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At least 991 records · Page 55Linked to original sources
PubMed1989

Decreased binding of vasoactive intestinal peptide to intestinal epithelial cells from hypothyroid rats.

The binding of vasoactive intestinal peptide (VIP) and stimulation of adenylate cyclase by VIP were studied in intestinal epithelial cells during hypothyroidism. Experimental hypothyroidism was induced in rats by the administration of KC10(4). The binding capacity, but not the affinity, of VIP receptors decreased in the hypothyroid rats. Besides, the stimulation of cyclic AMP production by VIP was also diminished in cells from hypothyroid rats. These observations indicate a decrease of the responsiveness of intestinal epithelial cells to VIP in the hypothyroid status, suggesting a role of the peptide in the pathophysiologic mechanism of intestinal manifestations during hypothyroidism.

Animals↗
PubMed1990

Stomatocytic or discoidal erythrocyte ghosts containing only spectrin.

We extracted Triton-treated erythrocyte ghosts with 2 M KCl (Triton/KCl/ghosts), and then with 1.2 M KBr at pH 5.5 (Triton/KCl/KBr ghosts). Triton/KCl/KBr ghosts were very similar in shape to untreated ghosts, Triton ghosts and Triton/KCl ghosts under a phase-contrast microscope at various pH vales and salt concentrations, despite having lost most of their phospholipids and proteins, except for spectrin. Negatively stained Triton ghosts, Triton/KCl ghosts and Triton/KCl/KBr ghosts appeared similar to each other, but the regularity of the spectrin network structure decreased somewhat in that order. Triton/KCl/KBr ghosts were stabilized by adding both actin and band 4.1, but not by adding either alone. These and previous findings strongly suggest that the spectrin network is visible and the simplest inframembrane structure.

Bromides↗
PubMed1990

Metabolism of ethyl 2-carbamoyloxybenzoate (4003/2), a prodrug of salicylic acid, carsalam and salicylamide.

The metabolites of 4003/2 observed in vivo have been produced by incubation in vitro of 4003/2 with liver post-mitochondrial supernatants from rat, rabbit and dog. The metabolites were characterized by UV, i.r., NMR, MS and HPLC. All the metabolites detected have been or are in use as drugs for the relief of pain and inflammation. Hence, the new drug 4003/2 is a pro-drug of salicylic acid, carsalam and salicylamide.

Animals↗
PubMed1992

Ceruletide, a CCK-like peptide, attenuates dopamine release from the rat striatum via a central site of action.

Ceruletide (CLT), a cholecystokinin-like peptide was given subcutaneously or via the perfusate to rats to clarify the site of action (peripheral vs. central location) of CLT, using in vivo microdialysis techniques. Striatal dopamine (DA) release induced by haloperidol (HPD) was significantly inhibited by subcutaneously administered CLT (160 micrograms/kg) when given with a perfusate containing 15 mM K+. Subdiaphragmatic vagotomies failed to block the inhibitory effect of CLT. CLT (10(-15)-10(-11) M) locally applied, via a dialysis tube, produced an inhibitory effect on HPD-induced DA release in the striatum in a dose-dependent manner. The inhibitory effect of CLT given subcutaneously on DA release was antagonized by both locally applied proglumide and systemically administered L-365,260. These findings suggest that systemically administered CLT can directly act on the striatal neurons via CCK-B receptors and produce an inhibitory effect on DA release in the striatum under appropriate depolarization.

Animals↗
PubMed1993

Selective alterations in transglutaminase activity of rat superior cervical ganglia in response to neurotransmitters, high potassium and sialic acid-containing compounds.

