scholarly journals Hydrogen Sulfide Impairs Meiosis Resumption in Xenopus laevis Oocytes

Cells ◽  
2020 ◽  
Vol 9 (1) ◽  
pp. 237
Author(s):  
Armance Gelaude ◽  
Sylvain Slaby ◽  
Katia Cailliau ◽  
Matthieu Marin ◽  
Arlette Lescuyer-Rousseau ◽  
...  
Keyword(s):  
Hydrogen Sulfide ◽  
Xenopus Laevis ◽  
Xenopus Laevis Oocytes ◽  
Oocyte Meiosis ◽  
M Phase ◽  
Dependent Inhibition ◽  
Mercaptopyruvate Sulfurtransferase ◽  
Amplification Loop ◽  
Dose Dependent Inhibition

The role of hydrogen sulfide (H2S) is addressed in Xenopus laevis oocytes. Three enzymes involved in H2S metabolism, cystathionine β-synthase, cystathionine γ-lyase, and 3-mercaptopyruvate sulfurtransferase, were detected in prophase I and metaphase II-arrested oocytes and drove an acceleration of oocyte meiosis resumption when inhibited. Moreover, meiosis resumption is associated with a significant decrease in endogenous H2S. On another hand, a dose-dependent inhibition was obtained using the H2S donor, NaHS (1 and 5 mM). NaHS impaired translation. NaHS did not induce the dissociation of the components of the M-phase promoting factor (MPF), cyclin B and Cdk1, nor directly impacted the MPF activity. However, the M-phase entry induced by microinjection of metaphase II MPF-containing cytoplasm was diminished, suggesting upstream components of the MPF auto-amplification loop were sensitive to H2S. Superoxide dismutase and catalase hindered the effects of NaHS, and this sensitivity was partially dependent on the production of reactive oxygen species (ROS). In contrast to other species, no apoptosis was promoted. These results suggest a contribution of H2S signaling in the timing of amphibian oocytes meiosis resumption.

Investigation on the antibacterial activity of electronic cigarette liquids (ECLs): a proof of concept study

2020 ◽  
Vol 21 ◽  
Author(s):  
Virginia Fuochi ◽  
Massimo Caruso ◽  
Rosalia Emma ◽  
Aldo Stivala ◽  
Riccardo Polosa ◽  
...  
Keyword(s):  
Antibacterial Activity ◽  
Bacterial Species ◽  
A549 Cells ◽  
Bactericidal Effect ◽  
Minimal Bactericidal Concentration ◽  
Viability Assay ◽  
Dependent Inhibition ◽  
Dose Dependent Inhibition ◽  
Dose Dependent

Background: The key ingredients of e-cigarettes liquid are commonly propane-1,2-diol (also called propylene glycol) and propane-1,2,3-triol (vegetal glycerol) and their antimicrobial effects are already established. The nicotine and flavors which are often present in e-liquids can interfere with the growth of some microorganisms. Objective: The effect of the combining these elements in e-liquids is unknown. The aim of the study was to investigate the possible effects of these liquids on bacterial growth in the presence or absence of nicotine and flavors. Methods: Susceptibilities of pathogenic strains (Klebsiella pneumoniae, Staphylococcus aureus, Pseudomonas aeruginosa, Acinetobacter baumannii, Escherichia coli, Enterococcus faecalis and Sarcina lutea) were studied by means of a multidisciplinary approach. Cell viability and antioxidant assays were also evaluated. Results: All e-liquids investigated showed antibacterial activity against at least one pathogenic strain. A higher activity was correlated to the presence of flavors and nicotine. Discussion: In most cases the value of minimal bactericidal concentration is equal to the value of minimal inhibitory concentration showing that these substances have a bactericidal effect. This effect was observed in concentrations up to 6.25% v/v. Antioxidant activity was also correlated to presence of flavors. Over time, the viability assay in human epithelial lung A549 cells showed a dose-dependent inhibition of cell growth. Conclusion: Our results have shown that flavors considerably enhance the antibacterial activity of propane-1,2-diol and propane-1,2,3-triol. This study provides important evidence that should be taken into consideration in further investigative approaches, to clarify the different sensitivity of the various bacterial species to e-liquids, including the respiratory microbiota, to highlight the possible role of flavors and nicotine.

