Weathering and evaporation controls on dissolved uranium concentrations in groundwater - A case study from northern Burundi.

The potential use of groundwater for potable water supply can be severely compromised by natural contaminants such as uranium. The environmental mobility of uranium depends on a suite of factors including aquifer lithology, redox conditions, complexing agents, and hydrological processes. Uranium concentrations of up to 734µg/L are found in groundwater in northern Burundi, and the objective of the present study was to identify the causes for these elevated concentrations. Based on a comprehensive data set of groundwater chemistry, geology, and hydrological measurements, it was found that the highest dissolved uranium concentrations in groundwater occur near the shores of Lake Tshohoha South and other smaller lakes nearby. A model is proposed in which weathering and evapotranspiration during groundwater recharge, flow and discharge exert the dominant controls on the groundwater chemical composition. Results of PHREEQC simulations quantitatively confirm this conceptual model and show that uranium mobilization followed by evapo-concentration is the most likely explanation for the high dissolved uranium concentrations observed. The uranium source is the granitic sand, which was found to have a mean elemental uranium content of 14ppm, but the exact mobilization process could not be established. Uranium concentrations may further be controlled by adsorption, especially where calcium-uranyl­carbonate complexes are present. Water and uranium mass balance calculations for Lake Tshohoha South are consistent with the inferred fluxes and show that high­uranium groundwater represents only a minor fraction of the overall water input to the lake. These findings highlight that the evaporation effects that cause radionuclide concentrations to rise to harmful levels in groundwater discharge areas are not only confined to arid regions, and that this should be considered when selecting suitable locations for water supply wells.

A competitive receptor binding assay for platelet-activating factor (PAF): quantification of PAF in rat brain.

A radioreceptor assay (RRA) was developed using rabbit platelet membrane preparations to quantify platelet-activating factor (PAF) and lyso-PAF, the deacylated derivative of PAF, in a variety of tissues and biological fluids. We examined PAF and lyso-PAF levels in different rat brain areas with regard to the many proven and postulated actions of PAF in brain functions. Human saliva was selected to check the validity of this RRA. The samples were extracted with methanol/chloroform/water and purified by high-performance liquid chromatography on a 5-microns Nucleosil Si column (overall recovery: 78%). Sample extracts were acetylated before chromatography to assay lyso-PAF. PAF itself was assayed in non-aceylated samples. A competitive binding assay was performed using aliquots of platelet membrane preparation and tritiated PAF. The minimum detectable amount of PAF was 144 pg per tube and the receptor was highly specific for PAF. In human saliva, we confirm the presence of PAF and lyso-PAF within the range expected. Moreover there was a good correlation between the RRA and the aggregation assay (r = 0.976). A defined cocktail of protease inhibitors allowed storage of platelet membrane preparations for at least 3 months at -20 degrees C with no change in binding properties. In the brain we observed the prevalent presence of lyso-PAF and large variations in PAF and lyso-PAF concentrations between the different brain areas analyzed. PAF was undetectable in the hypothalamus but the lyso-PAF concentration was 2.5 micrograms/g wet tissue. The PAF concentration in the cortex varied from 0 to 16 ng/g wet tissue while that of lyso-PAF was 0.7 micrograms/g wet tissue. Moreover the amount of lyso-PAF varied between the different brain areas analyzed. The hippocampus contained the highest amount (7 micrograms/g wet tissue), and relatively high levels were found in the hypothalamus, medulla oblongata and corpus striatum. The cerebellum and cortex contained the lowest levels of lyso-PAF. These findings show that PAF is present in the central nervous system mainly in its inactive form, lyso-PAF, and suggest that its effects as a modulator of brain function may be dependent on deacetylation, rather than synthesis.

Practical method for optimizing radioimmunoassay detection and precision limits.