We examined the in vitro effects of neurotransmitters, high KCl as well as sialic acid-containing compounds (GM1; SC) on transglutaminase (TG) activity in isolated superior cervical ganglia (SCG) one week after denervation or axotomy. Following denervation, TG activity in SCG decreased to 83% of the unoperated control value, whereas that of axotomized ganglia was 28% of control. Thus, TG activity was relatively unaffected when sympathetic ganglionic neurons were preserved, but was markedly reduced under conditions where neurons were degenerating. Addition of ACh (0.1 mM) to the medium during aerobic incubation stimulated TG activity more than 3-fold in denervated ganglia but had no effect on TG activity in axotomized ganglia. Similarly, the NE (0.05 mM)-induced decrease of TG activity observed in intact SCG was also seen following denervation (-49%) but not following axotomy. In denervated SCG, the stimulatory effects of ACh were virtually abolished by co-addition of the cholinergic antagonists, atropine or hexamethonium, while the suppressant effects of NE were blocked by the adrenergic antagonists, propranolol, prazosin or yohimbine. These results imply that transmitter-induced rapid changes in TG activity occur predominantly in ganglionic neurons. When the ganglia were depolarized by high KCl (50 mM), a significant increase in TG activity in each intact, denervated and axotomized SCG was seen with qualitatively similar manner, suggesting that high KCl-induced depolarization affects both neuronal and glial components in the SCG. The marked increase in ganglionic TG activity in response to GM1 (5 nM) and synthetic SC (0.02 mM) were lost in denervated SCG but only partially reduced in axotomized SCG.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1995

Cerebellar granule neurons develop elevated calcium responses when treated with interleukin-6 in culture.

In humans, elevated levels of cytokines are associated with several diseases (including HIV infection and Down Syndrome) that result in developmental abnormalities. Overexpression of interleukin-6 (IL-6) in the central nervous system has been shown to cause extensive neuronal abnormality in mice that becomes more evident with maturation. However, it is difficult to separate direct effects of IL-6 on the developing neurons of an intact animal from indirect effects involving effects on other cell types that possess cytokine receptors, such as microglia and astrocytes. We have found that IL-6 treatment of rat cerebellar granule neurons developing in the absence of other cell types in culture results in the persistence of large, depolarization or neurotransmitter-induced calcium transients, that are normally observed only in immature neurons. The cause of this appears to be the persistence of a calcium-induced calcium release (CICR) component of the calcium response to stimulation. This basic abnormality in neuronal development may contribute to the developmental abnormalities associated with human syndromes that involve elevated cytokine levels.

Age Factors↗
PubMed1995

HIV-1 coat protein gp120-induced increases in levels of intrasynaptosomal calcium.

The effects of human immunodeficiency virus type-1 (HIV-1) coat protein gp120 on levels of intrasynaptosomal calcium ([Ca2+]i) were determined in rat cortical synaptosomes. gp120 at concentrations of > or = 400 pM, significantly (P < 0.05) increased levels of [Ca2+]i. Treatment with 20 mM KCl, reduced the concentrations of gp120 necessary to produce significant (P < 0.001) increases in [Ca2+]i. gp120-evoked increases in [Ca2+]i were prevented either by treatment with dantrolene or by removal of extracellular calcium with BAPTA. The peak levels of gp120-induced increases in [Ca2+]i were not affected by calcium channel blockers lanthanum and nicardipine, by glutamate receptor antagonists MK-801 and NBQX, or by removal of endogenous glutamate with glutamate dehydrogenase. gp120-induced [Ca2+]i increases in presynaptic terminals may play a role in HIV-mediated effects in the central nervous system.

Animals↗
PubMed1996

Inhibition of regulatory volume decrease in swollen rat primary astrocyte cultures by methylmercury is due to increased amiloride-sensitive Na+ uptake.

Primary astrocyte cultures from neonatal rats were swollen by exposure to hypotonic buffer with and without 10 microM methylmercury (MeHg). We investigated the effects of MeHg on K+ (using 86Rb), taurine, D-aspartate (a non metabolizable analogue of glutamate) and Na+ fluxes during regulatory volume decrease (RVD), with an electrical impedance method for determination of cell volume, coupled with on-line measurements of efflux of radioactive ions and amino acids. Addition of 10 microM MeHg completely inhibited RVD in swollen astrocytes, increased the uptake of 22Na+, increased 86Rb release, and decreased 3H-taurine release. There was no effect on the rate of release of 3H-D-aspartate from swollen astrocytes. 0.5 mM amiloride completely inhibited MeHg-induced increased Na+ influx during RVD, while 1 mM furosemide had no effect. When Na+ in the hypotonic buffer was replaced with N-methyl-D-glucamine (NMDG), RVD in the presence of MeHg was indistinguishable from controls. These results indicate that MeHg increases cellular permeability to ions such as Na+ and K+, and that an increase in Na+ permeability via Na+/H+ exchange, offsetting K+ loss, is the primary mechanism in its inhibition of RVD in swollen astrocytes.

