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At least 19 recordsLinked to original sources
PubMed1984

Transport of calcium, germanium and rubidium ions in rice seedlings in deuterium oxide.

Deuterium oxide affected all types of transport processes of ions in rice seedlings. The processes of the active transport of Rb+, the passive diffusion of Ca2+, and the preferential and specific absorption of Ge by the seedlings in D2O solutions, were suppressively distorted by D2O. The suppressive effect on the translocation of all ions studied and the absorption of Rb+, was greater with higher concentrations of D2O. However, clear-cut relations of the effect of increasing D2O concentrations on the ion transport were not obtained. The extent of the replacement of H2O by D2O in the plant appeared to affect the movement of ions in the plant.

Biological Transport↗
PubMed2000

Suppression of microtubule dynamic instability and treadmilling by deuterium oxide.

Deuterium oxide (D(2)O) is known to promote the assembly of tubulin into microtubules in vitro, to increase the volume of mitotic spindles and the number and length of spindle microtubules, and to inhibit mitosis. Reasoning that its actions on cellular microtubules could be due to modulation of microtubule dynamics, we examined the effects of replacing H(2)O with D(2)O on microtubule dynamic instability, treadmilling, and steady-state GTPase activity. We found that replacing 50% or more of the H(2)O with D(2)O promoted microtubule polymerization and stabilized microtubules against dilution-induced disassembly. Using steady-state axoneme-seeded microtubules composed of pure tubulin and video microscopy, we found that 84% D(2)O decreased the catastrophe frequency by 89%, the shortening rate by 80%, the growing rate by 50%, and the dynamicity by 93%. Sixty percent D(2)O decreased the treadmilling rate of microtubules composed of tubulin and microtubule-associated proteins by 42%, and 89% D(2)O decreased the steady-state GTP hydrolysis rate by 90%. The mechanism responsible for the ability of D(2)O to stabilize microtubule dynamics may involve enhancement of hydrophobic interactions in the microtubule lattice and/or the substitution of deuterium bonds for hydrogen bonds.

Animals↗
PubMed1996

Interactions of intercalating fluorochromes with DNA analyzed by conventional and fluorescence lifetime flow cytometry utilizing deuterium oxide.

Deuterium oxide (D2O) has been shown in previous studies to increase both the fluorescence lifetime and fluorescence intensity of propidium iodide (PI) and ethidium bromide (EB) when bound to nucleic acid structures. We have used spectroscopic analysis and conventional and phase-sensitive flow cytometry to compare changes in PI and EB fluorescence intensity and lifetime bound to DNA and fixed Chinese hamster ovary (CHO) cells in the presence of D2O vs. phosphate-buffered saline (PBS). Spectroscopic and flow cytometric studies showed a twofold enhancement of fluorescence intensity of PI and EB bound to fixed CHO cells in D2O and a 5 ns increase in PI and EB fluorescence lifetimes in D2O. The fluorescence lifetime of HL-60 cells stained with PI or EB was found to be 1-2 ns different from that of CHO cells, indicating that the lifetime of these fluorochromes is sensitive to chromatin configuration in different cells types. Apoptotic subpopulations of HL-60 cells had a significantly reduced fluorescence lifetime compared to nonapoptotic subpopulations. Results indicate that different chromatin states, or differences in the structures of PI and EB, lead to alterations in the fluorescence intensity and fluorescence lifetime of these intercalating probes.

Animals↗
PubMed1991

Effect of substitution of hydrogen oxide by deuterium oxide on thermotropic transition between the interdigitated gel phase and the ripple phase of dihexadecylphosphatidylcholine.

