Neuromuscular sensitivity to hydrogen sulfide in the marine invertebrate Urechis caupo.

1998 ◽  
Vol 201 (9) ◽  
pp. 1393-1403
Author(s):  
D Julian ◽  
W E Dalia ◽  
A J Arp
Keyword(s):  
Hydrogen Sulfide ◽  
Marine Invertebrate ◽  
Complete Recovery ◽  
Reversible Binding ◽  
Contraction Amplitude ◽  
Anoxic Conditions ◽  
Urechis Caupo ◽  
Nerve Muscle ◽  
Evoked Contractions

Hydrogen sulfide (HS) is a well-known inhibitor of aerobic respiration via its reversible binding of mitochondrial cytochrome c oxidase, but recent studies have suggested that HS may have other non-respiratory actions. We have studied the effects of HS on spontaneous and evoked contractions in vitro under hypoxic and anoxic conditions in nerve-muscle preparations from the echiuran worm Urechis caupo. Contraction amplitude in response to electric field stimulation under anoxic conditions was completely abolished by HS within minutes in a classic dose-response relationship (Kd=31 mmol l-1, r2=0.86). Exposure of body wall and esophagus to HS in vitro for up to 6 h demonstrated that the contraction amplitude and frequency of spontaneous activity were relatively insensitive to anoxia, but that the sensitivity to HS was similar to that seen in field-stimulated muscle (Kd=2.7-32 mmol l-1). The toxic effects of HS were reversible, with almost complete recovery under anoxic conditions within the first hour. These data indicate that HS at millimolar concentrations can directly inhibit muscle contraction. Although the mechanism of this action is unknown, it does not appear to involve metabolic pathways or oxygen transport.

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.

Hypercoagulability Syndrome Due to Heparin Co-Factor Deficiency

1964 ◽  
Vol 11 (02) ◽  
pp. 485-496 ◽  
Author(s):  
B. J Koszewski ◽  
H Vahabzadeh
Keyword(s):  
Dynamic Process ◽  
Blood Clotting ◽  
Complete Recovery ◽  
Inhibition Test ◽  
Factor Deficiency ◽  
Heparin Resistance ◽  
Fever Therapy ◽  
Intensive Course ◽  
Plasma Infusions

SummaryA case of hypercoagulability syndrome in a 35 years old male is reported. An abnormal heparin resistance was found which could be defined by means of a heparin clot-inhibition test as a deficiency in heparin co-factor. The required anticoagulant doses of heparin were forty times as high as in cases with intact heparin co-factor. The factor seemed to be used up in the process of coagulation, as plasma, but not serum, was able to correct the deficiency in vitro. Plasma infusions were helpful for four days, but a complete recovery was achieved only after an intensive course of fever therapy.The phenomenon of blood clotting should be regarded as a dynamic process which is facilitated by an array of clot promoting factors and opposed by a system of natural anticoagulants.

scholarly journals H2S in acute lung injury: a therapeutic dead end(?)

2020 ◽  
Vol 8 (S1) ◽  
Author(s):  
Tamara Merz ◽  
Nicole Denoix ◽  
Martin Wepler ◽  
Holger Gäßler ◽  
David A. C. Messerer ◽  
...  
Keyword(s):  
Hydrogen Sulfide ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Circulatory Shock ◽  
Therapeutic Window ◽  
Pharmacokinetics And Pharmacodynamics ◽  
Clinical Reality ◽  
Dead End

AbstractThis review addresses the plausibility of hydrogen sulfide (H2S) therapy for acute lung injury (ALI) and circulatory shock, by contrasting the promising preclinical results to the present clinical reality. The review discusses how the narrow therapeutic window and width, and potentially toxic effects, the route, dosing, and timing of administration all have to be balanced out very carefully. The development of standardized methods to determine in vitro and in vivo H2S concentrations, and the pharmacokinetics and pharmacodynamics of H2S-releasing compounds is a necessity to facilitate the safety of H2S-based therapies. We suggest the potential of exploiting already clinically approved compounds, which are known or unknown H2S donors, as a surrogate strategy.

Role of Muscle Activity in Nerve-Muscle Interaction in vitro

Nature ◽  
1974 ◽  
Vol 248 (5443) ◽  
pp. 70-71 ◽  
Author(s):  
J. H. STEINBACH
Keyword(s):  
Muscle Activity ◽  
Nerve Muscle

Mineral Density and Fluoride Content of in vitro Remineralized Lesions

1988 ◽  
Vol 67 (3) ◽  
pp. 577-581 ◽  
Author(s):  
Y. Jima ◽  
T. Koulourides
Keyword(s):  
Complete Recovery ◽  
Fluoride Content ◽  
Mineral Density ◽  
Acid Dissolution ◽  
Thin Sections ◽  
Partially Saturated ◽  
In Vitro Investigation ◽  
Bovine Enamel ◽  
Caries Lesions

This in vitro investigation studied the remineralization of experimental caries lesions in bovine enamel by use of three methods: (1) surface microhardness, (2) microradiography, and (3) abrasion biopsy for mineral density and fluoride content. The lesions were produced by a two-day exposure to 0.01 mol/L lactic acidlsodium hydroxide buffer partially saturated with 3.0 mmol/L Ca, 1.8 mmol/L P, in 1% CMC, at pH 4.0 and 37°C. The lesions were exposed to a remineralizing solution containing 3.0 mmol/L Ca, 1.8 mmol/L P, and 3 ppm F in 1% CMC at pH 7.0 and 37°C for two, six, and ten days, with solution changes every two days. The data derived from the three methods are presented in sequence from the baseline and at days two, six, and ten of the remineralizing treatment. Microhardness measurements showed hardness recoveries of 35.9, 78.9, and 87.5%, respectively. Microradiography suggested complete recovery with the ten-day remineralization. Abrasion biopsy of successive 10-μm layers to a depth of 100 μm indicated 15.2, 39.8, and 68.8% mineral density recoveries, with fluoride content of the surface layer increasing from a baseline of 300 ppm to 4600, 9000, and 9800 ppm F for the 2, 6, 10 days of remineralization, respectively. Subsequent acid-etching of thin sections from the ten-day-remineralized specimens showed that the fluoride-enriched remineralized area was more resistant to acid dissolution than was the underlying nonnal enamel.

Reversible binding of 5- and 8-methoxypsoralen to human serum proteins (albumin) and to epidermis in vitro

1979 ◽  
Vol 101 (6) ◽  
pp. 669-677 ◽  
Author(s):  
M. ARTUC ◽  
G. STUETTGEN ◽  
W. SCHALLA ◽  
H. SCHAEFER ◽  
J. GAZITH
Keyword(s):  
Human Serum ◽  
Serum Proteins ◽  
Reversible Binding ◽  
Human Serum Proteins

PL08 Homocysteine to Hydrogen Sulfide: in vitro, ex vivo and in vivo

Nitric Oxide ◽  
2013 ◽  
Vol 31 ◽  
pp. S15
Author(s):  
Suresh C. Tyagi
Keyword(s):  
Hydrogen Sulfide ◽  
Ex Vivo
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