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Biomedical subjects

R Spector

Publications and source records attributed to R Spector.

At least 127 records · Page 7Linked to original sources
PubMed1982

Riboflavin transport by rabbit kidney slices: characterization and relation to cyclic organic acid transport.

The transport of riboflavin and the relationship of riboflavin transport to the transport of the cyclic organic acids, aminohippurate and penicillin, were investigated in small renal slices in vitro. Riboflavin was accumulated by rabbit renal slices by a transport system that was inhibited by sugar-containing and sugarless flavins, cyclic organic acids including aminohippurate and penicillin, dinitrophenol and cold temperatures, but not by D-ribose or the weak base tolazoline. The transport of riboflavin into renal slices was not solely due to intracellular binding or metabolism of the riboflavin. Aminohippurate, penicillin and riboflavin inhibited the active accumulation of [14C] aminohippurate and [14C]penicillin by kidney slices. These studies support the notions that: 1) riboflavin is accumulated in kidney cortex slices by an energy-dependent saturable transport system; 2) riboflavin accumulation by kidney slices is inhibited by cyclic organic acids and sulfhydryl reagents, but not weak bases; and 3) riboflavin is a competitive inhibitor of aminohippurate as well as an inhibitor of penicillin G accumulation by kidney slices.

Aminohippuric Acids↗
PubMed1982

Pharmacokinetics and metabolism of cytosine arabinoside in the central nervous system.

The pharmacokinetics and metabolism of [3H] cytosine arabinoside in the central nervous system were investigated. In vitro, the ability of rabbit brain slices and the isolated choroid plexus to accumulate [3H] cytosine arabinoside from artificial cerebrospinal fluid (CSF) containing 5 nM [3H] cytosine arabinoside was studied. Although in both tissues the uptake of [3H] cytosine arabinoside was saturable, neither brain slices nor the isolated choroid plexus achieved tissue/medium ratios greater than 1.0 in 30 min. After 15-min incubations iin artificial CSF containing 5 nM [3H] cytosine arabinoside, 8 +/- 2 (S.E.M.;N = 3)% of the 3H within the choroid plexuses was [3H] cytosine arabinoside phosphates; after comparable 30-min incubations, 4 +/- 1 (N = 4)% of the 3H within brain slices was [3H] cytosine arabinoside phosphates. In vivo, 2 hr after the i.c.v. injection into rabbits of [3H] cytosine arabinoside and 0, 2 ro 20 mumol of unlabeled cytosine arabinoside, it was shown that: 1) high concentrations of cytosine arabinoside in the CSF decreased the clearance of cytosine arabinoside from the CSF; 2) cytosine arabinoside was taken up and phosphorylated by brain cells in all regions tested; and 3) although the phosphorylation of [3H] cytosine arabinoside in brain cells was saturable, a portion of the [3H] cytosine arabinoside in brain was phosphorylated to [3H] cytosine arabinoside triphosphate even when the i.c.v. injectate contained 20 mumol of unlabeled cytosine arabinoside.

Animals↗
PubMed1982

Verapamil.

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Humans↗
PubMed1982

Zomepirac.

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Analgesics↗
PubMed1981

Partial purification and characterization of a folate-binding protein from human choroid plexus.

A folate-binding protein (binder) from human choroid plexus was solubilized with Triton X-100 and partially purified in three steps: (1) affinity chromatography, (2) Sephadex G-200 column chromatography, and (3) polyacrylamide gel electrophoresis. When the partially purified binder was subjected to sodium dodecyl sulfate--polyacrylamide gel electrophoresis, the binding activity was located in the region of the gel with a molecular weight between 45,000 and 60,000. The specific activity of the binder after the three purification steps was 1.2 mu g folic acid/mg protein, a 316-fold purification. Binding activity of the partially purified binder decreased below pH 6.0 and above pH 8.0, was unaffected by treatment with ribonuclease or deoxyribonuclease, but was abolished with trypsin, chymotrypsin, or protease (Streptomyces griesus). The binding of folic acid to the human binder was inhibited by folate Greater Than H4-folate Greater Than methyl-H4-folate approximately dihydrofolate approximately pteroic acid Greater Than methotrexate approximately aminopterin.

