CARBON MONOXIDE: ITS ROLE IN MITOCHONDRIAL PATHWAY OF APOPTOSIS INDUCTION IN JURKAT CANCER CELLS
Abstract. This study demonstrates ability of carbon monoxide to trigger mitochondrial pathway of apoptosis induction of Jurcat cells. We have shown that proapoptotic action of carbon monoxide is coupled to permeabilization of cellular mitochondrial membranes. Imbalance in Bcl-2 family of regulatory...
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| Autores principales: | , , , , , |
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| Formato: | article |
| Lenguaje: | RU |
| Publicado: |
SPb RAACI
2014
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| Materias: | |
| Acceso en línea: | https://doaj.org/article/a3ada925b35a4c20860c40247081ddf3 |
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| Sumario: | Abstract. This study demonstrates ability of carbon monoxide to trigger mitochondrial pathway of apoptosis induction of Jurcat cells. We have shown that proapoptotic action of carbon monoxide is coupled to permeabilization of cellular mitochondrial membranes. Imbalance in Bcl-2 family of regulatory proteins may be considered among possible reasons of the membrane pore formation. We have shown downregulated cl-2 and Bcl-xl mRNA expression and decreased levels of antiapoptotic proteins, along wih decreased mRNA expression and increase of Bad proapototic protein level in Jurkat cells following incubation with 50 μm of CORM-2, a carbon monoxide donor. |
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