The role of intracellular gaseous transmitters hydrogen sulfide and nitric oxide in apoptosis regulation of normal and cancer cells

Investigation of influence of gases nitric oxide and hydrogen sulfide on apoptotic cell death of Jurlat cells and mononuclear leucocytes of healthy donors was conducted. It was shown that 100 mmol sodium nitroprussidi increased the apoptosis of T lymphoblast leukemia cells after 15’ incubation. 10 and 100 mmol donor of hydrogen sulfide caused apoptotic death of Jurkat cells after 15’ incubation. 15’ exposure of nitric oxide and hydrogen sulfide donors did not lead to the changes of cell death of mononuclear leucocytes. Gaseous transmitters NO and H2S increased necrosis of Jurkat cells and mononuclear leucocytes after 24 h incubation with the appropriate gase’s donor.

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INTRACELLULAR TARGETS OF PROAPOPTOTIC INFLUENCE OF GASEOUS TRANSMITTERS

Annals of the Russian academy of medical sciences ◽

10.15690/vramn.v67i10.420 ◽

2012 ◽

Vol 67 (10) ◽

pp. 77-81 ◽

Cited By ~ 1

Author(s):

L. A. Tashireva ◽

E. G. Starikova ◽

V. V. Novitskii ◽

N. V. Ryazantseva

Keyword(s):

Nitric Oxide ◽

Carbon Monoxide ◽

Hydrogen Sulfide ◽

Transmembrane Potential ◽

Molecular Targets ◽

Jurkat Cells ◽

Mitochondrial Transmembrane Potential ◽

Caspase 9 ◽

Gaseous Transmitters ◽

Intracellular Targets

Main molecular targets of nitric oxide, hydrogen sulfide and carbon monoxide proapoptotic action in Jurkat cells were determined in this study. Decrease of mitochondrial transmembrane potential was shown during all three gases action. Reason of this event is the Bcl-2 family members disbalance. Proapoptotic proteins release after mitochondrion membranes permeabilisation could be abolished by protein xIAP inhibition of caspase -9 and-3 activity during NO and CO application.

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Nitric oxide mediates epinephrine-induced apoptotic cell death of trabecular meshwork cellsin vitro

Korean Journal of Ophthalmology ◽

10.3341/kjo.2003.17.2.97 ◽

2003 ◽

Vol 17 (2) ◽

pp. 97 ◽

Cited By ~ 1

Author(s):

J W Kim ◽

S K Kim ◽

K H Kim

Keyword(s):

Nitric Oxide ◽

Cell Death ◽

Trabecular Meshwork ◽

Apoptotic Cell ◽

Apoptotic Cell Death

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Apoptotic cell death triggered by nitric oxide in pancreatic beta-cells

Diabetes ◽

10.2337/diabetes.44.7.733 ◽

1995 ◽

Vol 44 (7) ◽

pp. 733-738 ◽

Cited By ~ 59

Author(s):

H. Kaneto ◽

J. Fujii ◽

H. G. Seo ◽

K. Suzuki ◽

T. Matsuoka ◽

...

Keyword(s):

Nitric Oxide ◽

Cell Death ◽

Beta Cells ◽

Pancreatic Beta Cells ◽

Apoptotic Cell ◽

Apoptotic Cell Death

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CHANGES OF NITRIC OXIDE SYNTHASE AND HYDROGEN SULFIDE IN BLOOD LYMPHOCYTES IN THE ACUTE PERIOD OF POLYTRAUMA

Wiadomości Lekarskie ◽

10.36740/wlek201908110 ◽

2019 ◽

Vol 72 (8) ◽

pp. 1473-1476

Author(s):

Nataliya Matolinets ◽

Helen Sklyarova ◽

Eugene Sklyarov ◽

Andrii Netliukh

Keyword(s):

Nitric Oxide ◽

Hydrogen Sulfide ◽

Tissue Injury ◽

Traumatic Injury ◽

Cell Types ◽

No Synthase ◽

Septic Complications ◽

Acute Period ◽

Gaseous Transmitters ◽

The Moment

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 Role of Reactive Oxygen Species, Kinases, Hydrogen Sulfide, and Nitric Oxide in the Regulation of Autophagy and Their Impact on Ischemia and Reperfusion Injury in the Heart

Current Cardiology Reviews ◽

10.2174/1573403x16666201014142446 ◽

2020 ◽

Vol 16 ◽

Author(s):

Andrey Krylatov ◽

Leonid Maslov ◽

Sergey Y. Tsibulnikov ◽

Nikita Voronkov ◽

Alla Boshchenko ◽

...

Keyword(s):

Nitric Oxide ◽

Reactive Oxygen Species ◽

Hydrogen Sulfide ◽

Ischemia Reperfusion ◽

Reactive Oxygen ◽

Ischemia And Reperfusion ◽

Oxygen Species ◽

Ischemia And Reperfusion Injury ◽

Adaptive Process

: There is considerable evidence in the heart that autophagy in cardiomyocytes is activated by hypoxia/reoxygenation (H/R) or in hearts by ischemia/reperfusion (I/R). Depending upon the experimental model and duration of ischemia, increases in autophagy in this setting maybe beneficial (cardioprotective) or deleterious (exacerbate I/R injury). Aside from the conundrum as to whether or not autophagy is an adaptive process, it is clearly regulated by a number of diverse molecules including reactive oxygen species (ROS), various kinases, hydrogen sulfide (H2S) and nitric oxide (NO). The purpose this review is to address briefly the controversy regarding the role of autophagy in this setting and to examine a variety of disparate molecules that are involved in its regulation.

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Inhibition of Autophagy Enhances the Antitumor Effect of Thioridazine in Acute Lymphoblastic Leukemia Cells

Life ◽

10.3390/life11040365 ◽

2021 ◽

Vol 11 (4) ◽

pp. 365

Author(s):

Carina Colturato-Kido ◽

Rayssa M. Lopes ◽

Hyllana C. D. Medeiros ◽

Claudia A. Costa ◽

Laura F. L. Prado-Souza ◽

...

Keyword(s):

Cell Death ◽

Acute Lymphoblastic Leukemia ◽

Lymphoblastic Leukemia ◽

Clinical Problem ◽

Jurkat Cells ◽

Leukemia Cells ◽

Peripheral Mononuclear Blood ◽

Induced Apoptosis ◽

Cure Rates

Acute lymphoblastic leukemia (ALL) is an aggressive malignant disorder of lymphoid progenitor cells that affects children and adults. Despite the high cure rates, drug resistance still remains a significant clinical problem, which stimulates the development of new therapeutic strategies and drugs to improve the disease outcome. Antipsychotic phenothiazines have emerged as potential candidates to be repositioned as antitumor drugs. It was previously shown that the anti-histaminic phenothiazine derivative promethazine induced autophagy-associated cell death in chronic myeloid leukemia cells, although autophagy can act as a “double-edged sword” contributing to cell survival or cell death. Here we evaluated the role of autophagy in thioridazine (TR)-induced cell death in the human ALL model. TR induced apoptosis in ALL Jurkat cells and it was not cytotoxic to normal peripheral mononuclear blood cells. TR promoted the activation of caspase-8 and -3, which was associated with increased NOXA/MCL-1 ratio and autophagy triggering. AMPK/PI3K/AKT/mTOR and MAPK/ERK pathways are involved in TR-induced cell death. The inhibition of the autophagic process enhanced the cytotoxicity of TR in Jurkat cells, highlighting autophagy as a targetable process for drug development purposes in ALL.

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