Thermotropic transitions of dihexadecylphosphatidylcholine (DHPC) dispersions in hydrogen oxide (1H2O) and deuterium oxide (2H2O) were investigated by differential scanning calorimetry (DSC). In DHPC dispersions, transition temperature between interdigitated gel phase (L beta I) and ripple phase (P beta') is lower in 2H2O than in 1H2O, and transition between the ripple phase (P beta') and fluid phase (L alpha) in 2H2O occurs at a temperature slightly higher than in 1H2O. In dipalmitoylphosphatidylcholine (DPPC) dispersions, on the other hand, transition temperature between lamellar gel phase (L beta') and ripple phase is higher in 2H2O than in 1H2O. These results suggest that the interdigitated gel phase is more stable in 1H2O than in 2H2O. To account for the shift of transition temperature by the water substitution, difference of interfacial energies between these aqueous environments is discussed.

Calorimetry, Differential Scanning↗
PubMed1984

Deuterium-oxide-induced histamine release from basophils of allergic subjects. I. Responsiveness to deuterium oxide requires an activation step.

Basophils from many atopic persons, and especially asthmatic patients, have been shown to release histamine in response to 44% deuterium oxide (D2O), whereas basophils from nonatopic persons do not release histamine. The present experiments analyzed the mechanisms by which D2O mediated release. It was found that although D2O induced release from washed leukocytes, it failed to induce release from whole blood or from leukocytes that had sedimented but had not been washed. The kinetics of release after washing were rapid and were equivalent regardless of the temperature at which cells were sedimented (O degrees or 37 degrees C). Washed cells became desensitized to the action of D2O within 30 to 60 min at 37 degrees C, whereas unwashed leukocytes did not become desensitized. Serum or plasma inhibited D2O-induced release, although high concentrations (1/5) were less inhibitory than lower ones (1/10 to 1/100). Basophils from D2O responders also released histamine in response to a "platelet enhancing factor" (PEF), whereas those from D2O nonresponders did not. As with D2O-mediated release, PEF-mediated release occurred only with washed leukocytes, desensitized within 30 to 60 min at 37 degrees C, and was inhibited by serum. These results suggest that D2O induces histamine release by augmenting the effects of an endogenous activation mechanism, and that PEF acts on the same (D2O-responsive) donors to augment this activation mechanism. Cell activation, as well as desensitization of this activation mechanism, occurs rapidly when basophils are washed free of plasma inhibitors and placed at 37 degrees C.

Asthma↗
PubMed1991

Radioprotection of cultured cells by preincubation in medium containing deuterium oxide.

Pretreatment with deuterium oxide (D2O) has been shown to protect mice against lethal effects of X-rays. In contrast, X-irradiation of cultured mammalian cells in D2O-containing medium has previously been reported to result in increased cell killing. Therefore, the effects of preincubation in medium containing 20% D2O on radiosensitivity were tested, using cells of a heat-sensitive cell-cycle mutant (21-Tb) of the murine mastocytoma P 815-X2. The mutant cells proliferate at 33 degrees C and are arrested in G1 phase in a state of reversible proliferative quiescence at 39.5 degrees C. Prior to irradiation with single X-ray doses of 0-10 Gy, the cells were cultured in normal or D2O-containing medium, either for 96 h at 33 degrees C ('proliferating cells'), or for 72 h at 33 degrees C followed by 24 h at 39.5 degrees C ('arrested cells'). After X-irradiation the cells were resuspended in normal medium, and cell survival was determined by the capacity of cells to form colonies in fibrin gels. Preincubation in medium containing 20% D2O resulted in a radioprotective effect on both proliferating and arrested cells, particularly at the higher X-ray doses. This radioprotection was manifested as a decreased slope of the semilogarithmic survival curves, whereas pretreatment with D2O had no significant effect on postirradiation repair as judged from Dq values. These results support the interpretation that the increase in postirradiation survival may be attributed to incorporation of deuterium into cellular metabolites during the period of preincubation.

Cell Line↗
PubMed1979

Taste responses to deuterium oxide.