Amiloride↗
PubMed1996

Presynaptic glutamatergic function in dentate gyrus in vivo is diminished by chronic exposure to inorganic lead.

Reductions in membrane Ca2+ channel currents and depolarization-evoked neurotransmitter release have been repeatedly observed as a result of acute exposure to Pb2+. This study was performed to determine whether hippocampal glutamate and GABA release are impaired in intact animals chronically exposed to lead (Pb). As paired-pulse facilitation in the hippocampus is primarily mediated by an enhancement of glutamate release, this neurophysiological measure was also assessed in the dentate gyrus of Pb-exposed animals. Pregnant dams received 0.2% Pb acetate in the drinking water at parturition, and male offspring were weaned to the same solution as that given their dams. Control animals were maintained on distilled water. As adults, animals had intracerebral dialysis probes inserted through guide cannulae implanted 2-4 days previously and the hippocampal CAI-dentate area was perfused with modified Ringer's solution. Transmitter release was induced by perfusion with 150 mM K+ with half the animals in each group tested with Ca2+ present in the perfusate (total release) and the other half with Ca2+ absent (Ca(2+)-independent release). K(+)-stimulated total glutamate release was reduced in Pb-exposed animals relative to controls. No group differences were observed under Ca(2+)-free conditions, indicating that Ca(2+)-dependent glutamate release was decreased in exposed rats. In contrast no group differences in K(+)-stimulated total GABA release were evident, whereas an augmentation in GABA release under Ca(2+)-free conditions was revealed in Pb-exposed animals. The effects of exposure on the Ca(2+)-dependent components of release are consistent with in vitro evidence indicating an inhibitory action of Pb2+ at voltage-sensitive Ca2+ channels. A separate group of animals was prepared under urethane anesthesia with stimulating and recording electrodes placed in the perforant path and dentate gyrus, respectively. Pairs of stimulus pulses were delivered at interpulse intervals (IPI) of 10-250 ms. Pb exposure induced an increase in paired-pulse depression at the 20 ms 1PI and reduced paired-pulse facilitation at the 30 ms IPI. Decreases in paired-pulse facilitation could not be attributed to the reported effects of Pb2+ on N-methyl-D-aspartate (NMDA) receptors as MK-801 (1.0 mg/kg, s.c.) administration produced an opposing pattern of effects on paired-pulse measures. The Pb-induced suppression of paired-pulse facilitation is consistent with exposure-related decreases in total glutamate release. The impact of these effects of Pb exposure on hippocampal glutamatergic transmission may contribute to the reported effects of Pb on other forms of synaptic plasticity including long-term potentiation, a model of learning and memory.

Animals↗
PubMed1988

Changes in composition and structure of wheat bran resulting from the action of human faecal bacteria in vitro.

Cell-wall material of wheat bran was incubated with human faecal bacteria for 24-72 h and the resulting structural changes were studied by methylation analysis. Of the carbohydrate content, approximately 39% was degraded after 24 h, increasing to only 44% after 72 h. Arabinoxylans and mixed-linkage beta-D-glucans from the aleurone layer were degraded preferentially. After treatment of the bran with alkali, the extent of degradation was increased three-fold as a result of saponification of ester cross-links which facilitated increased degradation of the polymers from both the aleurone and outer, lignified, layers. There was evidence that ester linkages between the glucuronosyl residues, attached to O-2 of the (1----4)-linked xylosyl residues, and phenolic groups of lignin were also saponified. The treatment with alkali also rendered the cellulose more susceptible to bacterial attack. The alkali-soluble acidic arabinoxylan fractions of the bran were degraded readily by bacterial action, but the xyloglucans cross-linked to arabinoxylans by phenolics were relatively resistant.

Arabinose↗
PubMed1982

Uptake of hexavalent chromium by bovine erythrocytes and its interaction with cytoplasmic components; the role of glutathione.

