scholarly journals Effect of three-day Glutathione introduction on hydrogen sulfide metabolism in liver of rats under experimental nephropathy conditions

2019 ◽  
Vol 0 (1(58)) ◽  
pp. 18-21
Author(s):  
E. O. Ferenchuk ◽  
I. V. Gerush
2018 ◽  
Vol 17 (3) ◽  
Author(s):  
I. V. Gerush ◽  
N. P. Grigorieva ◽  
I. O. Kolianyk ◽  
Ye. O. Ferenchuk ◽  
M. V. Dikal

Author(s):  
E. O. Ferenchuk ◽  
I. V. Gerush

Introduction. Kidney diseases are a worldwide health problem. The renal dysfunctions cause the production of reactive oxygen species and can co-exist with different liver disease, or stimulate their development, so scientists are becoming more interested in the study of the influence of antioxidants such as glutathione on metabolic pathways of the body under conditions of different disease. Hydrogen sulfide has anti-inflammatory, anti-oxidant and anti-apoptotic effects that are mediated by its ability to downregulate the synthesis of lipid peroxides and reactive oxygen species-producing enzymes and may play an important role in the mechanism of development of nephropathy. The aim of the study – to learn the effect of glutathione introduction within 7 days on the system of H2S production in the liver of rats under conditions of experimental nephropathy. Research Methods. The experiment was conducted on albino mature male rats. The animals in experimental group were administered a single intraperitoneal dose of folic acid (250 mg/kg). Glutathione was introduced intragastral (100 mg/kg) within 7 days after intoxication. The activity of H2S-producing enzymes, the concentration and production of H2S were measured in the liver. Results and Discussion. Under conditions of experimental nephropathy there was a decrease in the concentration and production of hydrogen sulfide compared with the control group. The introduction of glutathione increased the content of hydrogen sulfide and promoted the growth of the activities of H2S-producing enzymes in the liver of rats. Conclusions. It was found that the content and production of hydrogen sulfide in the group of animals with nephropathy were diminished by a decrease in the activities of hepatic H2S-producing enzymes. The introduction of glutathione increased the content of hydrogen sulfide by stimulation the activities of cystathionine-β-synthase and cysteinaminotransferase in the liver of rats. As reasons for this effect, antioxidant properties of glutathione and the possibility of including tripeptide as a source of cysteine in the synthesis of hydrogen sulfide are considered.


2019 ◽  
Vol 133 (20) ◽  
pp. 2045-2059 ◽  
Author(s):  
Da Zhang ◽  
Xiuli Wang ◽  
Siyao Chen ◽  
Selena Chen ◽  
Wen Yu ◽  
...  

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.


Author(s):  
Roberto González-De Zayas ◽  
Liosban Lantigua Ponce de León ◽  
Liezel Guerra Rodríguez ◽  
Felipe Matos Pupo ◽  
Leslie Hernández-Fernández

The Cenote Jennifer is an important and unique aquatic sinkhole in Cayo Coco (Jardines del Rey Tourist Destination) that has brackish to saline water. Two samplings were made in 1998 and 2009, and 4 metabolism community experiments in 2009. Some limnological parameters were measured in both samplings (temperature, salinity, pH, dissolved oxygen major ions, hydrogen sulfide, nutrients and others). Community metabolism was measured through incubated oxygen concentration in clear and dark oxygen bottles. Results showed that the sinkhole limnology depends on rainfall and light incidence year, with some stratification episodes, due to halocline or oxycline presence, rather than thermocline. The sinkhole water was oligotrophic (total nitrogen of 41.5 ± 22.2 μmol l−1 and total phosphorus of 0.3 ± 0.2 μmol l−1) and with low productivity (gross primary productivity of 63.0 mg C m−2 d−1). Anoxia and hypoxia were present at the bottom with higher levels of hydrogen sulfide, lower pH and restricted influence of the adjacent sea (2 km away). To protect the Cenote Jennifer, tourist exploitation should be avoided and more resources to ecological and morphological studies should be allocated, and eventually use this aquatic system only for specialized diving. For conservation purposes, illegal garbage disposal in the surrounding forest should end.


Author(s):  
Tetyana V Shimanskaya ◽  
Yulia V. Goshovska ◽  
Olena M. Semenykhina ◽  
Vadim F. Sagach

Author(s):  
Olena M. Semenykhina ◽  
Olga V. Bazilyuk ◽  
Yulia P. Korkach ◽  
Vadim F. Sagach

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