Deuterium Tracer Studies on Hydrotreating Catalysts—Isotopic Exchange between Hydrogen and Hydrogen Sulfide on Sulfided NiMo/Al2O3

1997 ◽  
Vol 167 (1) ◽  
pp. 1-11 ◽  
Author(s):  
C. Thomas ◽  
L. Vivier ◽  
J.L. Lemberton ◽  
S. Kasztelan ◽  
G. Pérot
Keyword(s):  
Hydrogen Sulfide ◽  
Isotopic Exchange ◽  
Tracer Studies ◽  
Hydrotreating Catalysts

Dissociation of dihydrogen and hydrogen sulfide over a sulfided NiMo-alumina catalyst as evidenced by D2S-H2 isotopic exchange

1995 ◽  
Vol 34 (3-4) ◽  
pp. 375-378 ◽  
Author(s):  
P. d'Araujo ◽  
C. Thomas ◽  
L. Vivier ◽  
D. Duprez ◽  
G. P�rot ◽  
...  
Keyword(s):  
Hydrogen Sulfide ◽  
Isotopic Exchange ◽  
Alumina Catalyst

Isotopic dilution of CO2 as an estimate of CO2 production during substrate oxidation studies

1989 ◽  
Vol 257 (2) ◽  
pp. E296-E298 ◽  
Author(s):  
C. L. Kien
Keyword(s):  
Correction Factor ◽  
Isotopic Exchange ◽  
Numerical Estimate ◽  
Substrate Oxidation ◽  
Isotopic Dilution ◽  
Co2 Production ◽  
Isotopic Enrichment ◽  
Tracer Studies ◽  
Co2 Excretion

The rate of oxidation of a substrate is often divided by the numerical estimate of a correction factor for the proportion of labeled CO2 that is excreted during the course of the experiment. This factor, derived from tracer studies of bicarbonate kinetics, equals the product of the net rate of respiratory CO2 excretion and the ratio of the plateau isotopic enrichment of CO2 to the rate of infusion of labeled bicarbonate. The inverse of this ratio may be equated to the rate of appearance of unlabeled CO2. When one substitutes the expression for the correction factor into a typical equation for the rate of substrate oxidation, the rate of appearance of CO2 substitutes for both net CO2 excretion and the correction factor in the original oxidation equation. Thus the rate of appearance of CO2 is an index of CO2 production that takes into account both net fixation of CO2 and isotopic exchange of labeled CO2; it also may have application as an index of net CO2 production.

Deuterium Tracer Studies on Hydrotreating Catalysts. 2. Contribution of the Hydrogen of the Alumina Support to H-D Exchange

1998 ◽  
Vol 179 (2) ◽  
pp. 495-502 ◽  
Author(s):  
C. Thomas ◽  
L. Vivier ◽  
A. Travert ◽  
F. Maugé ◽  
S. Kasztelan ◽  
...  
Keyword(s):  
Tracer Studies ◽  
Alumina Support ◽  
Hydrotreating Catalysts

Lactate-pyruvate interconversion in blood: implications for in vivo tracer studies

1994 ◽  
Vol 266 (3) ◽  
pp. E334-E340 ◽  
Author(s):  
J. A. Romijn ◽  
D. L. Chinkes ◽  
J. M. Schwarz ◽  
R. R. Wolfe
Keyword(s):  
Production Rate ◽  
Whole Blood ◽  
Isotopic Exchange ◽  
Average Rate ◽  
Compartmental Modeling ◽  
Tracer Studies ◽  
Net Production ◽  
Lactate And Pyruvate

We have evaluated lactate and pyruvate kinetics in whole blood or plasma by the addition of [1-13C]lactate (n = 5) or [1-13C]pyruvate (n = 5) and application of compartmental modeling to the resulting data. Pyruvate and lactate concentrations and tracer-to-tracee ratios were measured at frequent intervals for 45 min. Pyruvate and lactate tracer-to-tracee ratios equilibrated almost completely within 3-4 min in whole blood, whereas there was no isotopic exchange in plasma. The average rate of interconversion between unlabeled lactate and pyruvate was four to five times (pyruvate to lactate) and three to four times (lactate to pyruvate) the net production rate of lactate. We conclude that there is a very rapid interconversion between lactate and pyruvate in blood that has to be considered in the interpretation of in vivo tracer studies.

Endogenous hydrogen sulfide sulfhydrates IKKβ at cysteine 179 to control pulmonary artery endothelial cell inflammation

2019 ◽  
Vol 133 (20) ◽  
pp. 2045-2059 ◽  
Author(s):  
Da Zhang ◽  
Xiuli Wang ◽  
Siyao Chen ◽  
Selena Chen ◽  
Wen Yu ◽  
...  
Keyword(s):  
Hydrogen Sulfide ◽  
Endothelial Cell ◽  
Pulmonary Artery ◽  
Cell Model ◽  
Site Directed Mutagenesis ◽  
Critical Event ◽  
Hypertensive Rats ◽  
Pulmonary Artery Endothelial Cell

Abstract Background: Pulmonary artery endothelial cell (PAEC) inflammation is a critical event in the development of pulmonary arterial hypertension (PAH). However, the pathogenesis of PAEC inflammation remains unclear. Methods: Purified recombinant human inhibitor of κB kinase subunit β (IKKβ) protein, human PAECs and monocrotaline-induced pulmonary hypertensive rats were employed in the study. Site-directed mutagenesis, gene knockdown or overexpression were conducted to manipulate the expression or activity of a target protein. Results: We showed that hydrogen sulfide (H2S) inhibited IKKβ activation in the cell model of human PAEC inflammation induced by monocrotaline pyrrole-stimulation or knockdown of cystathionine γ-lyase (CSE), an H2S generating enzyme. Mechanistically, H2S was proved to inhibit IKKβ activity directly via sulfhydrating IKKβ at cysteinyl residue 179 (C179) in purified recombinant IKKβ protein in vitro, whereas thiol reductant dithiothreitol (DTT) reversed H2S-induced IKKβ inactivation. Furthermore, to demonstrate the significance of IKKβ sulfhydration by H2S in the development of PAEC inflammation, we mutated C179 to serine (C179S) in IKKβ. In purified IKKβ protein, C179S mutation of IKKβ abolished H2S-induced IKKβ sulfhydration and the subsequent IKKβ inactivation. In human PAECs, C179S mutation of IKKβ blocked H2S-inhibited IKKβ activation and PAEC inflammatory response. In pulmonary hypertensive rats, C179S mutation of IKKβ abolished the inhibitory effect of H2S on IKKβ activation and pulmonary vascular inflammation and remodeling. Conclusion: Collectively, our in vivo and in vitro findings demonstrated, for the first time, that endogenous H2S directly inactivated IKKβ via sulfhydrating IKKβ at Cys179 to inhibit nuclear factor-κB (NF-κB) pathway activation and thereby control PAEC inflammation in PAH.

Sign in / Sign up

Export Citation Format

Share Document