Substitution of deuterium oxide (D2O) as the solvent in taste stimuli elicits neural responses which differ from ordinary water (H2O). Previous reports have shown that D2O is toxic to many animals and rats avoid drinking it when offered H2O simultaneously. In the current study, summated responses were recorded from the chorda tympani nerves of rats after NaCl, KCl, sucrose and quinine were applied to the tongue in solutions of either D2O or H2O. Both solvents were used as the adapting or rinse solution in separate series. On tongues adapted to H2O, D2O elicited mean responses which were equivalent to 29% of the response to 0.1 M NaCl. The threshold concentration of D2O in H2O was between 25% and 50%. Solutes in D2O yielded responses which were greater than corresponding solutions of H2O when adapting rinse was H2O. Adaptation to D2O diminished the responses to D2O solutions of NaCl, KCl and sucrose but not quinine. This observation suggests that some portion of the augmented response to stimuli in D2O is due to the solvent itself. The taste of water has been examined by both electrophysiological methods and by behavior, but none of the mechanisms espoused for its effect seem adequate to explain the response to D2O. Water structure at the interface between molecular components of the cell membrane and the bulk phase of the surrounding medium is considered as a locus for disparity in the taste responses to D2O and H2O in the rat.

Animals↗
PubMed1983

Effect of deuterium oxide on gastrin release from rat antral mucosal fragments.

The effects of the microtubule stabilizing agent, deuterium oxide, on in vitro rat antral gastrin release were examined under basal conditions and during stimulation with isobutyl methylxanthine and bombesin plus isobutyl methylxanthine. Basal gastrin release from antral mucosal fragments was unaffected by increasing media concentration of deuterium oxide (12.5 to 75% v/v) during 1 h incubations. Gastrin release stimulated by isobutyl methylxanthine (0.1 mM), a potent inhibitor of phosphodiesterase activity, was inhibited completely by 12.5% deuterium oxide. Bombesin (1 X 10(-8) M) in the presence of IBMX (0.1 mM) stimulated gastrin release (29.7 +/- 1.9% of total gastrin). This was significantly greater than gastrin released under control conditions and with IBMX alone: 12.0 +/- 1.1 (P less than 0.001) and 20.2 +/- 2.6% of total gastrin (P less than 0.02), respectively. Partial inhibition of bombesin-IBMX stimulated gastrin release was achieved with 12.5% and 25% deuterium oxide and stimulation of gastrin release was inhibited completely by 50% deuterium oxide. In contrast to these results, gastrin release stimulated by the calcium ionophore A23187 was not inhibited by 50% deuterium oxide. Additional studies were performed to assess reversibility of the effects of deuterium oxide on stimulated gastrin release. Antral tissue exposed to initial culture medium containing deuterium oxide (50%) and bombesin-IBMX for 60 min was exchanged for medium without deuterium oxide. Restimulation of antral tissue during the second hour of culture resulted in gastrin release that was comparable to that observed in cultures not exposed to deuterium oxide during the first hour of culture. Reversibility of the effects of deuterium oxide suggest that a functional alteration in microtubular function is restored by removal of heavy water from the culture medium. Results of these experiments indicate that deuterium oxide is capable of inhibiting gastrin release stimulated by the peptide hormone bombesin and by the phosphodiesterase inhibitor isobutyl methylxanthine. Furthermore, these results suggest that increased levels of intracellular calcium achieved by the action of ionophore A23187 prevent microtubular stabilization by deuterium oxide.

1-Methyl-3-isobutylxanthine↗
PubMed1975

Scanning isoelectric focusing in small density-gradient columns. IV. The use of deuterium oxide for preparing the density gradient and its effects on isoelectric points of proteins.

