THE INTERACTION OF HYDROGEN SULFIDE WITH NO-SYNTHASE AND NO DONORS TRIGGERS SPECIFIC VASOACTIVE EFFECTS IN ISOLATED ARTERIES OF RATS AND PATIENTS WITH ARTERIAL HYPERTENSION

Introduction: Polytrauma patients have high risk of shock, septic complications and death during few years of follow-up. In recent years a lot of attention is paid to gaseous transmitters, among which are nitrogen oxide (NO) and hydrogen sulfide (H2S). It is known that the rise of NO and its metabolites levels occurs during the acute period of polytrauma. Nitric oxide and hydrogen sulfide are produced in different cell types, among which are lymphocytes. The aim: To investigate the levels of NO, NOS, iNOS, еNOS, H2S in lymphocytes lysate in patients at the moment of hospitalization and 24 hours after trauma. Materials and methods: We investigated the levels of NO, NO-synthase, inducible NO-synthase, endothelial NO-synthase, H2S in lymphocytes lysate in patients at the moment of hospitalization and 24 hours after trauma. Results: The study included 20 patients with polytrauma who were treated in the intensive care unit (ICU) of the Lviv Emergency Hospital. Tissue injury was associated with an increased production of NO, NOS, iNOS, еNOS during the acute period of polytrauma. At the same time, the level of H2S decreased by the end of the first day of traumatic injury. Conclusions: In acute period of polytrauma, significant increasing of iNOS and eNOS occurs with percentage prevalence of iNOS over eNOS on the background of H2S decreasing.

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The prognostic implications of perioperative endogenous hydrogen sulfide and nitric oxide levels in children with congenital heart disease complicated by pulmonary arterial hypertension

European Journal of Pediatrics ◽

10.1007/s00431-020-03897-w ◽

2021 ◽

Author(s):

Yanling Tan ◽

Sa Wang ◽

Xinrui Ren ◽

Chao Zhang ◽

Feng Xu

Keyword(s):

Nitric Oxide ◽

Congenital Heart Disease ◽

Hydrogen Sulfide ◽

Heart Disease ◽

Pulmonary Arterial Hypertension ◽

Arterial Hypertension ◽

Congenital Heart ◽

Pulmonary Arterial ◽

Prognostic Implications

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In vitro anticancer activity of hydrogen sulfide and nitric oxide alongside nickel nanoparticle and novel mutations in their genes in CRC patients

Scientific Reports ◽

10.1038/s41598-021-82244-x ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Zjwan Housein ◽

Tayeb Sabir Kareem ◽

Abbas Salihi

Keyword(s):

Nitric Oxide ◽

Cell Proliferation ◽

Hydrogen Sulfide ◽

Direct Sequencing ◽

Scorpion Venom ◽

Enos Gene ◽

Cytotoxic Activities ◽

No Donors ◽

The Impact

AbstractThis study was carried out to assess the impact of nickel nanoparticles (NiNPs) as well as scorpion venom on colorectal cancer (CRC) cells in the presence and/or absence of 5-fluorouracil (5-FU), hydrogen sulfide (H2S), and nitric oxide (NO) donors and to determine alterations in endothelial NO synthase (eNOS) and cystathionine γ-lyase (CSE) enzyme-producing genes in CRC patients. The IC50 of both H2S and NO donors, along with NiNPs, were determined. The CRC cells were treated for 24hrs, and the cytotoxic activities were assessed using the MTT test. Moreover, the apoptosis was determined after 24hrs and 48hrs using TUNEL assay. Furthermore, the mutations in the eNOS gene (intron 4, -786T>C and 894 G>T) and CSE gene (1364GT) were determined using direct sequencing. The IC50 values for sodium disulfide (Na2S) and sodium nitroprusside (SNP) at 24hrs treatment were found to be 5 mM and 10−6 M, respectively, while the IC50 value for 5-FU was reached after 5-days of treatment in CRC cell line. Both black and yellow scorpion venoms showed no inhibition of cell proliferation after 24hrs treatment. Furthermore, Na2S showed a significant decrease in cell proliferation and an increase in apoptosis. Moreover, a co-treatment of SNP and 5-FU resulted in inhibition of the cytotoxic effect of 5-FU, while a combination treatment of NiNPs with Na2S, SNP, and 5-FU caused highly significant cytotoxicity. Direct sequencing reveals new mutations, mainly intronic variation in eNOS gene that has not previously been described in the database. These findings indicate that H2S promotes the anticancer efficiency of 5-FU in the presence of NiNPs while NO has antiapoptotic activity in CRC cell lines.

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Nitric Oxide: Potential of NO Donors and NO Synthase Inhibitors for the Treatment of Pain

Analgesics ◽

10.1002/3527605614.ch16 ◽

2005 ◽

pp. 555-566

Author(s):

Corinna Maul ◽

Hagen-Heinrich Hennies ◽

Bernd Sundermann

Keyword(s):

Nitric Oxide ◽

No Synthase ◽

No Donors

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Nitric oxide stimulates cellular degradation of human CYP51A1, the highly conserved lanosterol 14α-demethylase

Biochemical Journal ◽

10.1042/bcj20170459 ◽

2017 ◽

Vol 474 (19) ◽

pp. 3241-3252 ◽

Cited By ~ 8

Author(s):

Ji Won Park ◽

Aria Byrd ◽

Choon-myung Lee ◽

Edward T. Morgan

Keyword(s):

Nitric Oxide ◽

Proteasome Inhibitors ◽

No Synthase ◽

Cytochrome P450 Enzymes ◽

Human Hepatoma Cells ◽

Down Regulation ◽

Regulation Of Expression ◽

No Donors ◽

Huh7 Cells ◽

Ubiquitin Proteasome

Nitric oxide (NO) is known to down-regulate drug-metabolizing cytochrome P450 enzymes in an enzyme-selective manner. Ubiquitin–proteasome-dependent and -independent pathways have been reported. Here, we studied the regulation of expression of human CYP51A1, the lanosterol 14α-demethylase required for synthesis of cholesterol and other sterols in mammals, which is found in every kingdom of life. In Huh7 human hepatoma cells, treatment with NO donors caused rapid post-translational down-regulation of CYP51A1 protein. Human NO synthase (NOS)-dependent down-regulation was also observed in cultured human hepatocytes treated with a cytokine mixture and in Huh7 cells expressing human NOS2 under control of a doxycycline-regulated promoter. This down-regulation was partially attenuated by proteasome inhibitors, but only trace levels of ubiquitination could be found. Further studies with inhibitors of other proteolytic pathways suggest a possible role for calpains, especially when the proteasome is inhibited. NO donors also down-regulated CYP51A1 mRNA in Huh7 cells, but to a lesser degree, than the down-regulation of the protein.

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