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Sodium benzylideneascorbate induces apoptosis in HIV‐replicating U1 cells
Author(s) -
Aokia Kazumasa,
Nakashima Hideki,
Hattori Toshihiro,
Shiokawa Daisuke,
Ni-imi Ei-ichi,
Tanimoto Yutaka,
Maruta Hideharu,
Uchiumi Fumiaki,
Kochi Mutsuyuki,
Yamamoto Naoki,
Tanuma Sei-ichi
Publication year - 1994
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(94)00832-9
Subject(s) - apoptosis , human immunodeficiency virus (hiv) , chemistry , microbiology and biotechnology , sodium , virology , biophysics , biology , biochemistry , organic chemistry
U1 cells, a subclone of U937 cells chronically infected with human immunodeficiency virus type 1 (HIV‐1), produced HIV‐1 only in the presence of inducers such as 12‐ O ‐tetradecanoxylphorbol 13‐acetate (TPA) or tumor necrosis factor (TNF)‐α. The expression of HIV‐antigen on U1 cells induced by TPA or TNF‐α was found to be prevented by sodium 5,6‐benzylidene‐ l ‐ascorbate (SBA) in a concentration‐dependent manner. Treatment of U1 cells with SBA in the presence of inducers resulted in cell death with cell shrinkage, chromatin condensation and DNA fragmentation into nucleosomal oligomers, characteristics of apoptosis. In contrast, SBA had scarcely any apoptotic effect on U1 cells in the absence of inducers. SBA did not also induce apoptosis in parental U937 cells in the presence or absence of inducers. These results suggest that HIV‐replicating U1 cells selectively undergo apoptosis on treatment with SBA.