The use of deuterium oxide as a substitute for sucrose in preparing density gradients for small isoelectrofocusing columns has been investigated. A density gradient was created directly in a 1.5-ml column by free inter-diffusion of three deuterium oxide solutions for 3 min. The resulting deuterium oxide concentration course (as shown by measurement of the refractive-index gradient) had a very high degree of linearity. Test runs with beta-lactoglobulin and sperm-whale myoglobin showed that the strength and stability of the deuterium oxide density gradient should normally be sufficient for stabilization of protein zones against convection during isoelectric focusing. The isoelectric points of beta-lactoglobulins A and B were found to increase as the concentration ratio of deuterium oxide to water at focusing level increased. Within the limits of experimental error, the pI shift corresponding to a given change in solvent composition was equal for both components. These findings are accounted for in terms of the deuterium isotope effect on the dissociation constants of protolytic groups and the shift in the asymmetry potential of the glass electrode in deuterium oxide as compared with water. The spontaneous reduction of sperm-whale metmyoglobin to ferrous myoglobin, which occurs on prolonged isoelectric focusing, is discussed, as are the benefits and drawbacks of deuterium oxide as a density-gradient solute.

Animals↗
PubMed1968

Protein aggregation. The effect of deuterium oxide on large protein aggregates of C-phycocyanin.

The amount of 11s aggregate in phycocyanin, normally stimulated by hydrophobic forces, is dramatically increased by the presence of deuterium oxide. Proteins in which hydrophobic forces are not proposed as a mechanism for aggregation are unaffected by deuterium oxide. These observations are consistent with the lower critical micelle concentration reported for ionic detergents in deuterium oxide. Phycocyanin samples containing a majority of material sedimenting faster than 11s were also investigated in the presence of deuterium oxide with the following findings: the most rapidly sedimenting species in water buffer is 24s; in deuterium oxide more than 10% of the protein sediments at 67s and substantial amounts of other species with sedimentation coefficients larger than 24s are present. These large quantities of species sedimenting faster than 24s are found in deuterium oxide buffers from pD5.5 to 7.0. Sucrose-density-gradient studies in deuterium oxide at pD6.0 confirm the presence of large amounts of more rapidly sedimenting species. Spectrophotometric studies on fractions from the sucrose-density-gradient experiments indicate with the presence of higher aggregates a red shift of the visible-absorption maximum and an enhancement of the E(620)/E(280) ratio. Fluorescence-emission studies show a greater relative fluorescence efficiency for these higher aggregates and are consistent with the suggested enhancement of higher aggregates in deuterium oxide. The existence of phycocyanin aggregates of such a large size is suggested to be of importance in vivo, with phycocyanin playing a role as a structural protein.

Centrifugation, Density Gradient↗
PubMed1991

Deuterium oxide prevents hypertension and elevated cytosolic calcium in hypertensive rats.

Increased calcium uptake in vascular tissue, leading to elevated cytosolic free calcium, has been implicated in the pathophysiology of hypertension. This study examined the dose-dependent effect of deuterium oxide (5%, 10%, or 20% in drinking water) on systolic blood pressure, aortic calcium uptake, and platelet cytosolic free calcium in spontaneously hypertensive rats. Starting at age 8 weeks, spontaneously hypertensive rats were divided into four groups of six animals each. The drinking water of groups 1, 2, 3, and 4 was replaced by 100% water and 5%, 10%, and 20% deuterium oxide in water, respectively, for another 7 weeks. Ten Wistar-Kyoto rats, age 8 weeks, were given 100% water for the next 7 weeks. The usual increase in systolic blood pressure and the associated increase in aortic calcium uptake and platelet cytosolic free calcium in spontaneously hypertensive rats at age 15 weeks was lowered in a dose-dependent manner by deuterium oxide. Deuterium oxide also prevented renal vascular changes in spontaneously hypertensive rats. A minimum dose of 10% deuterium oxide was needed to completely prevent the development of hypertension, elevated aortic calcium uptake, platelet cytosolic free calcium, and renal vascular changes in spontaneously hypertensive rats.

Animals↗
PubMed1976

Potentiation of cutaneous reactivity and blood leucocyte histamine release by deuterium oxide in human beings.

