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PubMed2004

Cationic vesicles consisting of 1,2-dioleoyl-3-trimethylammonium propane (DOTAP) and phosphatidylcholines and their interaction with erythrocyte membrane.

We studied the formation and stability of vesicles consisting of 1,2-dioleoyl-3-trimethylammonium propane (DOTAP) and phosphatidylcholines by electron spin resonance (ESR) analysis and observation of their hemolytic activities. In contrast with previous findings on dimethyldialkylammoniums, DOTAP formed vesicles at 37 degrees C with phosphatidylcholines containing either saturated acyl chains such as dimyristoylphosphatidylcholine (DMPC) or unsaturated acyl chains such as dilinoleoylphosphatidylcholine (DLPC). Phosphatidylcholines made the bilayer more rigid and significantly reduced the hemolytic activity of DOTAP. In the presence of equimolar concentration of DOTAP and phosphatidylcholines, formation of tightly aggregated structures of several erythrocytes was observed, as previously reported for the vesicles containing dimethyldipalmitylammonium. These findings indicate that DOTAP vesicles were stabilized by phosphatidylcholines with either saturated acyl chains or unsaturated acyl chains, and the interaction with the lipid bilayer of biological membranes as cationic vesicles became prominent with minimal membrane damage by DOTAP monomers.

Animals↗
PubMed1998

Mobilization of mercury and arsenic in humans by sodium 2,3-dimercapto-1-propane sulfonate (DMPS).

Sodium 2,3-dimercapto-1-propane sulfonate (DMPS, Dimaval) is a water-soluble chelating agent that can be given by mouth or systemically and has been used to treat metal intoxication since the 1960s in the former Soviet Union and since 1978 in Germany. To better approximate the body burdens of Hg and As in humans, DMPS-Hg andDMPS-As challenge tests have been developed. The tests involve collecting an overnight urine, administering 300 mg DMPS at zero time, collecting the urine from 0 to 6 hr, and determining the urinary Hg before and after DMPS is given. The challenge test, when applied to normal college student volunteers with and without amalgam restorations in their mouths, indicated that two-thirds of the Hg excreted in the urine after DMPS administration originated in their dental amalgams. In addition, there was a positive linear correlation between the amalgam score (a measure of amalgam surface) and urinary Hg after the challenge test. When the DMPS-Hg challenge test was used to study dental personnel occupationally exposed to Hg, the urinary excretion of Hg was 88, 49, and 35 times greater after DMPS administration than before administration in 10 dental technicians, 5 dentists, and 13 nondental personnel, respectively. DMPS also was used to measure the body burden of humans with a history of drinking water containing 600 microgram As/liter. DMPS administration resulted in a tripling of the monomethylarsonic acid percentage and a halving of the dimethylarsinic acid percentage as related to total urinary As. Because South American animals studied were deficient in arsenite methyltransferase, a hypothesis is presented that arsenite and arsenite methyltransferase may have had a role in the evolution of some South American animals.

Adult↗
PubMed1990

Potentiation of doxorubicin cytotoxicity by (+)-1,2-bis-(3,5-dioxopiperazinyl-1-yl) propane (ICRF-187) in human leukemic HL-60 cells.

The bisdioxopiperazine propane, ICRF-187, has been reported to potentiate doxorubicin cytotoxicity in certain tumor cell lines; however, the mechanism of this interaction is not known. In order to define the mechanism of this interaction, we examined the effects of ICRF-187 on doxorubicin cytotoxicity, free radical formation, and drug accumulation in human leukemia HL-60 cells. Studies show that ICRF-187 synergistically potentiated doxorubicin cytotoxicity in HL-60 cells. This potentiation of doxorubicin cytotoxicity by ICRF-187 appeared to result from enhanced drug dependent free radical formation without effecting doxorubicin uptake in HL-60 cells.

Biological Transport↗
PubMed2005

Effect of 2-amino-2-(2-(4-octylphenyl) ethyl) propane-1,3-diol hydrochloride (FTY 720) on immune liver injury in mice.