scholarly journals The protective role of the 3-mercaptopyruvate sulfurtransferase (3-MST)-hydrogen sulfide (H2S) pathway against experimental osteoarthritis

2020 ◽  
Vol 22 (1) ◽  
Author(s):  
Sonia Nasi ◽  
Driss Ehirchiou ◽  
Athanasia Chatzianastasiou ◽  
Noriyuki Nagahara ◽  
Andreas Papapetropoulos ◽  
...  
Keyword(s):  
Hydrogen Sulfide ◽  
Protective Role ◽  
Mercaptopyruvate Sulfurtransferase ◽  
Experimental Osteoarthritis

scholarly journals Uterine Dysfunction in Diabetic Mice: The Role of Hydrogen Sulfide

Antioxidants ◽  
2020 ◽  
Vol 9 (10) ◽  
pp. 917
Author(s):  
Emma Mitidieri ◽  
Domenico Vanacore ◽  
Carlotta Turnaturi ◽  
Raffaella Sorrentino ◽  
Roberta d’Emmanuele di Villa Bianca
Keyword(s):  
Hydrogen Sulfide ◽  
Cyclic Nucleotides ◽  
Nod Mice ◽  
Diabetic Mice ◽  
Uterine Contractions ◽  
Female Reproductive Health ◽  
Spontaneous Motility ◽  
Mercaptopyruvate Sulfurtransferase

It is well-known that the physiological uterine peristalsis, related to several phases of reproductive functions, plays a pivotal role in fertility and female reproductive health. Here, we have addressed the role of hydrogen sulfide (H2S) signaling in changes of uterine contractions driven by diabetes in non-obese diabetic (NOD) mice, a murine model of type-1 diabetes mellitus. The isolated uterus of NOD mice showed a significant reduction in spontaneous motility coupled to a generalized hypo-contractility to uterotonic agents. The levels of cyclic nucleotides, cAMP and cGMP, notoriously involved in the regulation of uterus homeostasis, were significantly elevated in NOD mouse uteri. This increase was well-correlated with the higher levels of H2S, a non-specific endogenous inhibitor of phosphodiesterases. The exposure of isolated uterus to L-cysteine (L-Cys), but not to sodium hydrogen sulfide, the exogenous source of H2S, showed a weak tocolytic effect in the uterus of NOD mice. Western blot analysis revealed a reorganization of the enzymatic expression with an upregulation of 3-mercaptopyruvate-sulfurtransferase (3-MST) coupled to a reduction in both cystathionine-β-synthase (CBS) and cystathionine-γ-lyase (CSE) expression. In conclusion, the increased levels of cyclic nucleotides dysregulate the uterus peristalsis and contractility in diabetic mice through an increase in basal H2S synthesis suggesting a role of 3-MST.

scholarly journals Proteomic screen for potential regulators of M-phase entry and quality of meiotic resumption in Xenopus laevis oocytes

2010 ◽  
Vol 73 (8) ◽  
pp. 1542-1550 ◽  
Author(s):  
Romain D'Inca ◽  
Gaëlle Marteil ◽  
Franck Bazile ◽  
Aude Pascal ◽  
Nathalie Guitton ◽  
...  
Keyword(s):  
Xenopus Laevis ◽  
Xenopus Laevis Oocytes ◽  
Proteomic Screen ◽  
M Phase ◽  
Phase Entry

scholarly journals Cell cycle dynamics of an M-phase-specific cytoplasmic factor in Xenopus laevis oocytes and eggs.