Hexavalent chromium (Cr(VI)) anion gradually penetrated into bovine erythrocytes and bound with cytoplasmic components. Its penetration was strongly inhibited by the NH2-reactive agent, 4-acetamido-4'-isothiocyano-stilbene-2,2'-disulfonic acid (SITS) and the SH-reactive agent, N-ethylmaleimide (NEM). Gel filtration showed that the intracellular component that bound to chromium was hemoglobin. The binding affinity of Cr(VI) to hemoglobin in the absence of glutathione in vitro was found to be much less than in intact erythrocytes. However, in the presence of glutathione, the binding affinity of Cr(VI) to hemoglobin became much higher. This indicates that reduction of hemoglobin or Cr(VI) by glutathione is involved in the binding. Cr(VI) interacted only weakly with the membrane and did not cause hemolysis of bovine erythrocytes, unlike heavy metals such as Hg2+.

4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfo↗
PubMed1995

In vitro reduction of Cr(VI) by low molecular weight biomimetic components: a comparative study using UV-Vis spectroscopy.

Chromium(VI) reduction has been carried out by a variety of molecules of cellular and soil importance, such as thiol containing ones, ascorbic acid, saccharides and their derivatives, and nucleotides and their components using absorption spectroscopy. Based on the absorption data, the reductive abilities of these molecules have been obtained and the trend has been found to be ascorbic acid > thiols >> saccharides > nucleotides.

Ascorbic Acid↗
PubMed1984

Stimulation of ATP synthesis in hypothermically perfused dog kidneys by adenosine and PO4.

During continuous hypothermic perfusion of dog kidneys there occurs a gradual decrease in ATP from about 1.4 to 0.6 mumol/g wet wt after 5 days of preservation. The loss of ATP can be prevented by including both adenosine (10 mM) and PO4 (25 mM) in the perfusate. Under these conditions kidney cortex ATP levels were more than double control values--3.5 mumol/g wet wt. Both adenosine and PO4 were necessary since omission of one substance resulted in no net synthesis of ATP. Furthermore, these high levels of ATP were obtained only if adequate concentrations of adenosine were maintained during perfusion. Following 3 days of perfusion the adenosine level in the perfusate decreased to about 1 mM and under this condition ATP levels were low. Adenosine levels were maintained in the perfusate by two methods: (1) addition of fresh perfusate or (2) pretreatment of the kidney with the adenosine deaminase inhibitor--deoxycoformycin. The increased levels of ATP appear directly related to the availability of nucleotide precursors and the presence of inhibitors of the enzymes involved in the catabolism of nucleotides and nucleosides (PO4 and deoxycoformycin). Mitochondrial activity was similar in kidneys with high or low ATP levels following 5 days of preservation.

Adenine Nucleotides↗
PubMed1983

Intracellular microinjection of alkaline buffers reversibly inhibits the initial phase of hormone action in meiosis reinitiation of starfish oocytes.

Intracellular microinjection of alkaline Hepes-KOH buffers, which increases intracellular pH (pHI) from 6.92 to 7.70 in fully grown prophase-blocked oocytes of the starfish Marthasterias glacialis, like external application of ammonia and other weak bases (M. Doree, K. Sano, and H. Kanatani, 1982, Dev. Biol. 90, 13-17), inhibited meiosis reinitiation induced by 1-methyladenine (1-MeAde) or dithiothreitol (DTT), a mimetic of the hormone. Oocytes could be released from inhibition by raising the concentration of hormone or of its mimetic. Increasing pHI to 7.70 neither inhibited nor delayed meiosis reinitiation when pH was clamped after the end of the hormone-dependent period, the period during which 1-MeAde is required in the external medium for meiosis to occur, whereas it blocked the action of the hormone at low concentration when performed before the end of the hormone-dependent period. When hormone concentration was higher, germinal vesicle breakdown (GVBD) occurred, but duration of the hormone-dependent period was increased. Delay introduced by alkalinization for oocytes to reach GVBD after 1-MeAde addition was smaller at high than at medium concentrations of the hormone. Increasing pHI did not inhibit action of MPF, the cytoplasmic maturation factor which induces GVBD and the subsequent process of meiotic maturation following hormonal treatment of prophase-blocked oocytes.

Adenine↗