AIM: To investigate the protective effect against two immune liver injury models in mice by 2-amino-2-(2-(4-octylphenyl) ethyl) propane-1,3-diol hydrochloride and its possible mechanisms in Con A-induced liver damage. METHODS: Liver tissue or hepatocyte injury was monitored biochemically by measuring alanine aminotransferase (sALT) and aspartate aminotransferase (sAST) activity. Hematoxylin and eosin (HE) staining was used for histopathological examination. To evaluate the role of IFN-gamma and IL-4 in the liver injury, serum levels of IFN-gamma and IL-4 were determined using commercially available ELISA kit at 12 h after Con A challenge. We also determined FTY 720-induced spleen cell apoptosis by flow cytometry analysis or spleen cell proliferation test. RESULTS: Different doses of FTY 720 treatment dramatically reduced circulating markers of hepatocyte injury in two kinds of immunological liver injury models. FTY 720 dramatically reduced the elevated serum IFN-gamma and IL-4 levels after Con A injection. Effect of spleen cell supernatants treated with Con A or FTY 720 on hepatocytes showed that ALT activities in cultured hepatocyte supernatants in Con A treatment group increased markedly and FTY 720 could reduce this elevated ALT activities in FTY 720 treatment group. FTY 720 dose-dependently increased the percentage of apoptotic cells in T cells and inhibited splenocyte proliferation induced by Con A. CONCLUSION: Pretreatment with FTY 720 was shown to produce protective effect on the immune liver injury in mice. The possible mechanism of FTY 720 on Con A-induced liver damage is that it could inhibit lymphocyte proliferation and induce lymphocyte apoptosis, resulting in the reduction of IL-4 or IFN-gamma release, and subsequently protecting liver from being damaged by Con A.

Acute Disease↗
PubMed1998

Effects of 1-(2,6-dimethylphenoxy)-2-(3,4-dimethoxyphenylethylamino) propane hydrochloride on heart function, lactate dehydrogenase and its isoenzymes in rats with cardiac hypertrophy.

AIM: To investigate the effects of 1-(2,6-dimethylphenoxy)-2-(3,4-dimethoxyphenylethylamino) propane hydrochloride (DDPH) on cardiac systolic and diastolic function, lactate dehydrogenase (LDH) activity, and LDH isoenzymes in rats with cardiac hypertrophy. METHODS: The cardiac hypertrophy of rats was induced by partly occluding abdominal aorta. The rats were given i.g. DDPH for 8 wk 4 wk after operation, and isolated working heart was made. RESULTS: Eight wk later, in model group, left ventricle systolic pressure (LVSP), LV + dp/dtmax, -dp/dtmax and aorta pressure (AP) decreased by 20.2%, 20.0%, 41.4%, and 13.6%, respectively. Left ventricle ending diastolic pressure (LVEDP) increased by 173.9%. The hemodynamic study showed that flowing liquid of aorta (AF) and coronary (CF) and cardiac output (CO) decreased by 49.4%, 41.2%, and 48.9%, respectively. After the rats were given i.g. DDPH, the all above-mentioned parameters recovered to different degrees. Under condition of cardiac hypertrophy, LDH isoenzymes and subunits changed significantly. Isoenzymes LDH3, LDH4, and LDH5, especially LDH5 increased, LDH1 decreased, subunit M in hypertrophied heart increased 1.69 times than that in normal heart. DDPH could decrease subunit M and increase subunit H. CONCLUSION: DDPH can increase cardiac function, coronary flow and reverse changes of LDH isoenzymes in rats with cardiac hypertrophy.

Animals↗
PubMed2000

Mechanism-based inactivation of cytochromes P450 2B1 and P450 2B6 by 2-phenyl-2-(1-piperidinyl)propane.