1984 ◽  
Vol 98 (4) ◽  
pp. 1247-1255 ◽  
Author(s):  
J Gerhart ◽  
M Wu ◽  
M Kirschner
Keyword(s):  
Cell Cycle ◽  
Xenopus Laevis ◽  
Germinal Vesicle ◽  
Small Scale ◽  
Xenopus Laevis Oocytes ◽  
Germinal Vesicle Breakdown ◽  
Cytoplasmic Factor ◽  
M Phase ◽  
Cytostatic Factor ◽  
Meiotic Cycle

We have examined the regulation of maturation-promoting factor (MPF) activity in the mitotic and meiotic cell cycles of Xenopus laevis eggs and oocytes. To this end, we developed a method for the small scale extraction of eggs and oocytes and measured MPF activity in extracts by a dilution end point assay. We find that in oocytes, MPF activity appears before germinal vesicle breakdown and then disappears rapidly at the end of the first meiotic cycle. In the second meiotic cycle, MPF reappears before second metaphase, when maturation arrests. Thus, MPF cycling coincides with the abbreviated cycles of meiosis. When oocytes are induced to mature by low levels of injected MPF, cycloheximide does not prevent the appearance of MPF at high levels in the first cycle. This amplification indicates that an MPF precursor is present in the oocyte and activated by posttranslational means, triggered by the low level of injected MPF. Furthermore, MPF disappears approximately on time in such oocytes, indicating that the agent for MPF inactivation is also activated by posttranslational means. However, in the absence of protein synthesis, MPF never reappears in the second meiotic cycle. Upon fertilization or artificial activation of normal eggs, MPF disappears from the cytoplasm within 8 min. For a period thereafter, the inactivating agent remains able to destroy large amounts of MPF injected into the egg. It loses activity just as endogenous MPF appears at prophase of the first mitotic cycle. The repeated reciprocal cycling of MPF and the inactivating agent during cleavage stages is unaffected by colchicine and nocodazole and therefore does not require the effective completion of spindle formation, mitosis, or cytokinesis. However, MPF appearance is blocked by cycloheximide applied before mitosis; and MPF disappearance is blocked by cytostatic factor. In all these respects, MPF and the inactivating agent seem to be tightly linked to, and perhaps participate in, the cell cycle oscillator previously described for cleaving eggs of Xenopus laevis (Hara, K., P. Tydeman, and M. Kirschner, 1980, Proc. Natl. Acad. Sci. USA, 77:462-466).

scholarly journals Intracellular Sodium Regulates Opioid Signalling in Peripheral Neurons

2017 ◽  
Author(s):  
Alexandros H. Kanellopoulos ◽  
Jing Zhao ◽  
Edward C. Emery ◽  
John N Wood
Keyword(s):  
Protein Kinase ◽  
Sodium Channel ◽  
Protein Kinase A ◽  
Fold Increase ◽  
Intracellular Sodium ◽  
Peripheral Neurons ◽  
Dependent Inhibition ◽  
Dose Dependent Inhibition ◽  
Kinase A

AbstractOpioid receptors signal more effectively in sensory neurons from pain-free mice lacking the voltagegated sodium channel Nav1.7. Type-A GPCRs are known to be regulated through a specific sodium binding site, the occupancy of which diminishes agonist binding. We have used an electrophysiological assay of Protein Kinase A activity to examine the role of intracellular sodium on opioid signalling. Phosphorylation of sodium channel Nav1.8 by activation of Protein Kinase A with db-cAMP is unaffected by altered intracellular sodium. By contrast, there is a dose-dependent inhibition of fentanyl action on Nav1.8 currents when intracellular sodium is increased from 0 mM to 20 mM. Fentanyl shows a 50% loss of activity and 80-fold increase in EC50 with 20 mM intracellular sodium. These data demonstrate that altered intracellular sodium levels modulate opioid receptor signalling.

scholarly journals The T-cell CD2 determinant mediates inhibition of erythropoiesis by the lymphokine cascade

Blood ◽  
1988 ◽  
Vol 72 (2) ◽  
pp. 770-775 ◽  
Author(s):  
S Burdach ◽  
M Shatsky ◽  
B Wagenhorst ◽  
L Levitt
Keyword(s):  
T Cells ◽  
T Cell ◽  
Interleukin 2 ◽  
Receptor Expression ◽  
Isotype Control ◽  
Isotype Control Antibody ◽  
Dependent Inhibition ◽  
Neutralizing Monoclonal Antibody ◽  
Dose Dependent Inhibition

