Fractional Tritium Research Articles

Effects of external energetic factors on tritium release from the EXOTIC 8-3/13 neutron-irradiated beryllium pebbles

Tritium release from samples of 9–13 mg of the EXOTIC 8-3/13 neutron-irradiated beryllium pebbles under the separate and simultaneous action of temperature 490–770 K, 5 MeV fast-electron radiation 14 MGy h −1 for 3 h and magnetic field (MF) of 1.7 T was investigated. The pebbles were found to be very dissimilar with respect to their total tritium content—2.5–9 MBq g −1. The batch contained also some coarse agglomerates of the pebbles containing 10–19 MBq g −1 of tritium having also a high tritium release. For the pebbles having the total tritium 2.5–5.3 MBq g −1, the electron radiation for 3 h caused the fractional tritium release 17–26% ( B = 0) and 21–29% ( B = 1.7 T), the temperature of the pebbles being <550 K. The annealing of the pebbles at the temperature ramp at 5 K/min to 553 K and at 553 K for 3 h caused the fractional tritium release 10–19% ( B = 0) and 14% ( B = 1.7 T). For the pebbles having the total tritium 3.6–5.8 MBq g −1, the annealing of the pebbles at the temperature ramp at 5 K/min to 770 K and at 770 K for 1 h caused the fractional tritium release 17–24% ( B = 0) and 25% ( B = 1.7 T), but with the simultaneous additional action of the electron radiation for 3 h the fractional tritium release was 24–42% ( B = 0) and 32–37% ( B = 1.7 T).

Tritium sorption and desorption from JET beryllium tiles under temperature, electron radiation and magnetic field

Tritium release at annealing of samples cut from beryllium tiles exposed to D + D, D + T plasma in the Joint European Torus (JET) was investigated under 5 MeV fast-electron radiation at the dose rate 14 MGy h −1 and in a magnetic field of 1.7 T separately and simultaneously in order to evaluate possible effects of these factors. Abundances of chemical forms of tritium—molecular T 2 (44%), atomic T 0 (42%), and ionic T + (14%) and their distribution were determined in the plasma-exposed beryllium samples with lyomethods. Fast-electron radiation considerably increased the fractional tritium release at annealing by a factor of approximately 5. The magnetic field increased the fractional tritium release at annealing both without and under electron radiation by approximately 25%. Sorption of tritium in samples cut from an unused beryllium tile was investigated at about 1 Pa of T 2 at 773 K for 3 h both with and without simultaneous electron radiation and/or magnetic field. The amount of the tritium sorbed was found to be 3.3–6.2 kBq cm −2. Most of the tritium sorbed was localized in subsurface layers up to a depth of 80 μm of the beryllium samples.

Subcellular Distribution of Organically Bound Tritium in the Rat Liver after Ingestion of Tritiated Water and Some Tritiated Organic Compounds

Tritiated water and some tritiated organic compounds (leucine, glucose and thymidine) were administered to rats by oral ingestion and the content of organically bound tritium (OBT) in subcellular fractions (cold PCA soluble, ethanol-ether soluble, hot PCA soluble and alkali soluble) of the liver were determined at various time points after ingestion. In the case of tritiated water, the initial OBT content was high in the cold PCA soluble fraction, which contains low molecular weight components, but as the time proceed the OBT was distributed to other fractions, which contains relatively high molecular weight components. Significant time variation in the OBT content was observed in the hot PCA soluble fraction containing nucleic acids, in which the OBT content, expressed as percentage of OBT content in all fractions, changed from 1 % at 12 hours to 15 % at 50 days. In the cases of tritiated organic compounds, the subcellular distribution of OBT was widely changed owing to their biochemical and metabolic characteristics. Thus, the OBT distribution among subcellular fractions was changed depending on the chemical form at ingestion and on the time after ingestion. The OBT distribution among four subcellular fractions after 22 day’ continuous ingestion was also dependent on the chemical form of ingested tritium. Present results should be taken into account for internal dose estimation of tritium in different chemical forms.