2-Phenyl-2-(1-piperidinyl)propane (PPP), an analog of phencyclidine, was tested for its ability to inactivate cytochrome P450s (P450s) 2B1 and 2B6. PPP inactivated the 7-(benzyloxy)resorufin O-dealkylation activity of liver microsomes obtained from phenobarbital-induced rats with a K(I) of 11 microM. The 7-ethoxy-4-(trifluoromethyl)coumarin O-deethylation activity of purified rat liver P450 2B1 and expressed human P450 2B6 was inactivated by PPP in a reconstituted system containing NADPH-cytochrome P450 reductase and lipid. In the presence of NADPH, the loss of activity was time- and concentration-dependent, and followed pseudo first order kinetics. The rate of inactivation for P450 2B1 was 0.3 min(-1), and the concentration of PPP required to achieve half-maximal inactivation was 12 microM. The time for 50% of the P450 2B1 to become inactivated at saturating concentrations of PPP was 2.5 min. P450 2B6 was inactivated with a k(inact) of 0.07 min(-1), a K(I) of 1.2 microM, and a t(1/2) of 9.5 min. The inactivated P450s 2B1 and 2B6 lost about 25 and 15%, respectively, of their ability to form a CO-reduced complex, suggesting that the loss of activity was caused by a PPP modification of the apoprotein rather than the heme. The estimated partition ratio for P450s 2B1 and 2B6 with PPP was 31 and 15, respectively. The inactivation was not reversible and reductase activity was not affected. Coincubation of P450 2B1 and 2B6 with PPP and NADPH in the presence of an alternate substrate protected both enzymes from inactivation. The exogenous nucleophile GSH did not affect the rate of inactivation. PPP-inactivated P450s 2B1 and 2B6 were recognized on Western blots by an antibody generated to phencyclidine that had been conjugated to BSA. Stoichiometries of 1.4:1 and 0.7:1 were determined for the binding of a [3H]PPP metabolite to P450 2B1 and 2B6, respectively.

Animals↗
PubMed2000

Inhibitory effect of 1-(2, 6-dimethylphenoxy)-2-(3, 4-dimethoxyphenyl-ethylamino) propane hydrochloride on inward rectifier and delayed rectifier K+ currents in guinea pig ventricular myocytes.

AIM: To study the effects of 1-(2,6-dimethylphenoxy)-2-(3,4-dimethoxyphenyl-ethylamino) propane hydrochloride (DDPH) on action potential (AP), inward rectifier K+ current (IK1), and delayed rectifier K+ current (IK) in isolated guinea pig ventricular myocytes. METHODS: Whole cell patch-clamp recording techniques. RESULTS: DDPH 0.1-100 mumol.L-1 decreased 50% duration of action potential (APD50) concentration-dependently. APD50 was shortened from (493 +/- 58) to (262 +/- 38) ms (n = 7 cells from 5 guinea pigs, P < 0.01) by DDPH 10 mumol.L-1. However, 90% duration of action potential (APD90) was increased by DDPH (> 1 mumol.L-1). At high concentration (> 10 mumol.L-1) DDPH decreased resting membrane potential (RP) and amplitude of action potential (APA). DDPH inhibited tail current of IK (IK.tail) concentration-dependently, 46% at 10 mumol.L-1 and 78% at 100 mumol.L-1. EC50 for DDPH inhibiting IK was 13.3 (11.6-16.7) mumol.L-1. DDPH also blocked IK1. DDPH at high concentration (> 10 mumol.L-1) shifted the reverse potential of IK1 positively. All the effects of DDPH were reversible after washout. CONCLUSION: DDPH blocked both IK1 and IK current in guinea pig ventricular myocytes.

Action Potentials↗
PubMed2000

[Antagonistic characterization of 1-(2,6-dimethylphenoxyl)-2-(3,4-dimethylphenyl ethylamino) propane hydrochloride on alpha 1-adrenoceptor].

