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PubMed1996

Changes in extracellular acid-base homeostasis in cerebral ischemia.

The purpose of this study was to examine the changes in extracellular CO32- and lactate concentration produced by ischemia, especially in relation to the occurrence of anoxic depolarization, and how some of these changes are altered by the inhibition of organic acid transport systems with probenecid. These data demonstrate that (i) the transmembrane mechanisms contributing to intracellular acid-base regulation (Na+/H+ and HCO3-/Cl- exchanges, and lactate/H+ cotransport) are markedly activated during ischemia; (ii) the efficacy of these mechanisms is abolished as the cellular membrane permeability to ions, including H+ and pH-changing anions, suddenly increases with anoxic depolarization; and (iii) efflux of intracellular lactate during ischemia, and its reuptake with reperfusion, mainly occur via a transporter. These findings imply that residual cellular acid-base homeostasis persists as long as cell depolarization does not occur, and strengthen the concept that anoxic depolarization is a critical event for cell survival during ischemia.

Acid-Base Equilibrium↗
PubMed1994

Nephrotoxicity of 4-amino-3-S-glutathionylphenol and its modulation by metabolism or transport inhibitors.

The nephrotoxicity of 4-amino-3-S-glutathionylphenol (PAP-GSH), a known metabolite of 4-amino-phenol (PAP), was determined in male Fischer 344 rats. Administration of a single dose of 40 or 60 mumol kg-1 caused a marked elevation in blood urea nitrogen and an increase in the urinary excretion of glucose, protein and gamma-glutamyltransferase (GGT). These changes were associated with histological alterations in the proximal tubule, where at the lower dose the lesion was restricted to the S3 region of the proximal tubule in the medullary rays, while at the higher dose the lesion extended to affect the S3 region in both the medullary rays and the outer stripe of the outer medulla. Studies with [35S]-PAP-GSH at 40 mumol kg-1 showed selective retention of radioactivity in the kidney, relative to other organs 24 h after dosing and that some radioactivity was covalently bound to renal proteins. Pretreatment of animals with probenecid, an inhibitor of renal organic anion transport, or aminooxyacetic acid, an inhibitor of cysteine conjugate beta-lyase, had little or no effect on the toxicity. In contrast, pretreatment of animals with acivicin, an inhibitor of gamma-glutamyltransferase, or co-administration of PAP-GSH with ascorbic acid almost completely protected against the nephrotoxicity. This protection was associated with a decreased concentration of radioactivity from [35S]-PAP-GSH in the kidneys and a decrease in the amount covalently bound to renal protein. Thus, the nephrotoxicity of PAP-GSH may be mediated by oxidation and further processing of the glutathione conjugate via gamma-glutamyltransferase.

Aminooxyacetic Acid↗
PubMedDate not supplied

Renal elimination of the hypoxic cell radiosensitizer misonidazole in Wistar rats: influence of some drugs on its excretion.

The hypoxic cell radiosensitizing drug, misonidazole (Miso) (Ro 07-0582) and its demethylated metabolite were administered to Wistar rats at different dose levels to examine their renal elimination. The data were consistent with a model in which Miso is eliminated mainly after biotransformation into desmethylmisonidazole (Demiso) which is eliminated according to its renal clearance. The study of Miso renal elimination process shows a tubular reabsorption. So we analyzed the interaction of various drugs on urinary 24 hours elimination of this radiosensitizer. Following results were observed: Furosemide and acetazolamide do not change the rate of renal elimination of the drug; Soludactone increases the elimination level of unmetabolized Miso (p less than 0.01); Under probenecid treatment, the elimination of Miso and its O-demethylated derivative are increased; On the other hand, after a pretreatment with phenobarbital, the urinary level of desmethylmisonidazole is strongly increased (p less than 0.001).

Animals↗
PubMed2001

Uraemia suppresses central dopaminergic metabolism and impairs motor activity in rats.

