PubMed · 14780472
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F HIRSCHBERG. 1950-03-24. [The bicarbonate test].. https://pubmed.ncbi.nlm.nih.gov/14780472/
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Excessive fluoride ingestion predominantly comes from drinking water sources. However, prevalence and severity of dental and skeletal fluorosis in northern Tanzania have been reported to be higher than would be expected from ingestion of fluoride through drinking water alone. This study aimed at investigating the contribution of "trona" (also locally known as magadi) a food additive, to the prevalence and severity of fluorosis in northern Tanzania. The study was carried out in four villages (Embaseni, Kitefu and Ngurdoto) in Maji ya Chai ward; and Nkoanekoli in Poli ward, in Arusha region, Tanzania. Analysis of fluoride concentrations was carried out in drinking water sources as well as in magadi samples. Assessment of the prevalence of dental fluorosis using Dean's Index Method was carried out for a population of 2217 pupils in four primary schools located in the case study area. Fluoride concentration in drinking water sources was found to range from 1.7 to 11.3 mg/l, while the concentration in magadi samples in case study villages were in the range of 0.21 to 0.9 mg/g. Total fluoride ingestion through magadi and water were established to be 11.74 mg/person/day in Embaseni, 36.1 mg/person/day in Ngurdoto, 10.88 mg/person/day in Kitefu and 5.7 mg/person/day in Nkoanekoli villages. Levels of total fluoride ingestion were directly correlated with Community Fluorosis Index (CFI) values, which were found to be 3.32 (in Embaseni), 3.67 (in Ngurdoto), 2.2 (in Kitefu) and 1.47 (in Nkoanekoli). The village with the highest fluoride consumption rate showed the highest CFI as well. High levels of fluoride concentrations in magadi suggest that excessive fluorosis in northern Tanzania may be due to the use of magadi in food preparations.
Cyclopropane synthases catalyze the cyclopropanation of unsaturated fatty acid using S-adenosyl-L-methionine as the methylene donor. The crystal structure of three cyclopropane synthases from Mycobacterium tuberculosis showed a bicarbonate ion bound in the active site that was proposed to act as a general base in the reaction mechanism [Huang, C., Smith, V., Glickman, M. S., Jacobs, W. R., and Sacchettini, J. C. (2002) J. Biol. Chem. 277, 11559-11569]. Because the in vitro activity of M. tuberculosis cyclopropane synthases has not yet been reported and because the ligands of the bicarbonate ion are all strictly conserved in cyclopropane synthases, we used the closely related Escherichia coli cyclopropane fatty acid synthase for this study. The putative ligands that share a hydrogen bond with the bicarbonate through their side chains were mutated. H266A, Y317F, E239A, and E239Q mutants were thus constructed and purified, and their catalytic efficiencies were 5.3, 0.7, 0.2, and <0.02%, respectively. C139 that is bound to the bicarbonate by its NH amide had already been mutated to serine in a previous work, and this mutant retains 31% of the activity of the wild-type enzyme. Kinetic analyses and binding studies using spectrofluorimetry showed that these mutations affected the catalytic constant rather than the binding of the substrates. While addition of free bicarbonate had almost no effect on the wild-type enzyme activity, all mutants, with the exception of E239A and E239Q, were rescued by the addition of free bicarbonate. The catalytic efficiencies of the rescued mutants were 85, 16, and 14% for C139S, H266A, and Y317F, respectively. This effect was specific to bicarbonate. The kinetic parameters of the rescued mutants were determined, and it is shown that the rescuing effect is due to an increase in kcat. These data are interpreted by assuming that the E. coli cyclopropane fatty acid synthase specifically binds a bicarbonate ion that is involved in catalysis, as proposed for the M. tuberculosis enzymes, and that mutation of the bicarbonate ligands decreases the affinity for that ion. However, because the E239Q mutation could not be rescued, we propose that E239 forms a catalytic dyad with the bicarbonate to perform the proton abstraction necessary in the chemical pathway to the cyclopropane ring.
The metabolic fate of substrates in humans can be examined by the use of stable isotopes, one of which, [13C]bicarbonate, may serve to estimate CO2 production rate. In view of minimizing the burden of metabolic studies for preterm infants, the authors determined whether intragastric and intravenous infusions of [13C]bicarbonate would achieve the same 13CO2 enrichment in expired air during steady state. A second aim of this study was to determine the minimum time required to reach steady state during intragastric infusion. Ten preterm infants received a primed continuous [13C]bicarbonate infusion intragastrically, followed by an intravenous infusion the next day. Breath samples were obtained every 30 min by the direct sampling method. 13CO2 isotopic enrichment, expressed as atom percent excess, was measured by isotopic ratio mass spectrometry. Two-tailed t tests were used to detect statistically significant differences between the infusion routes. The isotopic enrichment at plateau did not differ between intragastric and intravenous infusion. A steady state of 13CO2 enrichment was achieved after 60 min of intravenous infusion and after 120 min of intragastric infusion. In conclusion, intragastric infusion of [13C]bicarbonate may serve to estimate the whole-body CO2 production rate in preterm infants. To reach 13CO2 steady state, a minimum of 120 min of bicarbonate administration is required.