AIM: To study the antagonistic effect of 1-(2,6-dimethylphenox)-2-(3,4-dimethylphenyl ethylamino) propane hydrochloride (DDPH) on alpha 1-adrenoceptor (AR). METHODS: Radioligand binding assay was used. Specific 125I-BE2254 (2-beta(4-hydroxyphenyl)-ethyl aminomethyl-tetralone) binding was measured by incubating membrane of rat cerebral cortex, spleen and the three cloned alpha 1-AR subtypes (alpha 1A, alpha 1B, alpha 1D) stably expressed in human embryonic kidney 293 cell preparation with a single concentration of 125I-BE2254 in the presence of 14 concentrations of DDPH. Equilibrium binding constant (KI) and Hill coefficients (nH) were determined from Hill plots. The -log value of the KI was expressed as pKI. Contractile responses of isolated rat aorta, renal artery ring and spleen were determined. The pA2 values for DDPH in competitively inhibiting NE-stimulated contraction of tissues were measured with the method of Ainlakshana and Schild. RESULTS: DDPH competitively inhibited binding of 125I-BE2254 to alpha 1-AR in a concentration-dependent manner. The pKI values for DDPH in rat cerebral cortex and spleen were 7.17 +/- 0.06 and 7.41 +/- 0.11, respectively, and the Hill efficiency values were not significantly different from unit. The pKI values for cloned alpha 1A, alpha 1B and alpha 1D-AR were 7.21 +/- 0.12, 6.88 +/- 0.04 and 7.26 +/- 0.06, respectively, and the Hill efficiency values were not significantly different from unit. Contractile studies showed that DDPH competitively antagonized the NE concentration-response curve with a pA2 values of 7.40 +/- 0.23 in aorta, 7.41 +/- 0.04 in renal artery and 7.63 +/- 0.07 in spleen and the slopes of schild plot were not significantly different from unit. The pKI values for DDPH in tissues and the cloned alpha 1A or alpha 1D-AR were shown to fit well in with the pA2 values in antagonizing NE-induced constriction in rat isolated aorta, renal artery and spleen. CONCLUSION: These results suggest that DDPH appear to be a non-subtype selective competitive antagonist for alpha 1-AR.

Adrenergic alpha-Antagonists↗
PubMed1997

[Effects of 1-(2,6-dimethylphenoxy)-2-(3,4-dimethoxyphenylethylamino) propane hydrochloride on proliferation of vascular smooth muscle cells and PDGF-B, bFGF, c-sis, c-myc in spontaneously hypertensive rat].

In order to determine the effects of 1-(2, 6-dimethylphenoxy)-2-(3, 4-dimethoxyphenylethylamino) propane hydrochloride(DDPH) on proliferation of vascular smooth muscle cells(VSMC), growth factor PDGF-B, bFGF and expression of oncogene c-sis and c-myc in spontaneously hypertensive rat(SHR), 3H-thymidine(3H-TdR) incorporation, electronic microscopy, immunohistochemistry and in situ hybridization assays were used. The results showed that after DDPH administration (50 mg i.g. q.d. x8 wk to SHR), morphological change of VSMC was antagonized, blood pressure and 3H-TdR incorporation were significantly reduced. Furthermore, DDPH was shown to reverse the enhanced antigen PDGF-B and bFGF and reverse the reduced expression of oncogene c-sis and c-myc in SHR. These results suggest that DDPH may inhibit VSMC proliferation in SHR, which may be relevant to the molecular biological mechanism of growth factors and oncogene control.

Animals↗
PubMed1975

Pharmacological studies of 3-[bis(3,3-diphenylpropyl)-amino]-propan-1-ol hydrochloride, (PF-244), a new cerebral vasodilator.

Pharmacological effects of 3-[bis(3,3-diphenylpropyl)-amino]-propan-1-ol-hydrochloride (PF-244) mainly on cerebral and cardiovascular systems, were studied. PF-244 indicated a potent cerebral vasodilation effect and a marked increase in oxygen supply to cerebral tissue with only weak inotropic action and depressor effect. This cerebral vasodilation was more potent and specific than that of papaverine hydrochloride in regional cerebral flow. PF-244 also indicated an antibarium action, although it did not show the properties related to the cholinergic and/or adrenergic mechanism. PF-244 appears to be one of the potent cerebral vascular dilators, and the nature of its mechanism was discussed.

Animals↗
PubMed1999

[Analysis of 2-acrylamido-2-methyl propane sulfonic acid by thin layer chromatography].