Mechanism of resistance to alpha-adrenergic receptor antagonists of renal nerve stimulation-induced vasoconstriction at low frequencies.

To determine why renal vasoconstriction elicited by periarterial nerve stimulation (RNS) at lower frequencies (< 4 Hz) is resistant to alpha-adrenergic receptor blockade in the rat kidney, we reevaluated the effect of alpha-receptor antagonists on the vasoconstrictor response to norepinephrine (NE) and to RNS and on the release of adrenergic transmitter. The alpha-receptor antagonist prazosin (PZ) at 0.2 and 7 nM reduced the vasoconstrictor response to NE, and 2.4 microM PZ abolished it. PZ (0.2 or 7 nM) reduced RNS-induced vasoconstriction without altering the fractional tritium overflow. PZ (2.4 microM) enhanced fractional tritium overflow and reduced the vasoconstrictor response to RNS at 2-10 Hz, but not at 0.5 or 1 Hz. The effect of 0.2 nM PZ to reduce RNS-induced vasoconstriction was reversed by increasing the concentration to 2.4 microM. Corynanthine (COR; 2.6 microM), a preferential alpha-receptor blocker, or phenoxybenzamine (PBZ; 30 nM) abolished the vasoconstrictor response to NE but only partially reduced response to RNS and enhanced the fractional tritium overflow. Rauwolscine (RW; 2.5 nM), a preferential alpha 2-receptor antagonist, did not alter the vasoconstrictor response to NE but potentiated RNS-induced vasoconstriction and fractional tritium overflow. RW (7.7 microM) inhibited NE-induced vasoconstriction but potentiated the vasoconstrictor response to RNS and fractional tritium overflow. PZ (7 nM) abolished the potentiation by RW and reduced the vasoconstrictor response to RNS. These data suggest that a component of RNS-induced vasoconstriction in the rat kidney is attributable to co-release of a nonadrenergic transmitter with NE. The diminished effect of alpha-receptor antagonists at higher concentrations (e.g., PZ 2.4 microM) to reduce RNS-induced vasoconstriction is caused by their prejunctional action to enhance co-release of the nonadrenergic transmitter.

Neuropeptide Y inhibits adrenergic transmitter release in cultured rat superior cervical ganglion cells by restricting the availability of calcium through a pertussis toxin-sensitive mechanism

Neuropeptide Y has been reported to inhibit the release of the adrenergic transmitter from sympathetic nerves in many tissues. The purpose of this study was to determine the mechanism of the inhibitory effect of neuropeptide Y on the release of the adrenergic transmitter in cultured superior cervical ganglion cells prelabeled with tritiated norepinephrine. In cultured superior cervical ganglion cells superfused with a HEPES-buffered saline, electrical field stimulation (1 Hz, 30 pulses, 1 ms, 60 V) increased the fractional overflow of tritium. Neuropeptide Y (50 nM) attenuated this depolarization-induced increase in transmitter release. The nonhydrolyzable cAMP analog, 8-(4-chlorophenylthio)cyclic AMP (100 μM) and the potassium channel blockers, tetraethylammonium chloride (1 mM) and 4-aminopyridine (300 μM) potentiated the electrically stimulated increase in fractional tritium overflow but failed to alter the inhibitory effect of neuropeptide Y on fractional tritium overflow. Increasing the calcium concentration in the superfusion fluid from 1.8 to 5.4 mM potentiated the electrically stimulated increase in fractional tritium overflow and attenuated the inhibitory effect of neuropeptide Y. Reduction of superfusion fluid calcium concentration to 0.5 mM decreased electrically stimulated fractional tritium overflow and augmented the inhibitory effect of NPY on release of tritium. The fractional release of tritium in response to the calcium ionophore, ionomycin, was not significantly altered by neuropeptide Y. In Fura-2-loaded isolated sympathetic neurites obtained from superior cervical ganglia explants, the depolarization-induced (54 mM KC1) increase in cytosolic calcium was attenuated by neuropeptide Y (50 nM). Pertussis toxin (100 ng/ml for 4 h) pretreatment abolished both the neuropeptide Y-induced decrease in electrically stimulated fractional tritium overflow and the reduction in depolarization-induced increase in cytosolic calcium. These data suggest that NPY inhibits adrenergic transmitter release in cultured superior cervical ganglion cells by decreasing the availability of calcium for the release process by a pertussis toxin-sensitive mechanism.