OBJECTIVE: Uraemia often provokes various neurological disorders, such as mental changes, malperception, confusion, seizures and coma. Since changes in neurotransmissions induce neurological symptoms, we investigated changes in the monoamine metabolism and motor activity in uraemic rats. DESIGN: Prospective, randomised, controlled animal study. SUBJECTS: Male Wistar rats. INTERVENTIONS: Acute renal failure was induced by occlusion of bilateral renal arteries for 60 min, and the motor activity and brain monoamine turnover were examined 48 h later. The brain monoamine turnover was evaluated by the depletion of norepinephrine (NE) and dopamine (DA) induced by alpha-methyl-p-tyrosine (alpha-MT), or the accumulation of 5-hydroxyindoleacetic acid (5-HIAA) induced by probenecid. MEASUREMENTS AND RESULTS: Marked damage in renal function was found in animals subjected to renal ischaemia 48 h after the operation. The motor activity of the uraemic rats was impaired. The turnover of DA in the striatum, mesencephalon and hypothalamus was decreased in these rats. The turnover of NE and 5-hydroxytryptamine (5-HT) was unchanged in all regions examined. CONCLUSIONS: Suppression of the central DA turnover appears to be involved in the impairment of motor activity in uraemic rats.

Acute Kidney Injury↗
PubMed1995

Effect of inhibitors and substrates on methyl mercury uptake by rat erythrocytes.

Methyl mercury (MeHg) uptake by isolated erythrocytes from rats was studied at 20 degrees C. Inhibitors and substrates were used to test which transport system was involved in MeHg uptake. Ouabain and ATP were used to test the active transport system. Glycine was used to test system Gly. DL-Methionine was used to test system L. Cysteine was used to test the cysteine-facilitated transport system. The effects of Ca2+, Mg2+ and Na+ on MeHg uptake have been examined. MeHgCl and 4,4'-diisothiocyano-2,2'-stilbenedisulfonic acid (DIDS) were used to test C1- ion transport system. D-Glucose and cytochalasin B were used to test the facilitated diffusive D-Glucose transport system. Colchicine and vinblastine were used to test the microtubule system. Probenecid was used to test the organic acid transport system. Valinomycin was used to test the effect of the membrane potential on MeHg uptake. The results showed that MeHg uptake at 20 degrees C might be involved in the following transport systems: 1) an active transport system; 2) a cysteine-facilitated transport system; 3) a C1- ion transport system; 4) a facilitated diffusive D-glucose transport system; 5) an organic acid transport system. The transport systems for MeHg uptake were sensitive to the membrane potential.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed2002

Tumour cell uptake of the metastasis inhibitor ruthenium complex NAMI-A and its in vitro effects on KB cells.

PURPOSE: The uptake of NAMI-A (imidazolium trans-imidazoledimethylsulphoxidetetrachlororuthenate) by KB cells in vitro was compared with the effects of this compound on the cell cycle phase distribution of the cells. METHODS: NAMI-A uptake was determined by flameless atomic absorption spectroscopy, and the cell cycle phase distribution was determined by flow cytometry. RESULTS: NAMI-A uptake was proportional to its concentration in the incubation medium. The use of a number of incubation conditions showed that NAMI-A uptake from MEM was independent of the presence of serum and dependent on the presence of amino acids in the incubation medium, and that NAMI-A uptake was markedly higher when the cells were incubated in PBS. The uptake increase observed in PBS did not occur when the cells were kept at 0-4 degrees C, suggesting the presence of active transportation of NAMI-A into cells. In addition, the presence of divalent cations such as Ca(2+) and Mg(2+), appeared to facilitate NAMI-A uptake. The anionic substance transport inhibitor probenecid significantly reduced the active transportation of NAMI-A into cells. The effects of NAMI-A on cell cycle distribution were strictly dependent on its uptake by tumour cells and not on its extracellular concentration. CONCLUSIONS: These findings suggest the interaction of NAMI-A with biological components resulting in possible consequences for the distribution of the compound itself. Furthermore, NAMI-A enters tumour cells both by passive diffusion and by active transportation.

Amino Acids↗
PubMed2006

Potential gamma-hydroxybutyric acid (GHB) drug interactions through blood-brain barrier transport inhibition: a pharmacokinetic simulation-based evaluation.