A method for the analysis of 2-acrylamido-2-methyl propane sulfonic acid(AMPS) by TLC is described. The plate was Silica GF254. We selected benzene/methanol as developing agent from several developing systems and fixed the best ratio: V(benzene):V(methanol) = 2:1. The experiment indicated that the Rf value of AMPS was 0.36 while that of AM(acrylamide), the main impurity in crude AMPS sample, was 0.64. The minimum detectable limit of AMPS was 5 micrograms and the developing time was about 25 minutes. Compared with ether/methanol and chloroform/methanol, benzene/methanol system has the advantages of more easily controlling its ratio, better repeatability and much rapid developing rate. This method may be helpful in the control of AMPS in quality.

Acrylamides↗
PubMed1992

Human pharmacokinetics and radiopharmacological studies of the myocardial perfusion agent: technetium (2-carbomethoxy-2-isocyano-propane)6+.

The myocardial perfusion agent technetium (2-carbomethoxy-2-isocyano-propane)6+ (99mTc-CPI) is unique from other cationic technetium isonitrile complexes in that it exhibits moderate washout from the heart and rapid hepatobiliary clearance in animal models and human volunteers. Dynamic imaging and HPLC analysis were performed in humans and guinea pigs to outline the pharmacological basis of its pharmacokinetics. Enzymatic hydrolysis of the terminal ester groups in blood was found to occur at a moderate rate producing new species that have been shown not to accumulate in heart tissue. However, after extraction by the heart, liver or kidneys, the 99mTc-CPI complex undergoes metabolism at a much slower rate than observed in the blood. Differences in hydrolysis rate and products obtained indicate separate mechanisms of hydrolysis occurring in blood and other organs. It is proposed that the heart washout occurring after hydrolysis produces a neutral compound which is no longer retained by the negative cytosolic and mitochondrial membrane potentials in myocardial tissue.

Adult↗
PubMed2003

[Protective effects of 1-(2,6-dimethylphenoxy)-2-(3,4-dimethoxyphenylethylamino) propane hydrochloride(DDPH) on brain ischemia injury in rats].

AIM: To study the effects of 1-(2,6-dimethylphenoxy)-2-(3,4-dimethoxyphenylethylamino) propane hydrochloride(DDPH) on brain ischemia injury in rats. METHODS: By using the middle cerebral artery occlusion (MCAO) induced by nylon surgical thread inserted through the internal carotid artery into the anterior cerebral artery in rats, the effects of DDPH on neuron defects(ND) and infarct size(IS) were investigated. Using incomplete cerebral ischemia in rats, the effects of DDPH on superoxide dismutase (SOD) activity and malondialdehyde (MDA) content in brain tissue and pathological changes in rats were studied. RESULTS: DDPH at the dose of 10 mg.kg-1 i.p. 30 min before ischemia decreased the ND 3 h after ischemia. The IS declined 24 h after ischemia as well. Meanwhile, DDPH was found to increase SOD activity and reduce the MDA content, as well as mitigate pathological damage, of neuron after brain ischemia in rats. CONCLUSION: DDPH showed protective effects on brain ischemia, probably related to its properties of calcium antagonistic effect and increasing the activity of superoxide dismutases.

Animals↗
PubMed2004

1,3-Bis(2-hydroxyiminomethylpyridinium) propane as the potential reactivator of the acetylcholinesterase inhibited by nerve agents.

The oxime K005 [1,3-bis(2-hydroxyiminomethylpyridinium) propane dibromide] for the reactivation of the enzyme acetylcholinesterase (AChE) inhibited by cyclosarin and VX was tested. Its reactivation potency was not better in comparison with the currently used AChE reactivator--pralidoxime. On the other hand, the oxime K005 has its maximum reactivation ability at the concentration 10(-4) M, which could be achieved for human use. The maximum concentration of pralidoxime was reached at the concentrations 10(-1) M (for cyclosarin) and 10(-3) M (for VX) but these concentrations are not available for the use in vivo.

Acetylcholinesterase↗
PubMed2005

Protective effect of 1-(2,6-dimethylphenoxy)-2-(3,4-dimethoxyphenylethylamino) propane hydrochloride on myocardial ischemia-reperfusion injury in rats.