Cyclic AMP modulates but does not mediate the inhibition of [ 3H]norepinephrine release by activation of alpha-2 adrenergic receptors in cultured rat ganglion cells

The purpose of this study was to determine whether a decrease in cyclic AMP accumulation mediates the inhibition of norepinephrine release in response to alpha-2 adrenergic receptor activation in cultured rat superior cervical ganglion cells. Superior cervical ganglia from neonatal rats were dissociated and cultured on collagen-coated plastic strips. Neurotransmitter release was assessed by measuring the fractional overflow of tritium in superfused cells prelabeled with [ 3H]norepinephrine. Intracellular cyclic AMP accumulation was measured using radioimmunoassay. Electrical field stimulation at 1 Hz, 30 pulses, 1 ms duration at 20 min intervals produced an increase in the fractional overflow of tritium that was composed predominantly of intact [ 3H]norepinephrine. The alpha-2 adrenergic receptor agonist UK-14,304 dose-dependently attenuated the increase in fractional tritium overflow elicited by electrical field stimulation. The adenylyl cyclase activator, forskolin, increased cyclic AMP accumulation in superior cervical ganglion cells and UK-14,304 dose-dependently inhibited forskolin-stimulated cyclic AMP accumulation. UK-14,304 had no effect on basal cyclic AMP accumulation or cyclic AMP accumulation during electrical field stimulation. Forskolin (1–10 μM) or the non-hydrolysable cAMP analog, 8-(4-chlorophenylthio)adenosine 3′,5′-cyclic monophosphate (1–100 μM), slightly increased basal and dose-dependently potentiated the increase in fractional tritium overflow in response to electrical stimulation. Despite enhancement by forskolin and 8-(4-chlorophenylthio)adenosine 3′,5′-cyclic monophosphate of fractional tritium overflow caused by electrical field stimulation, UK-14304 (1–10 μM) reduced release to a similar degree as that observed in the absence of forskolin or 8-(4-chlorophenylthio)adenosine 3′,5′-cyclic monophosphate. These data suggest that in cultured rat superior cervical ganglion cells, stimulation of alpha-2 adrenergic receptors decreases cyclic AMP accumulation when adenyl cyclase is activated. A decrease in cyclic AMP does not mediate the inhibition of [ 3H]norepinephrine release in response to alpha-2 adrenergic receptor activation, although elevations in cyclic AMP can enhance electrically-stimulated release of [ 3H]norepinephrine.

Allicin-induced hypotension in rabbit eyes.

The intent of this work was to examine the actions of allicin on 1) intraocular pressure (IOP) in normal and unilaterally sympathectomized (SX) rabbits; 2) cAMP accumulation in the rabbit iris-ciliary body (ICB) and cultured nonpigmented epithelial (NPE) ciliary body cells; and 3) 3H-norepinephrine (NE) release by calculating fractional tritium overflow in response to electrical field stimulation (EFS, 5 Hz, 12 V/cm) in isolated, perfused rabbit ICBs. Allicin, one of the active compounds produced by garlic, was evaluated on IOP and it was determined that allicin (1, 2.5, or 10 micrograms), topically, but not the precursor, alliin (10 micrograms), lowered the IOP unilaterally in normal rabbits. Allicin (10 micrograms) reduced the IOP by 6 +/- 1 mmHg (n = 4) in normal rabbits at 2 hrs (maximum response) whereas no change occurred in sympathectomized rabbit eyes. Moreover, allicin (0.01, 0.1, or 1 microM) caused 40, 40, or 52% inhibition, respectively, of 3H-NE overflow in response to EFS. Isoproterenol (ISO, 1 microM) stimulated cAMP accumulation by 3.6 and 9 fold in isolated rabbit ICB and cultured NPE cells, respectively. Allicin (1 microM) had no effect on basal cAMP level while it inhibited ISO-stimulated cAMP accumulation by 40% and 23% in ICB and NPE cells, respectively. This study suggests that allicin lowered IOP, in part, by dual actions at the neuroeffector junction.