Deuterium oxide (D2O) is known to potentiate non-cytotoxic histamine release in vitro. It has been shown (5) that D2O could also potentiate in vivo immediate-type hypersensitivity in dogs and monkeys. Present studies demonstrate potentiation in vivo by D2O of the cutaneous reactivity in 48/80, PHA and Dermatophagoides cutaneous reactions in human beings. PHA histamine release from human leucocytes is also potentiated by D2O in vitro.

Deuterium↗
PubMed1994

Fructose-induced hypertension, hypertriglyceridemia and elevated cytosolic calcium in rats: prevention by deuterium oxide.

We examined the effect of 5% deuterium oxide (D20) in drinking water on systolic blood pressure, platelet cytosolic free calcium, aortic calcium uptake and plasma insulin, glucose and triglycerides in rats with fructose-induced hypertension. Eighteen male Wistar-Kyoto (WKY) rats, age 8 weeks, were divided into 3 groups of 6 animals each. Animals in group I were given water; group II, 8% fructose and group III, 8% fructose + 5% D20 as their drinking water for the next 15 weeks. Systolic blood pressure in the fructose treated rats was significantly higher (p < 0.01) than in animals on water after 2 weeks and remained higher throughout the study. At 15 weeks, systolic blood pressure, platelet cytosolic calcium, aortic calcium uptake and plasma glucose, insulin and triglycerides were significantly higher (p < 0.01) in the fructose treated rats compared with rats from other groups. Deuterium oxide given together with fructose prevented development of high blood pressure and the associated increase in platelet cytosolic calcium, aortic calcium uptake and plasma triglycerides. D20 treatment did not prevent fructose induced increases in plasma insulin and glucose. The parallel increase in systolic blood pressure, cytosolic free calcium, and in vascular calcium uptake suggests that an increased cytosolic free calcium is involved in the pathophysiology of hypertension. D20 prevents this hypertension by normalizing cytosolic free calcium.

Animals↗
PubMed1997

Measurement of total body water content in horses, using deuterium oxide dilution.

OBJECTIVE: To measure total body water (TBW) content in horses, using deuterium oxide (D2O) dilution. ANIMALS: Six 8- to 10-year-old healthy untrained mixed-breed horses, weighing (mean +/-SD) 503.4 +/- 64.0 kg. PROCEDURE: After a 12-hour nonfeeding period, 6 horses were given D2O (0.14 g/kg of body weight) via nasogastric tube. Blood samples were collected from a preplaced indwelling jugular vein catheter prior to and 1 to 8, 10, 12, 14, and 24 hours after administration of D2O. Blood samples were centrifuged immediately, and plasma was collected and stored at -70 C until analysis. The D2O content in plasma was measured by zinc reduction to deuterium gas. The resulting gas was measured, using an isotope ratio mass spectrometer. RESULTS: Deuterium oxide was rapidly absorbed from the gastrointestinal tract of all horses, and reached peak (mean +/- SD) plasma concentration (1,454.4 +/- 163 delta D/ml or parts/thousand) 1 hour after administration. Plasma concentration decreased slowly during the next 2 to 3 hours, then remained statistically constant from 2 to 5 hours (early plateau phase) and 3 to 7 hours (late plateau phase) after administration. Mean +/- SEM TBW content was 623.0 +/- 2.2 ml/kg (62.3% of body weight) for the early plateau phase and 630.3 +/- 2.2 ml/kg (63.0% of body weight) for the late plateau phase. CONCLUSION: Deuterium oxide dilution appears to be of value for measurement of TBW content in horses, and has a 4-hour plateau effect. Equilibration of D2O with large intestinal water may be the reason for the prolonged equilibrium time and plateau effect seen in these horses. CLINICAL RELEVANCE: Deuterium oxide appears safe and efficacious for determining TBW content in horses and may be helpful for determining changes in TBW content during exercise and disease.

Animals↗
PubMed1990

Deuterium oxide normalizes blood pressure and vascular calcium uptake in Dahl salt-sensitive hypertensive rats.