Recreational abuse or overdose of gamma-hydroxybutyric acid (GHB) results in dose-dependent central nervous system (CNS) effects including death. As GHB undergoes monocarboxylic acid transporter (MCT)-mediated transport across the blood-brain barrier (BBB), one possible strategy for the management of GHB toxicity/overdose involves inhibition of GHB BBB transport. To test this strategy, interactions between GHB and MCT substrates (salicylic acid or probenecid) were simulated. Competitive, noncompetitive and uncompetitive inhibition mechanisms were incorporated into the GHB-MCT substrate interaction model for inhibitor dosing either pre-, concurrent or post-GHB administration. Simulations suggested that salicylic acid was the better candidate to limit GHB accumulation in the CNS. A time window of effect (> 10% change) was observed for salicylic acid pre- and post-administration, with maximal transport inhibition occurring within 12 hr of pre- and 2 hr of post-administration. Consistent with the prediction that reduced GHB brain concentrations could translate to decreased pharmacodynamic effects, a pilot study in rats showed that the pronounced GHB sedative/hypnotic effects (24.0 +/- 6.51 min; n = 4) in the control group (1.58 mmol/kg GHB plus saline) were significantly (p < 0.05) abrogated by salicylic acid (1.25 mmol/kg) coadministration.

Administration, Oral↗
PubMed2006

The efflux of flavonoids morin, isorhamnetin-3-O-rutinoside and diosmetin-7-O-beta-D-xylopyranosyl-(1-6) -beta-D-glucopyranoside in the human intestinal cell line caco-2.

PURPOSE: In this study, we chose three of the flavonoids isorhamnetin-3-O-rutinoside(IRR) diosmetin-7-O-beta-D-xylopyranosyl-(1-6)-beta-D-glucopyranoside(DXG) and morin, which showed obvious efflux, to test the hypothesis that a specific efflux transporter is responsible for their transportation. METHODS: The intestinal epithelial membrane transport of the flavonoids were examined using the monolayer of the human Caco-2 cell line grown in Transwells, a common model of intestinal absorption. The flavonoids were measured by high performance liquid chromatography with UV detector. RESULT: The efflux of morin, IRR and DXG, across Caco-2 cell monolayers was examined over the concentration range from 2 to 200 microM and showed a saturable process. The depletion of the cellular ATP stores with 5 mM iodoacetamide led to a significant inhibition of the efflux. Fifty micromolar verapamil, a chemical inhibitor of P-glycoprotein, had no effect on the transport of the three flavonoids, while the presence of 50 microM MK-571 and 1 mM probenecid, MRP inhibitors, resulted in an obvious reduction in the efflux. Moreover, inhibition of morin transport by MK-571 demonstrated concentration dependence. The transportation of the three flavonoids was compared with apigenin. CONCLUSION: These data support a role for MRPs in the intestinal transcellular efflux of morin, IRR, DXG and possibly other hydrophilic flavonoid aglycons and glycosides.

Adenosine Triphosphate↗
PubMed1985

Ceftazidime therapy in patients with cystic fibrosis and multiply-drug-resistant pseudomonas.

The in vitro activity of ceftazidime against Pseudomonas aeruginosa and P. cepacia isolates from patients with cystic fibrosis was compared with that of other antipseudomonal drugs. Ceftazidime was as potent as imipenem against P. aeruginosa and the only drug effective against P. cepacia. An evaluation of the elimination kinetics of ceftazidime in 20 cystic fibrosis patients revealed an elimination half-life of 1.76 hours, an apparent distribution volume of 0.27 liters/kg, and a serum clearance rate of 133.9 ml/minute/1.73m2. Urinary recovery of ceftazidime was 87 percent within the first 24 hours after administration of the drug, with 65 percent recovered in the first two-hour fraction. Probenecid administration had no effect on the elimination kinetics of ceftazidime. Forty-three patients who had either shown no response to conventional therapy or had sputum Pseudomonas isolates that were susceptible only to ceftazidime received 75 courses of therapy. In 67 percent of these patients, the clinical response, when evaluated using an objective clinical efficacy scoring system, was considered favorable. Clinical failures were not associated with the development of drug resistance. Thus, ceftazidime can be recommended for the treatment of acute pulmonary exacerbations in patients with cystic fibrosis.

Adolescent↗
PubMed1987

Norfloxacin in the treatment of uncomplicated gonococcal infections.

