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

https://doi.org/10.20538/1682-0363-2011-6-40-44

Abstract

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.

About the Authors

Ye. G. Starikova
Сибирский государственный медицинский университет
Russian Federation


N. V. Ryazantseva
Сибирский государственный медицинский университет
Russian Federation


V. V. Novitsky
Сибирский государственный медицинский университет
Russian Federation


L. A. Tashireva
Сибирский государственный медицинский университет
Russian Federation


Yu. V. Starikov
Сибирский государственный медицинский университет
Russian Federation


Ye. A. Stepovaya
Сибирский государственный медицинский университет
Russian Federation


I. A. Osikhov
Сибирский государственный медицинский университет
Russian Federation


O. A. Vasiliyeva
Сибирский государственный медицинский университет
Russian Federation


Y. D. Yakushina
Сибирский государственный медицинский университет
Russian Federation


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Review

For citations:


Starikova Ye.G., Ryazantseva N.V., Novitsky V.V., Tashireva L.A., Starikov Yu.V., Stepovaya Ye.A., Osikhov I.A., Vasiliyeva O.A., Yakushina Y.D. The role of intracellular gaseous transmitters hydrogen sulfide and nitric oxide in apoptosis regulation of normal and cancer cells. Bulletin of Siberian Medicine. 2011;10(6):40-44. (In Russ.) https://doi.org/10.20538/1682-0363-2011-6-40-44

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ISSN 1682-0363 (Print)
ISSN 1819-3684 (Online)