This study examined the effect of 25% deuterium oxide in drinking water on systolic blood pressure, uptakes of calcium, and rubidium 86 by aortas of Dahl salt-sensitive rats on 0.4% (low) and 8% (high) sodium chloride (salt) diet. Twenty-four rats were divided into four groups. Groups I and II were on the low salt diet and groups III and IV on the high salt diet from 6 weeks of age. Additionally, at 10 weeks of age groups I and III were placed on 100% water and groups II and IV on 25% deuterium oxide. At 14 weeks, systolic blood pressure, uptakes of calcium, and rubidium 86 by aortas were significantly higher (p less than 0.01) in rats on the high salt diet as compared with those on the low salt diet. Deuterium oxide intake normalized systolic blood pressure and aortic calcium uptake but not aortic rubidium 86 uptake in hypertensive rats on the high salt diet. Deuterium oxide had no effect on blood pressure or aortic calcium uptake in rats on the low salt diet. The parallel increase in systolic blood pressure and vascular calcium uptake suggests that increased calcium uptake mechanisms are associated with hypertension in salt-sensitive Dahl rats. Furthermore, deuterium oxide appears to normalize elevated blood pressure in salt-sensitive hypertensive rats by normalizing elevated vascular (aortic) calcium uptake.

Animals↗
PubMed1988

Validation of the deuterium oxide method for measuring average daily milk intake in infants.

The deuterium oxide elimination method for measuring average daily milk intake was validated against measured formula intake in 16 studies of 11 infants in a metabolic ward. Deuterium oxide (approximately 0.10 g/kg body wt) was given orally. Deuterium enrichment was measured in urine samples collected predose, as available for 6-h postdose for TBW determination, and at 24 h and 5-10 d postdose for HDO elimination calculated according to the two-point method. Urine samples were vacuum distilled, water was reduced to hydrogen gas, and deuterium enrichment was measured by isotope-ratio mass spectrometry. Milk intake was measured throughout the elimination period from prefeeding and postfeeding bottle weights (n = 12) or volumes (n = 4). Without corrections for atmospheric water influx, milk intake was overestimated by 76 g/d (6%). With corrections for estimated metabolic water production, isotopic fractionation, and atmospheric water influx, deuterium measured 98% +/- 3% or 1300 g milk intake/d compared with actual milk intake of 1329 +/- 206 g/d.

Body Water↗
PubMed2000

Mechanisms associated with the negative inotropic effect of deuterium oxide in single rat ventricular myocytes.

Deuterium oxide (D2O) is known to cause a negative inotropic effect in muscle although the mechanisms associated with this response in cardiac muscle are not well understood. We studied the effects of D2O in single rat ventricular myocytes in order to characterise the mechanisms associated with its negative inotropic effect and to assess its possible use as an acute modulator of microtubules. D2O rapidly reduced the magnitude of contraction in rat ventricular myocytes, and there was some recovery of contraction in the presence of D2O. Colchicine, an agent known to depolymerise microtubules, did not modify the effect of D2O. D2O decreased the L-type Ca2+ current (ICa), measured under whole cell and perforated patch clamp conditions. Slowing of the time to peak and a delay in inactivation of ICa were observed. Intracellular calcium ([Ca2+]i) and sodium ([Na+]i) were measured using the fluorescent indicators fura-2 and SBFI, respectively. The fall in contraction upon exposure to D2O was not associated with a fall in the [Ca2+]i transient; this response is indicative of a reduction in myofilament Ca2+ sensitivity. Both the [Ca2+]i transient and [Na+]i increased during the partial recovery of contraction in the presence of D2O. We conclude that a decrease in the myofilament sensitivity for Ca2+ and a reduction in Ca2+ influx via ICa are principally responsible for the negative inotropic effect of D2O in cardiac muscle. We found no evidence to explain the negative inotropic effect of D2O in terms of microtubule proliferation. In addition we suggest that acute application of D2O is not a useful procedure for the investigation of the role of microtubules in excitation-contraction coupling in cardiac muscle.

Animals↗