Norfloxacin, an oral fluoroquinolone antibacterial, is active in vitro against a variety of gram-positive and gram-negative pathogens, including both penicillinase-producing and non-penicillinase-producing strains of Neisseria gonorrhoeae. An earlier study demonstrated that a two-dose regimen of norfloxacin was as effective as standard therapy with spectinomycin for treating gonococcal urethritis, including infections caused by penicillinase-producing organisms. In this randomized study of treatment for uncomplicated gonococcal infection in men and women, three oral treatment regimens were compared: patients received either two doses of norfloxacin (600 mg twice daily), a single dose of norfloxacin (800 mg), or a single-dose ampicillin (3.5 g)/probenecid (1.0 g) regimen (as recommended by the Centers for Disease Control). All three treatment regimens achieved similar cure rates. Although the number of patients treated was too small to yield statistically significant conclusions, it appears that norfloxacin may be slightly better treatment for rectal and pharyngeal gonococcal infections than ampicillin and probenecid. Additionally, norfloxacin was well tolerated in this study. Thus, based on a review of these data, norfloxacin appears to be an alternative, single-dose, oral treatment regimen for uncomplicated gonococcal infection.

Adult↗
PubMed1992

Treatment of early Lyme disease.

PURPOSE: To compare the safety and efficacy of azithromycin, amoxicillin/probenecid, and doxycycline for the treatment of early Lyme disease, to identify risk factors for treatment failure, and to describe the serologic response in treated patients. PATIENTS AND METHODS: Fifty-five patients with erythema migrans and two patients with flu-like symptoms alone and fourfold changes in antibody titers to Borrelia burgdorferi were randomized to receive (1) oral azithromycin, 500 mg on the first day followed by 250 mg once a day for 4 days; (2) oral amoxicillin 500 mg and probenecid 500 mg, three times a day for each for 10 days; or (3) doxcycline, 100 mg twice a day for 10 days. If symptoms were still present at 10 days, treatment was extended with amoxicillin/probenecid or doxycycline for 10 more days. Evaluations were done at study entry and 10, 30, and 180 days later. RESULTS: Three of the patients who initially had symptoms suggestive of spread of the spirochete to the nervous system, one from each antibiotic treatment group, subsequently developed neurologic abnormalities, but symptoms in the other 54 patients resolved within 3 to 30 days after study entry. Six of the 19 patients (32%) (95% confidence interval, 13% to 57%) given amoxicillin/probenecid developed a drug eruption, whereas none of the patients given azithromycin or doxycycline had this complication. The presence of dysesthesias at study entry was the only risk factor significantly associated with treatment failure (p less than 0.001). By convalescence, 72% of the patients were seropositive, and 56% still had detectable IgM responses to the spirochete 6 months later. CONCLUSIONS: The three antibiotic regimens tested in this study were generally effective for the treatment of early Lyme disease, but the regimens differ in the frequency of side effects and in ease of administration.

Adult↗
PubMed1991

A randomized trial of ofloxacin versus cefoxitin and doxycycline in the outpatient treatment of acute salpingitis.

The object of this randomized study was to compare the safety and efficacy of oral ofloxacin, 400 mg twice daily for 10 days, versus intramuscular cefoxitin, 2 gm, plus oral probenecid, 1 gm, followed by oral doxycycline, 100 mg twice daily for 10 days, in the outpatient treatment of uncomplicated acute salpingitis. Thirty-eight women (53%) had Neisseria gonorrhoeae from their pretreatment endocervical or endometrial cultures, and 18 had Chlamydia trachomatis (25%). Thirty-five of 37 women (95%) treated with the ofloxacin regimen were clinically cured, and 34 of 35 (97%) were cured with the cefoxitin-doxycycline regimen (p = 0.52). One clinical failure occurred in each group with N. gonorrhoeae infection, and one failure occurred in the ofloxacin group because of side effects. The bacteriologic response for N. gonorrhoeae in both groups was 100%. The eradication of C. trachomatis was 100% (10/10) for the cefoxitin/doxycycline group and 86% (6/7) for ofloxacin. The side effects were similar in both groups of subjects. In this study both regimens were effective for the outpatient treatment of uncomplicated acute salpingitis.

Acute Disease↗
PubMed1981

Secondary syphilitic uveitis.

