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Exposition of Phosphatidylserine in Lewis Carcinoma Cells under the Action of Anphen Sodium and Hydrogen Peroxide
The apoptotic effect of the antioxidant anphen sodium, a spatially hindered phenol, which has antitumor activity—in particular, inhibiting the development of tumor cells in sarcoma—has been studied. It was found that the administration of anphen sodium (10 –4 M) into a cell culture of Lewis carcinom...
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Published in: | Cell and tissue biology 2021, Vol.15 (1), p.61-66 |
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Main Authors: | , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | The apoptotic effect of the antioxidant anphen sodium, a spatially hindered phenol, which has antitumor activity—in particular, inhibiting the development of tumor cells in sarcoma—has been studied. It was found that the administration of anphen sodium (10
–4
M) into a cell culture of Lewis carcinoma of mice already after 1–1.5 h led to the exposure of phosphatidylserine and the beginning of the process of apoptosis in the cells (according to the fluorescence of annexin V-FITC). With the combined action of H
2
O
2
(5 μM) and anphen sodium, the permeability of cells to acridine orange increased, and the number of apoptotic cells also increased to 80–100%. The formation of both single and numerous apoptotic bodies inside the cell was observed in tumor cells. Under the same conditions, a smaller number of apoptotic cells (14–16%) were found in spleen cells (splenocytes) of healthy mice, probably due to the action on only cells ready for apoptosis. Previously, we discovered the effect of anphen sodium on antiapoptotic proteins of the Bcl-2 family and hypothesized that this compound leads to apoptosis by the mitochondrial pathway. Since H
2
O
2
at low concentrations can act as a secondary messenger and stimulate the external pathway of apoptosis, it is supposed that the joint action of H
2
O
2
and anphen sodium leads to increased apoptosis by activating the mitochondrial and extrinsic signaling pathways. |
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ISSN: | 1990-519X 1990-5203 |
DOI: | 10.1134/S1990519X21010089 |