Carrier Proteins↗
PubMed1981

No effect of maternal niacin deficiency on niacin metabolism in newborn brain.

The effects of maternal niacin and tryptophan deficiency on: (1) total niacin levels and (2) niacinamide entry into brain, blood, and liver of newborn rabbits were studied. The deficient maternal diet produced a decreased concentration of the oxidized niacinamide-containing vitamers in the liver (73% of controls; P less than 0.05) but not in the brain of newborn rabbits. In both deficient and control newborn rabbits, the entry of [14C]niacinamide into brain and liver was saturable with an increasing [14C]niacinamide concentration in plasma. Also, the formation of [14C]NAD in brain and liver and [14C]niacinamide mononucleotide in blood was saturable. In vitro, the affinity of the saturable accumulation system for [14C]niacinamide in both newborn and adult rabbit brain slices was comparable (0.9 microM). The avid saturable, uptake system for niacinamide in rabbit brain contributes to total niacin homeostasis in brain.

Animals↗
PubMed1981

Lumiflavin and lumichrome transport in the central nervous system.

The transport of the lipid-soluble sugarless flavins, [14C]lumiflavin and [14C]lumichrome, into an from the isolated choroid plexus and brain slices was studied in vitro. The isolated choroid plexus accumulated both [14C]flavins by a saturable, energy-requiring process that did not depend on binding or intracellular metabolism of the [14C]flavins. Both sugar-containing and sugarless flavins, as well as cyclic organic acids, significantly inhibited [14C]lumiflavin and [14C]lumichrome uptake by the isolated choroid plexus. Within 2.5 min, 75% of the [14C]lumiflavin accumulated by the isolated choroid plexus was released into the medium. Brain slices accumulated [14C]lumiflavin by a saturable process that did not meet all the criteria for active transport. Ninety-five percent of the [14C]lumiflavin accumulated by brain slices was released into the medium within 7.5 min. In vivo, 2 h after the intraventricular injection of 6.5 nmol [14C]lumiflavin, almost all of the [14C]flavin was cleared from the CNS. Addition of 3.5 mumol FMN to the intraventricular injectate significantly decreased the clearance of [14C]lumiflavin from the CNS. These studies document that the sugarless flavins are transported by the flavin transport systems in the CNS.

Animals↗
PubMed1981

Development and localization of the thymidine phosphorylating systems in brain.

The development of the thymidine phosphorylating systems was studied in various regions of brain. Brain slices from cerebellum, brain stem, and forebrain of rabbits 2, 7, 14, 30, 90, 500, and 2500 days of age were incubated for various times in artificial CSF containing 3 nM-[3H]thymidine at 37 degrees C under 95% O2-5% CO2. When slices from all brain regions of 2-day-old rabbits were incubated in [3H]thymidine for 30 min, tissue-to-medium ratios of 3H were between 2 and 4 and declined with age, and the percentages of the total 3H in perchloric acid homogenates of brain slices as [3H]DNA were 26-29%, declining to low levels with age. However, at all ages and in all regions studied, 41--88% of the 3H within the slices was phosphorylated. After homogenization and subcellular fractionation of the brain slices incubated in [3H]thymidine for 30 min, the highest percentage of [3H]thymidine phosphates plus [3H]DNA was present in the nuclear (crude and purified) and mitochondrial fractions of all brain regions. The [3H]DNA content in the nuclear and mitochondrial fractions declined with age, but the percentage of [3H]thymidine phosphates did not. Thymidine phosphates were synthesized from thymidine in all brain regions tested throughout the entire life span.

Animals↗