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B Hoener

Publications and source records attributed to B Hoener.

8 recordsLinked to original sources
PubMed1991

Alpha-tocopherol succinate does not mitigate nitrofurantoin-induced changes in the glutathione and protein thiol status of the isolated perfused rat liver.

Because it had been suggested that alpha-tocopherol might protect protein thiols (PSH) from oxidation, we were interested in determining if alpha-tocopherol could prevent or mitigate nitrofurantoin-induced changes in the glutathione (GSH) or PSH status of the liver. Isolated rat livers were perfused in the single pass mode for 310 min with Krebs-Henseleit buffer or the same buffer containing 25 nmol/ml of alpha-tocopherol succinate. Treated livers were exposed to 1200 nmol/ml of nitrofurantoin from 30 to 90 min. In control (no nitrofurantoin or alpha-tocopherol) livers, tissue levels of GSH and PSH were maintained at 78 +/- 6% and 94 +/- 6% of their initial values, but alpha-tocopherol levels declined from 34.9 +/- 0.6 nmol/g to 26 +/- 1.5 nmol/g. In the nitrofurantoin-only livers, GSH and PSH tissue levels fell to 17 +/- 10% and 49 +/- 6% of their initial levels (P less than 0.05, vs. controls), alpha-Tocopherol levels fell from 31.7 +/- 4.8 nmol/g to 17.0 +/- 2.8 nmol/g. In the alpha-tocopherol-supplemented, nitrofurantoin-treated livers, initial tissue levels of alpha-tocopherol were elevated to 43.8 +/- 1.4 nmol/g (P less than 0.05), but fell to 26.1 +/- 4.2 nmol/g. Their GSH and PSH tissue levels also declined to 7 +/- 3% and 56 +/- 8% of their initial values (P less than 0.05, vs. controls). Thus, it appeared that alpha-tocopherol supplementation was unable to prevent nitrofurantoin-induced changes in the GSH or PSH status of the liver.

Animals↗
PubMed1989

Nitrofurantoin produces oxidative stress and loss of glutathione and protein thiols in the isolated perfused rat liver.

The effects of 150, 600 or 1,200 nmol/ml of nitrofurantoin on glutathione (GSH), glutathione disulfide (GSSG), protein thiols (PSH) and cell integrity were studied in the isolated perfused rat liver. Nitrofurantoin produced a dose-dependent, up to 3-fold, increase in bile flow and a marked, up to 150-fold, increase in biliary excretion of GSSG. By the conclusion of the experiment, tissue levels of GSH had fallen to 81 +/- 14, 41 +/- 10 and 16 +/- 5% of control values at the three dose levels. Tissue levels of GSSG rose from 18.3 +/- 2.3 to 45.3 +/- 8.0 nmol/g and from 20.0 +/- 6.0 to 187 +/- 47 nmol/g within 15 min at the two higher doses, but fell to initial levels by the end of the experiment. Only at the 1,200-nmol/ml dose did the tissue levels of PSH decline, to 64 +/- 14% of initial values, by the end of the experiment. Lactate dehydrogenase and transaminases were found in the perfusate only after the GSH and PSH levels had fallen. After a 60-min exposure to 1,200 nmol/ml of NFT followed by blank perfusate for 3 h, massive engorgement of the liver was noted. Microscopic examination revealed extensive interstitial edema, nuclear pyknosis, cytoplasmic shrinkage and vacuolization, and mitochondrial dense deposits. We conclude that toxic doses of nitrofurantoin can produce cellular depletion of GSH and PSH which, if not the direct cause, at least signal the loss of cell viability.

Animals↗
PubMed1981

Nitrofurantoin disposition.

Nitrofurantoin (50 mg) was administered in a three-way random crossover design to six healthy men. After a 45-min intravenous infusion the plasma concentration data could be described by a two-compartment open-body model with a terminal t 1/2 of 58.1 +/- 15 min. Oral availability of a tablet was 0.87 +/- 0.13 on a fasting stomach and 0.94 +/- 0.13 when taken with food. Although absorption appeared to be complete, the absorption rate profile was complex and erratic. Two subjects failed to achieve the minimum effective urine concentration of 32 micrograms/ml. After the intravenous infusion 47 +/- 13% of the dose was excreted unchanged in the urine and 1.2 +/- 0.3% was recovered as the reduced metabolite aminofurantoin.

Adult↗
PubMed1977

Rate and proposed mechanism of anhydrotetracycline epimerization in acid solution.

The pathway through which the toxic tetracycline degradation product epianhydrotetracycline forms in solution was studied using high-performance liquid chromatography and circular dichroism, taking advantage of the large difference in ellipticity between the reactant and the product at 285 nm. The epimerization of anhydrotetracycline followed a reversible first-order process, and both analytical methods yielded the same rate constants. The rate constants indicate that anhydrotetracycline epimerization is faster than tetracycline epimerization. The equilibrium favored anhydrotetracycline, and the activation energies for the forward and reverse rates were almost the same as those for tetracycline epimerization. The epimerization was catalyzed by phosphate. Activation energies in 0.1 and 1 M phosphate were essentially the same. The equilibrium constants for both anhydrotetracycline and tetracycline favored the natural configuration rather than the epi series. Possible rationalization based on conformational and hydrogen bonding effects is presented.

Chemical Phenomena↗
PubMed1977

High-performance liquid-chromatographic assay for nitrofurantoin in plasma and urine.

The high-performance liquid-chromatographic method described here for the quantitative analysis for nitrofurantoin in urine and plasma involves direct analysis of urine samples and analysis of plasma samples after protein precipitation by methanol. The assay, which requires only 0.2 ml of biological fluid and shows a linear relationship in the range 0.02 to 200 mg/liter, can be performed in 9 min and is reproducible (CV less than 2%). Results for nitrofurantoin so obtained correlate well with those obtained by the Hyamine 10-X spectrophotometric method (CV = 2%), but the present method is more sensitive. With no modification, the present procedure can also be used for nitrofurazone. The sensitivity, accuracy, and convenience of the method make it suitable for clinical monitoring and pharmacokinetic/bioavailability studies with 5-nitrofuran derivatives.

Chromatography, High Pressure Liquid↗
PubMedDate not supplied

Comparison of Fe-HBED and Fe-EHPG as hepatobiliary MR contrast agents.

The authors studied the biodisposition and hepatobiliary transport of two potential magnetic resonance imaging contrast agents, the iron (III) chelates of N,N'-bis(2-hydroxybenzyl)ethylene-diamine-N,N'-diacetic acid (HBED) and diastereomeric N,N'-ethylenebis(2-hydroxyphenylglycine) (EHPG). Fecal and urinary excretion (mean +/- standard deviation), respectively, of FE-59 over 7 days in rats given tracer doses of the contrast agents were 67% +/- 2% and 22% +/- 1% for Fe-59-HBED and 22% +/- 2% and 26% +/- 5% for Fe-59-EHPG. In bile duct-cannulated rats given 0.05-mmol/kg doses labeled with Fe-59, 52% +/- 8% of Fe-59 from Fe-59-HBED but only 17% +/- 3% of that from Fe-59-EHPG was excreted into the bile within 90 minutes. Bromosulfophthalein, but not taurocholate or oxyphenonium, was shown to compete with both agents for hepatobiliary transport. Enterohepatic recirculation of both agents was less than 1%.

Animals↗