Mechanism of Neurotransmitter Release Elicited by the Preferential ?1-Adrenergic Receptor Agonist Phenylephrine in Superfused Superior Cervical Ganglion Cells in Culture

Phenylephrine increased [3H]norepinephrine efflux and accumulation of cyclic AMP in cultured rat superior cervical ganglion cells superfused with Tyrode's solution. The purpose of this study was to determine the mechanism and relationship between these two events. Electrical stimulation (1-2 Hz), potassium chloride (50 mM), and the preferential alpha 1-adrenergic receptor agonist phenylephrine (1-100 microM) increased fractional tritium efflux, whereas methoxamine, cirazoline, and amidephrine were relatively ineffective. Phenylephrine, but not methoxamine and cirazoline, also increased cyclic AMP accumulation. Phenylephrine-induced tritium efflux was not altered by alpha- and beta-adrenergic receptor antagonists or by removal of extracellular calcium. Phenylephrine-induced cyclic AMP accumulation was blocked by the beta-adrenergic receptor antagonists propranolol and atenolol. Forskolin (10 microM) and the nonhydrolyzable cyclic AMP analogue 8-(4-chlorophenylthio)cyclic AMP (100 microM) had minimal effect on tritium efflux. However, phenylephrine-evoked increase in tritium efflux was dose dependently attenuated by the neuronal uptake blocker cocaine, and phenylephrine dose-dependently inhibited the incorporation of [3H]norepinephrine into neuronal stores. We conclude that the increase in tritium efflux induced by phenylephrine is independent of cyclic AMP accumulation and appears to be mediated by uptake of phenylephrine via the neuronal carrier-mediated amine transport process, which in turn promotes efflux of the adrenergic transmitter from its storage sites.

Effect of blockade of noradrenaline re‐uptake on evoked tritium overflow from mouse vasa deferentia and rat cortex slices

1. In tissues previously incubated with [3H]-noradrenaline exposure to cocaine (0.1 to 10 microM) or desmethylimipramine (0.01 to 1 microM) produced a concentration-dependent increase (up to 2 fold) in electrically evoked (3 Hz, 2 ms, 20 mA, 120s every 20 min) fractional overflow of tritium from rat brain cortex slices but not from mouse vas deferens (2.5 Hz, 2 ms, 400 mA, for 90s every 14 min). 2. Yohimbine and idazoxan (0.01 to 1 microM) increased fractional evoked overflow of tritium by up to 2 fold; in the presence of these drugs, cocaine (10 microM) produced an increase in both tissues (up to 3.5 fold over control). 3. In brain slice an increase in stimulation frequency (0.1, 0.5, 1, 3 and 6 Hz) decreased fractional evoked overflow of tritium per pulse but cocaine (10 microM) produced a significant enhancement at each frequency except 6 Hz. In vas deferens fractional tritium overflow per pulse changed little with increasing frequency and cocaine produced no effect. 4. In both tissues fractional evoked overflow of tritium was dependent on the stimulation current; cocaine (10 microM) increased fractional evoked overflow from brain slice at every current tested but was without effect in vas deferens. 5. Chromatographic separation of the released tritium showed there was little difference in the proportions of [3H]-noradrenaline and 3H-metabolites overflowing from the tissues. Cocaine increased the proportion of [3H]-noradrenaline and decreased the proportion of [3H]-DOPEG overflowing both at rest and during stimulation. 6. In brain slice an increase in electrically evoked overflow was produced by cocaine (10 microM) whether total tritium overflow (1.8 fold), overflow of [3H]-noradrenaline (1.8 fold) or overflow of unlabelled noradrenaline (1.8 fold) was measured. Evoked overflow from vas deferens was unaffected when assessed by any of these three methods. 7. The mechanism responsible for this differential effect of cocaine is unclear but may involve differences in the physical relationship between release sites, reuptake sites and presynaptic autoreceptors.

