PubMed · 1808292
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
M Odaka. 1991. [Replacement fluid for hemofiltration].. https://pubmed.ncbi.nlm.nih.gov/1808292/
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
N-Nitrosation in oxygenated nitric oxide (NO middle dot) solutions was previously shown to be significantly inhibited by phosphate and chloride presumably by anion scavenging of the nitrosating agent nitrous anhydride, N2O3 (Lewis, R. S., Tannenbaum, S. R., and Deen, W. M. (1995) J. Am. Chem. Soc. 117, 3933-3939). Here, bicarbonate is shown to exhibit this same inhibitory effect. Rate constants for reaction of morpholine, phosphate, and bicarbonate with N2O3 relative to N2O3 hydrolysis at pH 8.9 were determined to be (3.7 +/- 0.2) x 10(4) M-1, (4.0 +/- 0.9) x 10(2) M-1, and (9.3 +/- 1.5) x 10(2) M-1, respectively. The morpholine and phosphate rate constants at pH 8.9 are similar to those reported at pH 7.4 assuring that these results are relevant to physiological conditions. The rate constant for this previously unrecognized reaction of bicarbonate with N2O3 suggests the strong scavenging ability of bicarbonate; accordingly, bicarbonate may contribute to reducing deleterious effects of N2O3. This is biologically important due to substantial bicarbonate concentrations in vivo, approximately 30 mM. Bicarbonate was previously shown to alter peroxynitrite reactivity; however, carbon dioxide is the probable reactive species. Bicarbonate is therefore potentially important in determining the fate of two reactive species generated from nitric oxide, N2O3 and ONOO-, and may thus act as a regulator of NO middle dot-induced toxicity.
Peroxynitrite is a strong oxidant produced in vivo as the reaction product of superoxide anion and nitric oxide (k approximately 5 x 10(9) M-1 s-1) and can be formed and mediate reactions in the extracellular environment. It has recently been reported that peroxynitrite and carbon dioxide react in a second-order process (S. V. Lymar and K. Hurst (1995) J. Am. Chem. Soc. 117, 8867-8868). Since one of the most abundant constituents of the extracellular milieu is bicarbonate anion (25 mM in plasma) which is in equilibrium with carbon dioxide (1.3 mM in plasma) we have further studied the kinetics of the reaction between peroxynitrite and carbon dioxide/ bicarbonate and the effect of bicarbonate on different peroxynitrite-mediated oxidations. The apparent second-order rate constant for the reaction is (2.3 +/- 0.1) x 10(3) M-1 s-1 at 37 degrees C and pH 7.4 and a pH-independent second-order rate constant of (5.8 +/- 0.2) x 10(4) M-1 s-1 at 37 degrees C was obtained considering peroxynitrite anion and carbon dioxide as the reacting species. The enthalpy and entropy of activation are delta H* = +10.7 +/- 0.8 kcal mol-1 and delta S* = -6.5 +/- 0.5 cal mol-1 K-1, respectively. The presence of bicarbonate had variable influence on peroxynitrite-mediated oxidations. While bicarbonate significantly enhanced peroxynitrite-mediated nitration of aromatics, it partially inhibited the oxidation of thiols, dimethylsulfoxide, oxyhemoglobin, and cytochrome c+2 and totally inhibited the hydroxylation of benzoate. Spontaneous chemiluminescence studies suggest the formation of bicarbonate radicals during the interactions of peroxynitrite with carbon dioxide/ bicarbonate. Our results support that peroxynitrite anion rapidly reacts with carbon dioxide to yield an adduct (ONOOCO2-) which can participate in oxidation and nitration processes, thus redirecting the primary reactivity of peroxynitrite.
Membrane transport pathways for transplacental transfer of sulfate were investigated by assessing the possible presence of a bicarbonate-coupled anion exchange mechanism for sulfate in the maternal facing membrane of human placental epithelial cells. The presence of a SO42-/HCO3- exchange mechanism was determined from 35SO42-tracer flux measurements in preparations of purified brush-border membrane vesicles. Under 10% CO2/90% N2 the imposition of an outwardly directed bicarbonate gradient (pH0 6/pHi 7.5) stimulated sulfate uptake to levels approximately 4-fold greater than observed at equilibrium. Maneuvers designed to offset the development of ion gradient-induced diffusion potentials (valinomycin, [K+]0 = [K+]i) significantly reduced bicarbonate gradient-induced sulfate uptake but concentrative accumulation of sulfate persisted. Early time point determinations performed in the presumed absence of membrane potential suggest the reduced level of bicarbonate gradient-induced sulfate uptake resulted from a more rapid dissipation of the imposed bicarbonate gradient. Concentrative accumulation of sulfate was not observed in the presence of a pH gradient alone under 100% N2. suggesting a preference of bicarbonate over hydroxyl ions as substrates for exchange. Static head determinations of opposing sulfate and bicarbonate gradients resulting in zero net flux of sulfate suggests the anion exchange mechanism mediates the electroneutral exchange of 2 bicarbonate or 1 carbonate for each sulfate. Sulfate uptake was increased with increasing intravesicular concentrations of carbonate at constant bicarbonate but was constant with increasing intravesicular concentrations of bicarbonate at constant carbonate suggesting carbonate as a substrate for anion exchange. The mechanism mediating bicarbonate gradient-induced sulfate uptake was sensitive to inhibition by stilbene derivatives, furosemide, bumetanide and probenecid. Substrate specificity studies suggest possible interactions of the anion exchange mechanism with salicylate, butyrate, thiosulfate, sulfite, selenate, chromate and oxalate. The results of this study provide evidence for the presence of a bicarbonate-coupled anion exchange mechanism as an electroneutral pathway for sulfate transport across the maternal-facing membrane of human placental epithelial cells.