A patient with secondary syphilis had positive serum and cerebrospinal fluid findings. Fluorescent-antibody darkfield testing demonstrated spirochetes (Treponema pallidum) in the aqueous. There were clinical signs of secondary syphilis, including palmar skin lesions and frontal balding, and bilateral nasal altitudinal visual field loss. The discrete, waxy, yellow-white retinal lesions became increasingly pigmented and later migrated anteriorly into the vitreous chamber. The patient was treated with large amounts of penicillin (total dosage, 440 million units) and probenecid. Visual acuity improved to R.E. : 6/9 (20/30) and L.E.: 6/12 (20/40) and the inflammatory reaction disappeared. A second aqueous tap eight weeks after therapy ended showed no spirochetes by fluorescent-antibody testing.

Aqueous Humor↗
PubMed1989

Bioactivation mechanism of L-thiomorpholine-3-carboxylic acid.

L-Thiomorpholine-3-carboxylic acid (L-TMC) is a cyclized analog of S-(2-chloroethyl)-L-cysteine, which is cytotoxic in vitro and nephrotoxic in vivo. To determine whether L-TMC may play a role in S-(2-chloroethyl)-L-cysteine-induced toxicity, the cytotoxicity of L-TMC was studied in isolated rat kidney cells. L-TMC produced time- and concentration-dependent cytotoxicity. Probenecid, an inhibitor of the renal anion transport system, and L-alpha-hydroxyisocaproic acid, a substrate for L-amino acid oxidase, inhibited L-TMC-induced cytotoxicity. Rat kidney cytosol catalyzed the metabolism of L-TMC to a product absorbing at 300 nm. The increase in absorbance at 300 nm was accompanied by an increase in oxygen consumption and was inhibited by L-alpha-hydroxyisocaproic acid; moreover, the absorbance of the metabolite was quenched by addition of potassium cyanide or sodium borohydride, which indicated the formation of an imine. When L-TMC was incubated with rat kidney cytosol and sodium borodeuteride was added at the end of the incubation period, analysis by gas chromatography/mass spectrometry of the tert-butyldimethylsilyl ester of L-TMC showed the formation of [2H]TMC, indicating the intermediate formation of the imine 5,6-dihydro-2H-1,4-thiazine-3-carboxylic acid; chemically synthesized TMC imine showed similar behavior. The enzyme responsible for the metabolism of L-TMC was purified from rat kidney and was identified as L-amino acid oxidase. These observations indicate a role for L-amino acid oxidase in the bioactivation and cytotoxicity of L-TMC.

Amino Acid Oxidoreductases↗
PubMed1976

The binding of phenol red to rabbit renal cortex.

The binding of phenol red to the microsomal fraction of rabbit kidney cortex was rapid, reversible and consisted of two independent populations of binding sites: a high affinity and low capacity class which had an association constant of 11.29 - 10(3) M-1 and a binding capacity of 2.41 mumol phenol red bound per g of protein, and a low affinity binding population with an association constant of 0.80 - 10(3) M-1 and a maximal binding capacity of 55.06 mumol per g of protein. Probenecid (0.32 mM) competitively inhibited phenol red binding to only the high affinity binding site, whereas 2,4-dinitrophenol (0.77 mM) competitively inhibited phenol red binding to both the high and the low affinity population of binding sites. The binding of phenol red was highly sensitive to the cationic composition of the medium. The affinity of phenol red to the high and the low affinity binding populations was lowered by decreasing the sodium and potassium concentrations to 19 and 6 mequiv./l, respectively; however, the maximal binding capacity was unchanged. Calcium appeared to have no effect on the phenol red binding to the microsomes. All of these considerations suggest that the high affinity phenol red binding to the microsomal fraction may represent the interaction of phenol red with the physiological receptor necessary for organic acid transport at the peritubular membrane. Phenol red binding to the low affinity binding population may indicate an intracellular binding population which contributes to the intracellular accumulation of weak organic acids.

Animals↗
PubMed1992

Separation and inhibitor specificity of a second unidirectional efflux route for methotrexate in L1210 cells.

