and by NaNO2 plus either a thiol or ascorbate, was inhibited by methemoglobin, ferricyanide and methylene blue. These data suggest that the activation of guanylate cyclase by each of the compounds tested may occur through a common mechanism, perhaps involving nitric oxide. Moreover, these findings suggest that S-nitrosothiols could act as intermediates in the activation of guanylate cyclase by glyceryl trinitrate, NaNO2 and possibly nitroprusside.
Animals↗
Evaluation of porfimer sodium fluorescence for measuring tissue transformation.
BACKGROUND: Neoplastic tissue can be detected by its increased fluorescence compared with surrounding normal tissue after the injection of the tumor-localizing compound porfimer sodium (Photofrin; Quadra Logic Technologies, Vancouver, BC, Canada). In vivo fluorescence photometry is a nonimaging photodetector technique that detects specific 690 nm fluorescence of the porphyrin by subtracting nonspecific 612 nm excitation from 630 nm excitation. The technique was applied in the developmental stages of the 9,10 dimethyl-1,2-benzanthracene (DMBA)-induced hamster buccal cheek pouch carcinoma model to (1) quantitate and characterize porfimer sodium fluorescence and uptake as it relates to lesion progression and biochemical changes and (2) determine whether porfimer sodium-induced fluorescence will vary with promotional and inhibitory stimuli. METHODS: Groups of Syrian Golden hamsters had their cheek pouch buccal mucosa exposed to a 0.5% DMBA in acetone three times per week for 6 weeks (premalignant lesions), 12 weeks (squamous cell carcinomas), or other specified durations. The rate of malignant transformation was either promoted (by either carbon dioxide laser incision or continued DMBA application) or inhibited (by the administration of either somatostatin analogue RC-160 [D-Phe-Cys-Tyr-D-Trp-Lys-Val-Cys-Trp-NH2] or bombesin antagonist RC-3095 [D-Tpi-Gln-Trp-Ala-Val-Gly-His-Leu psi (CH2NH)Leu-NH2]). Groups of DMBA-exposed hamsters were subsequently injected with 1.0 mg/kg of porfimer sodium during the various stages of tumor development. Twenty-four hours after injection, fluorescence levels were measured by in vivo fluorescence photometry. Samples of tumors, dysplastic mucosal tissue, and normal-appearing oral mucosa were biopsied and used for either tissue extraction assays, histopathologic examination, or tyrosine kinase activity assay as an index of rate of transformation. RESULTS: Results demonstrated that porfimer sodium is retained in DMBA-treated tissue. Fluorescence is completely accounted for by porfimer sodium uptake. The duration of exposure to carcinogen is proportional to porfimer sodium fluorescence. This relationship establishes that premalignant lesions can be distinguished from normal tissue by porfimer sodium uptake and fluorescence. The changes in increased tyrosine kinase activity paralleled the increase in porfimer sodium fluorescence. Alterations in the rate of tissue transformation produced equivalent alterations in porfimer sodium-induced fluorescence. CONCLUSIONS: These results suggest that porfimer sodium uptake and fluorescence can be used in a prognostic manner to diagnose and determine the course of transformation of individual lesions.
9,10-Dimethyl-1,2-benzanthracene↗