Abstract
It was shown by immunoblotting that the introduction of an antitumor antioxidant, sodium 2-carboxy-2-(N-acetylamino)-3-(3,5-di-tert-butyl-4-hydrophenyl)propanoate (anphen sodium), into a suspension of Lewis carcinoma cells induces a sharp decrease in the contents of the monomer and homodimer of the anti-apoptotic Bcl-2 protein. According to fluorescence analysis, the number of apoptotic cells sharply increased 1 h after exposure to anphen sodium; preliminary addition of 5 μmol L-1 of hydrogen peroxide increased the cell membrane permeability of anphen sodium and the number of apoptotic cells. The onset of apoptosis detected using fluorophores is comparable in time with the start of the decline of the Bcl-2 level. It was assumed that the mechanism of action of anphen sodium may include the interaction of the agent with the hydrophobic (BH3) domain of Bcl-2 family proteins.
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