Abstract We examined the role of the T-cell antigen CD2 in the regulation of erythropoiesis by the lymphokine cascade. T-cell interleukin-2 (IL-2) receptors (p55) were induced via triggering of the antigen receptor- associated CD3 epitope. Before CD3 triggering T cells were preincubated with a CD2-blocking (Leu-5b) or isotype control antibody. T-cell pellets were employed during incubation to facilitate interaction between T-cell LFA-3 and CD2. CD2 blockade caused a 66% to 79% inhibition of p55 expression after three to six days of culture with IL- 2. Next we assessed the effect of CD2 blockade on IL-2. Next we assessed the effect of CD2 blockade on IL-2-induced inhibition of BFU-E in autologous cocultures containing CD3-triggered T cells. IL-2 caused a dose-dependent inhibition (52% to 92%) of BFU-E in the presence but not in the absence of CD3-triggered T cells. T-cell CD2 blockade prior to CD3 triggering caused a 65% to 87% abrogation of IL-2-induced inhibition of BFU-E at 10 to 10(2) U/mL IL-2. Preincubation of CD3- triggered T cells with isotype control antibody had no effect on IL-2- induced erythroid inhibition. Day 3 supernatants from CD3-triggered T cells or CD2-blocked, CD3-triggered T cells established in the presence of IL-2 were next assessed for modulation of BFU-E. CD3-triggered T- cell supernatants caused a 77% +/- 9% inhibition of BFU-E. Blockade of CD2 caused a 95% abrogation of T-cell-mediated BFU-E inhibition. In addition, CD2 blockade reduced interferon-gamma (IF gamma) release (84 to 128 U/mL) from CD3-triggered T cells by 81% at day 3 of culture. In control experiments, the addition of IF gamma-neutralizing monoclonal antibody to CD3-triggered T-cell supernatant established in the presence of IL-2 caused 75% abrogation of IL-2 inhibition of BFU-E. We conclude that blockade of the CD2 T-cell determinant induces down modulation of (a) T-cell p55 IL-2 receptor expression, (b) IL-2-induced inhibition of BFU-E, and (c) IL-2-induced marrow T-cell IF gamma release. These data suggest that the T-cell CD2 determinant can exert a regulatory effect on the control of erythropoiesis by the lymphokine cascade.

scholarly journals Role of Hydrogen Sulfide and 3-Mercaptopyruvate Sulfurtransferase in the Regulation of the Endoplasmic Reticulum Stress Response in Hepatocytes

Biomolecules ◽  
2020 ◽  
Vol 10 (12) ◽  
pp. 1692
Author(s):  
Theodora Panagaki ◽  
Elisa B. Randi ◽  
Csaba Szabo
Keyword(s):  
Endoplasmic Reticulum ◽  
Hydrogen Sulfide ◽  
Liver Disease ◽  
Er Stress ◽  
Chronic Liver Disease ◽  
Chronic Liver ◽  
Endoplasmic Reticulum Stress Response ◽  
Functional Responses ◽  
Mercaptopyruvate Sulfurtransferase

It is estimated that over 1.5 billion people suffer from various forms of chronic liver disease worldwide. The emerging prevalence of metabolic syndromes and alcohol misuse, along with the lack of disease-modifying agents for the therapy of many severe liver conditions predicts that chronic liver disease will continue to be a major problem in the future. Better understanding of the underlying pathogenetic mechanisms and identification of potential therapeutic targets remains a priority. Herein, we explored the potential role of the 3-mercaptopyruvate sulfurtransferase/hydrogen sulfide (H2S) system in the regulation of the endoplasmic reticulum (ER) stress and of its downstream processes in the immortalized hepatic cell line HepG2 in vitro. ER stress suppressed endogenous H2S levels and pharmacological supplementation of H2S with sodium hydrogen sulfide (NaHS) mitigated many aspects of ER stress, culminating in improved cellular bioenergetics and prevention of autophagic arrest, thereby switching cells’ fate towards survival. Genetic silencing of 3-MST or pharmacological inhibition of the key enzymes involved in hepatocyte H2S biosynthesis exacerbated many readouts related to ER-stress or its downstream functional responses. Our findings implicate the 3-MST/H2S system in the intracellular network that governs proteostasis and ER-stress adaptability in hepatocytes and reinforce the therapeutic potential of pharmacological H2S supplementation.

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