L1210 cells mediate the unidirectional and energy-dependent efflux of methotrexate. Efflux occurs primarily via a system which has a high sensitivity to prostaglandin A1, vincristine, reserpine, verapamil, and bromosulfophthalein, but evidence has also been obtained for a second efflux component with a lower response to these inhibitors. Pretreatment of L1210 cells with low concentrations of vincristine reduces methotrexate efflux by three fold and uncovers a second efflux component with an inhibitor specificity which is distinctly different from the primary efflux route. Vincristine treatment increased by 8-20-fold the concentration required for half-maximal efflux inhibition by prostaglandin A1, reserpine, bromosulfophthalein, and verapamil but had no effect on inhibition by probenecid, quinidine, or carbonylcyanide m-chlorophenylhydrazone. A selective block in the primary efflux system and retention of the second component was also achieved in cells exposed to low concentrations of prostaglandin A1 or bromosulfophthalein. These results support prior conclusions that L1210 cells contain both a primary and secondary unidirectional efflux route for methotrexate. The second system has been difficult to detect and quantitate since it comprises only 25% of total unidirectional efflux and shows a relatively low response to various efflux inhibitors.

Adenosine Triphosphate↗
PubMed1993

Fura-2 transport in toad urinary bladder epithelium: effects of antidiuretic hormone, colchicine and osmotic gradients.

Fluorescence is transferred across the toad urinary bladder when fura-2/AM is added to the mucosal or serosal sides of the epithelium. It was now observed that: (1) Oxytocin (20 nM, serosal) increased fluorescence transfer from the mucosal to the serosal but not from the serosal to the mucosal baths. The ratio between the fluorescence intensities recorded with excitation wavelengths of 340 and 380 nm indicates that the calcium sensitive probe (free fura-2) was transferred to the serosal but not to the mucosal compartment by an oxytocin sensitive transport. (2) Preincubation with probenecid did not change fluorescence transfer in basal conditions but significantly reduced the oxytocin induced increase in free fura-2 transport. (3) Fluorescence accumulation inside the tissue was strongly reduced by oxytocin, but only when fura-2/AM was added to the mucosal side. (4) An osmotic gradient, in the presence of oxytocin, further increased the transfer of fluorescence at 380 nm but not at 340 nm. This indicated that the transfer of a calcium-insensitive fraction was being stimulated. (5) Preincubation with colchicine strongly inhibited fluorescence transfer across the tissue, at both 340 and 380 nm (the 340/380 ratio did not change). (6) Tissue accumulation was increased by colchicine. (7) Vanadate did not inhibit fura-2 transfer in the toad urinary bladder. We conclude that intracellularly-generated free fura-2 is only transported across the basolateral border, and that this transfer is stimulated by ADH. The calcium-insensitive fraction is transferred by a temperature-dependent process, sensitive to an osmotic gradient and colchicine.

Animals↗
PubMed1996

Two kinetically-distinct components of UDP-glucuronic acid transport in rat liver endoplasmic reticulum.

Previous studies have documented the presence of protein-mediated transport of UDP-glucuronic acid (UDP-GlcUA) in rat liver endoplasmic reticulum (ER). Measurement of uptake at varying concentrations of high specific activity [beta-32P]UDP-GlcUA has revealed the presence of a two component UDP-GlcUA transporting system. Transport at low substrate concentrations occurred predominantly via a high affinity component (K(m) = 1.6 microM), whereas a low affinity component (K(m) = 38 microM) predominated at high substrate concentrations. The K(m) for the high affinity system is in agreement with that previously published, while the low affinity component is a new finding. The uptake of UDP-GlcUA was temperature-sensitive, time dependent, and saturable for both components. The high affinity transport was affected by trans-stimulation and cis-inhibition by UDP-N-acetylglucosamine (UDP-GlcNAc); however, the same concentrations of UDP-GlcNAc had less effect on the low affinity system. In order to further study the two transport components, various inhibitors of anion transport carriers were tested. The high affinity component was strongly inhibited by 4-acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic acid (SITS) and furosemide, while the low affinity system was less sensitive to these reagents. Dose-dependent inhibition by 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid (DIDS) was found for both transport systems. Probenecid was found to be a weak inhibitor of both components of the UDP-GlcUA uptake. Finally, the major metabolite of 3'-azido-3'-deoxythymidine, 3'-azido-3'-deoxythymidine monophosphate (AZTMP), was able to inhibit the uptake of UDP-GlcUA by both components. The results indicate the presence of two carrier-mediated UDP-glucuronic acid transporting components in rat liver ER.

4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfo↗