Tritium release from the various solid breeder materials irradiated in exotic experiments 1, 2 and 3

In-situ tritium release experiments have been performed on LiAlO b2, Li 2O, Li 2ZrO 3 and Li 2SiO 3 in the High Flux Reactor (HFR) at Petten. The experimental programme, EXOTIC, fits in the European Fusion Technology Programme on Blanket Technology and is jointly carried out by SNL-Springfields, SCK/CEN — Mol and ECN — Petten in cooperation with JRC — Petten. The vented capsules are purged with helium-0.1 vol% H 2. The main parameters were material density (75–95% TD), temperature (400–650°C), 6Li content, and irradiation time. During the steady state irradiation of EXOTIC-3 some temperature transients were carried out. They caused an immediate and strong effect on the release of tritium. More or less time was needed to restore steady-state tritium release. Almost complete tritium release was observed for: LiAlO 2 at 440°C, Li 2SiO 3 at 550°C, Li 2O at 600°C and Li 2ZrO 3 at 650°C for material densities of 75–80% TD. For 95% TD Li 2SiO 3 the fractional tritium release was < 70% at 630°C.

Tritium retention in the femoral bone marrow and spleens of mice receiving single intravenous injections of tritiated water and tritiated thymidine.

To derive parameters necessary for evaluating the possible hazards of tritium, retention of tritium in total and TCA-insoluble fractions of the femoral marrow and spleen of mice were observed after single intravenous injections of tritiated water and tritiated thymidine. Retention curves of tritium in TCA-insoluble fractions of the femoral marrow and spleen were resolved fairly well into two exponential components. After injecting tritiated thymidine, most of the activity was detected in the TCA-insoluble fraction. Tritium in this fraction decreased with half-times of 2.2 days in the femoral marrow and 3.6 days in the spleen as the first component, and 23.9 days and 30.5 days, respectively, as the second component. After tritiated water injections, the tritium incorporated into the TCA-insoluble fraction was quite small. Most of the activity was considered to be in the TCA-soluble fraction. Tritium in this fraction was estimated to decrease with half-times of 2.6 days in the femoral marrow and 2.3 days in the spleen as the first component, and 8.0 days and 8.2 days, respectively, as the second component. It is concluded that the retention curves of tritium in the bone marrow are similar to those in the spleen for tritiated water, but not for tritiated thymidine.

Some Basic Studies on Tritium Processing in CTR Solid Blanket

AbstractSome basic studies related to tritium processes in the solid blanket of CTR have been made.These are:(1) Evaluation of somewhat new blanket materials such as lithium-graphite intercalation compound. In this study, fractional tritium release was measured when lithium compound was heated after irradiated in a fast reactor.(2) Isotope effect, isotopic swamping effect and exchange reaction in tritiated water vapor adsorption on molecular sieve were studied. These are important items in the design of tritiated water vapor recovery in the gas cooled blanket.

Local modulation of neurotransmitter release in bovine splenic vein.