A model of the competitive radioimmunoassay standard curve, based on the Law of Mass Action, has been developed and used in conjunction with experimental and counting errors to predict the assay detection limit and precision profiles. We verified the model with hapten radioimmunoassays performed in our laboratory. The resulting computer program can be used to determine the optimum antiserum concentration--depending on its affinity--and labeled-antigen concentration--according to its specific activity and nonspecific binding. The graphical representation of this model provides radioimmunologists with a practical tool for assay optimization.

Hypothalamic prostaglandin E2 receptors coupled to an adenylyl cyclase.

We show that the effect of prostaglandin (PG) E2 on luteinizing hormone-releasing hormone (LHRH) release involves a receptor-mediated process coupled to an adenylyl cyclase system. The adenylyl cyclase activity in rat hypothalamus synaptic membrane preparations was stimulated by PGE2 and this stimulation was directly related to the presence of guanine nucleotide (GTP). PGE2 specifically bound to P2 membranes from rat and porcine hypothalami with similar characteristics. Computer-fitted saturation curves provided evidence for two binding components which may be two states of the same receptor (RH and RL). Experiments with Gpp(NH)p, a non-metabolizable analogue of GTP, suggested the interconversion of RH and RL. These results may reflect different states of the ternary complex (hormone-receptor-guanine binding protein). Magnesium (Mg2+) can modify the RH and RL binding parameters, but seems to act directly on the PGE2 receptor site.

Inhibitory effect of platelet-activating factor (PAF) on luteinizing hormone-releasing hormone and somatostatin release from rat median eminence in vitro correlated with the characterization of specific PAF receptor sites in rat hypothalamus.

Platelet-activating factor (PAF) exhibits a wide range of biological activities, including the stimulation of secretory processes in various cell types. However, little is known regarding its possible influence on the release of brain neuropeptides. In the present study we have examined the effect of PAF on the release of three hypothalamic releasing hormones in adult male rats, and have characterized the presence of specific PAF binding sites in rat hypothalamic membranes. PAF decreased LHRH and somatostatin (SRIF) release from the median eminence with a maximal inhibition at 10(-14) M for both neuropeptides, whereas GRF release was not significantly altered. Moreover, PAF strongly counteracted the Ca2+ ionophore A 23187-stimulated release of LHRH and SRIF from median eminence and medial basal hypothalamus (greater than 50% inhibition). These results suggest an involvement of Ca2+ dependent events in PAF action. This inhibitory effect was specifically exerted at a hypothalamic site because PAF failed to depress LH and GH release from the anterior pituitary. A specific, reversible and saturable binding of [3H]PAF to membrane preparations of rat hypothalamus was demonstrated and two classes of binding sites were characterized. The affinity (KD) of each binding class was 2.14 +/- 0.32 nM and 61.63 +/- 16.4 nM, respectively, and the corresponding maximal number of each binding class was 25.41 +/- 3.2 fmol/mg protein and 146.2 +/- 47.5 fmol/mg protein. In the same conditions no specific binding was observed using rat pituitary membranes. The specificity of PAF analogs for these binding sites was well correlated to their relative effectiveness in altering LHRH and SRIF release (order of potency: L-652,731, kadsurenone greater than BN 52021 greater than Lyso-PAF). These data suggest that the binding sites identified in the hypothalamus have the characteristics expected of a specific PAF receptor and that PAF effect on neuropeptides release is a receptor-mediated process.

[Control of growth hormone release by growth hormone-releasing factor and prostaglandin E2 in a system of perfused rat anterior pituitary cells]. / Contrôle de la libération de la GH par le GRF et la prostaglandine E2 dans un système de périfusion de cellules anté-hypophysaires de rat.

Using superfused rat pituitary cells we showed that the growth hormone-releasing factor (GRF) and prostaglandin E2 (PGE2) increased growth hormone (GH) secretion in a similar manner in terms of kinetics and amplitude of responses. Moreover, our data suggest that they stimulate GH secretion mainly by cAMP-dependent mechanisms.