The aim of the present study was to investigate the protective effect of 1-(2,6-dimethylphenoxy)-2-(3,4-dimethoxyphenylethylamino) propane hydrochloride (DDPH) on myocardial ischemia-reperfusion (I/R) injury in rats and the mechanism of its myocardial protection. For this purpose, 50 Wistar rats were divided into five groups: sham group, control group, verapamil treated group, and two DDPH treated groups (20 and 40 mg/kg, respectively). Myocardial I/R injury model was established by reperfusion for 120 min after 40 min ischemia induced by the ligation of left descending coronary artery in rats. The influence of DDPH on myocardial infarction size was observed and the levels of myocardial enzymes in serum were measured. The activities of oxygen free radical scavenging enzymes and the content of malondialdehyde (MDA) in myocardium and serum were determined. The pathological changes of myocardial tissue were observed. The results showed that DDPH significantly diminished myocardial infarction size, reduced the release of myocardial creatine phosphokinase (CPK), lactate dehydrogenase (LDH) and glutamic oxaloacetic aminotransferase (GOT), protected the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), and decreased the content of MDA in myocardium and serum as compared with the control group. The degree of myocardial injury was slighter in DDPH treated groups than in control group. These results suggest that DDPH produces a cardioprotective effect during myocardial I/R injury, which may be related to blocking calcium channels and inhibiting the formation of the oxygen free radical and subsequent peroxidation of lipid by DDPH.

Animals↗
PubMedDate not supplied

The enzymatic hydrolysis-activation of the adriamycin cardioprotective agent (+)-1,2-bis(3,5-dioxopiperazinyl-1-yl)propane.

The cardioprotective agent ICRF-187 [(+)-1,2-bis(3,5-dioxopiperazinyl-1-yl)propane, ADR-529] has shown a great deal of promise against what may be an iron-based adriamycin-induced cardiotoxicity. ICRF-187 likely exerts its actions through its rings-opened hydrolysis product, which has a structure similar to EDTA and like-wise strongly binds metal ions. The 105,000g soluble supernatant fraction of homogenates of porcine liver and kidney, but not of heart, enzymatically caused a ring-opening hydrolysis of ICRF-187 at the rate of 1.2, 1.4, and less than 0.15 nmol.(mg protein)-1.min-1, respectively. This enzymatic hydrolysis of ICRF-187 was completely abolished by 4-chlorobenzenesulfonamide, which suggested that dihydropyrimidine amidohydrolase (DHPase) might be, in large part, responsible for the ICRF-187 hydrolase activity. Bovine liver DHPase was isolated and was shown to enzymatically hydrolyze ICRF-187 with a Vmax of 14,900 nmol.(mg DHPase)-1.min-1, a value that exceeded that of its natural substrates. The KM for ICRF-187 of 6.7 mM was, however, much larger than that of its natural substrates. The enzyme kinetics were consistent with DHPase acting on ICRF-187 to form one-ring-opened hydrolysis product only. Thus, DHPase is not able to act on the one-ring-opened hydrolysis product to produce two-ring-opened product. The Ki for 4-chlorobenzenesulfonamide inhibition of DHPase was measured to be 26 microM.

Amidohydrolases↗
PubMedDate not supplied

Treatment of experimental Pneumocystis carinii pneumonia with 1,3-di(4-imidazolino-2-methoxyphenoxy)propane lactate.

An analogue of pentamidine, 1,3-di(4-imidazolino-2-methoxyphenoxy)propane (DMP) lactate, was tested against rat Pneumocystis carinii pneumonia (PCP). The drug was found to be highly active in the treatment of rat PCP at a dose of 1.75 mg/kg (parent molecule) when administered by intravenous (i.v.) injection (daily for 2 wk). The compound was also active against PCP when given orally, however, significantly higher doses of DMP were necessary when compared to the i.v. dosing regimen. Prophylactic doses (i.v.) of the drug also proved highly effective in preventing PCP.

Administration, Oral↗