Bovine splenic vein has an abundant sympathetic innervation. Isolated strips were used to examine whether autoinhibition of norepinephrine release from the noradrenergic nerve terminals could be demonstrated under various experimental conditions and whether additional local regulatory modulators of transmitter release could also be implicated. In particular, the possibility of a histamine interaction with presynaptic inhibitory receptors was examined because ultrastructural evidence disclosed a close spatial relationship between mast cells and noradrenergic nerve terminals in the vessel wall. To investigate the presence of presynaptic alpha-receptors the competitive blocking agent phentolamine was included in the superfusion medium at concentrations ranging from 1 to 50 microM during electrical field stimulation at frequencies between 1 and 10 Hz. Transmitter outflow was measured as fractional tritium release. Low frequency stimulation (1 Hz) with 1 microM phentolamine resulted in the typical increase in norepinephrine release characteristics for presynaptic alpha-receptor inhibition. In contrast, high frequency (10 Hz) stimulation in the presence of 50 microM phentolamine caused an unexpected decrease in norepinephrine outflow. This unusual result can be explained by additional pharmacological actions of phentolamine unrelated to alpha-receptor blockade, e.g. histamine release from the mast cells which subsequently can act on presynaptic inhibitory histamine receptors. This effect, manifested at higher phentolamine concentrations, would overcome the alpha-receptor blockade. The presence of histamine receptors was supported by the results from electrical stimulation in the presence of exogenous histamine. Histamine decreased norepinephrine outflow while increasing basal tension and the contractile response of the vein strip. Unexpectedly, these effects appeared to be mediated by histamine receptors of the H1-type because they were reduced after pyrilamine but unaffected by agonists and antagonists to receptors of the H2-type. It is speculated that interactions between mast cells and noradrenergic nerve terminals may serve to maintain homeostasis in the bovine splenic vein.

A maximum contraction and substantial quantities of tritium can be obtained from tetraethylammonium-treated [3H]-noradrenaline preloaded, rat vas deferens in response to a single electrical shock.

1 In the normal and phenoxybenzamine-treated vasa deferentia of the rat the overflow of tritium after preloading with [3H]-noradrenaline increased with the increase in frequency of transmural stimulation. Phenozybenzamine enhanced overflow by 5 to 7 fold. 2 After tetraethylammonium (TEA, 10 mM), fractional tritium overflow at 5 Hz increased from a control value of 2.8 to 53 X 10(-4), and at 0.5 Hz it reached 154 X 10(-4). Enhancement of overflow was inversely related to the frequency of stimulation. 3 Contractor responses of the vas deferens induced by transmural stimulation were markedly potentiated, both in amplitude and duration, by 10 mM TEA. The contraction developed in the presence of 10 mM TEA at 0.5 Hz was comparable to that obtained at 10 Hz in normal Krebs solution. 4 In the presence of 5 mM TEA, contractions of the vas deferens caused by exogenous noradrenaline were potentiated about 5 fold. 5 The overflow and contractor response induced by 45 mM K were enhanced about 5 fold in 10 mM TEA-Krebs solution. Facilitation of K-induced overflow by TEA was reduced over 50% by tetrodotoxin (TTX, 1 microM). 6 Delivery of a single shock (1.0 ms duration) to 10 mM TEA-treated vas deferens resulted in a 63% increase in tritium overflow over background overflow. The fractional overflow amounted to almost 720 X 10(-4) after a single shock, as compared to 154 X 10(-4) obtained at 0.5 Hz. 7 The vas deferens treated with 10 mM TEA and stimulated by a single shock developed a contraction which was greater in amplitude and duration than that seen in normal tissue at 10 Hz. 8 Five second serial samples collected from superfused 10 mM TEA-treated vas deferens contained maximum quantities of radioactivity in the first 5 s after a single shock. In subsequent samples, radioactivity gradually declined, and reached prestimulation level after about 25 s. 9 The fractional overflow caused by stimulation at 0.1 Hz in 10 mM TEA-treated tissue progressively increased as external Ca was gradually raised from 0.83 to 10 mM. 10 The mechanism of action of TEA in enhancing the overflow of sympathetic transmitter, particularly in response to a single shock, is discussed in relation to Ca.

Fusion reactivities and power multiplication factors of beam-driven toroidal reactors with both D and T injection

Key reactor parameters of intensely beam-driven toroidal plasmas with 50: 50 D-T composition maintained by neutral-beam injection of both D and T, together with plasma re-cycling, are determined. The deuterons and tritons are injected with equal intensity and velocity. This mode of operation is most appropriate for high-duty-factor, high-power-density operation, in the absence of pellet injection.The velocity distributions of energetic D and T ions are calculated from a relatively simple slowing-down model, but include a tail above the injection velocity that results from energy diffusion. Fusion power multiplication Q and fractional tritium burn-up are determined from fusion reactivities calculated for beam-target, hot-ion, and thermonuclear reactions. For conditions where Q ∼ 1, beam-target reactions are dominant, but reactions among the hot ions contribute substantially to the total reaction rate when nhot/ne ≳ 0.2. To maintain the bulk-plasma temperature at progressively smaller neτE, it is necessary to continuously increase nhot/ne, so that reactions among energetic ions serve to maximize the Q-value and power density in low-neτE-driven operation.

The subcellular localization of tritium after incubation of homogenates of rat brain with 3h-norepinephrine

Density gradient centrifugation of rat brain homogenates, after their incubation at 37° with 3H-norepinephrine (NE) revealed an uneven distribution of tritium among the five discrete fractions obtained. The bulk (76 per cent) of the tritium was found in the upper two fractions ( A and B) : the fraction lying between 0.29 and 0.88 M sucrose ( B) contained 46 per cent of the total tritium in the gradient. Pretreatment of the animal with reserpine, or incubation with 3H-NE at 4°, decreased the percentage of tritium in fraction B to approximately 36 per cent. The percentage distribution of tritium was uninfluenced by a fifty-fold increase in the quantity of 3H-NE added to the incubation medium. In contrast, the absolute amount of tritium in B bore a linear relationship to the concentration of added amine. The simultaneous addition of both nonisotopic NE and 3H-NE to the incubation medium decreased the tritium content of fraction B; the decrease was roughly proportional to the amount of nonisotopic NE present. Since over 80 per cent of the tritium in fractions A and B could be accounted for by unchanged norepinephrine, it is suggested that in this study the distribution of tritium in brain homogenates may accurately reflect that of endogenous catecholamine in intact neural structures.

Fate of tritium-labeled carnitine administered to dogs and rats.

dl-Carnitine hydrochloride, tritiated nonspecifically, was purified and shown to have the same chemical and biological properties as the original compound (ß-hydroxy, γ-trimethylammonium butyrate). About one-third of administered material was excreted in urine during a 7-hr period following the intravenous injection of carnitine HCl (2 mg/kg) to dogs. Tritium not excreted appeared primarily in the trichloroacetic acid (TCA)-soluble fraction of various tissues, with approximately half that administered being found in skeletal muscle. The concentrations of tritium in TCA-soluble fractions of all organs examined except brain were 4–30 times higher than plasma concentrations. No evidence of carnitine degradation was found. The tritiated material in TCA-soluble extracts moved as single peaks in three different chromatographic systems, having the same RF values as those of known samples of carnitine. Tritium in chloroform-soluble fractions accounted for less than 1% of that administered. Of the organs examined, liver had the highest relative amount of incorporation of tritium into lipids, with all activity being found in unidentified phospholipids, chiefly in the lecithin fraction. The possible physiological significance of carnitine in muscle is briefly discussed.

Origin of High Tritium Content of Atmospheric Methane, Hydrogen and Stratospheric Water

RECENT work (ref. 1 and Suess, H. E., private communication) has shown that atmospheric methane has a fractional tritium content orders of magnitude higher than that of rain water and approaching that of atmospheric hydrogen and stratospheric water. The rate of increase with time of this tritium in methane makes it appear likely that it originates in the testing of nuclear devices. (The finding by Bishop et al.1 that the specific activity of atmospheric methane appears to be lower in the troposphere than in the stratosphere or at the surface is, however, not obviously explained on the basis of origin in thermonuclear explosion, or for that matter by origin from any single source.) However, no satisfactory mechanism by which such tritium can be incorporated in methane has been advanced. The high temperature and oxidizing conditions supposed to exist in the bomb fireball seemed to rule it out as a source of tritiated methane1. Biological processes yielding methane of high specific activity are difficult to conceive; and indeed, sewage methane has little tritium content1. High atmosphere, radiation-induced mechanisms for exchange of methane with high specific activity atmospheric hydrogen can be formulated, but these mechanisms suggest that the methane is likely to be oxidized under the conditions required (Libby, W. F., private communication).