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Sodium benzylideneascorbate induces apoptosis in HIV-replicating U1 cells
K Aoki1, H Nakashima, T Hattori
1Department of Biochemistry, Faculty of Pharmaceutical Sciences, Science University of Tokyo, Japan.
FEBS Letters
|August 29, 1994
Summary
Sodium 5,6-benzylidene-L-ascorbate (SBA) selectively induces apoptosis in HIV-1-replicating U1 cells. This compound prevents HIV antigen expression and triggers programmed cell death in infected cells, but not in uninfected ones.
Area of Science:
- Virology
- Cell Biology
- Immunology
Background:
- U1 cells, a subclone of U937, are chronically infected with human immunodeficiency virus type 1 (HIV-1).
- HIV-1 production in U1 cells requires specific inducers like 12-O-tetradecanoylphorbol 13-acetate (TPA) or tumor necrosis factor-alpha (TNF-α).
Purpose of the Study:
- To investigate the effect of sodium 5,6-benzylidene-L-ascorbate (SBA) on HIV-1 replication and U1 cell viability.
- To determine if SBA can selectively induce apoptosis in HIV-1-infected cells.
Main Methods:
- U1 cells were treated with SBA in the presence and absence of inducers (TPA or TNF-α).
- HIV-1 antigen expression was monitored.
- Apoptosis was assessed by examining cell morphology, chromatin condensation, and DNA fragmentation.
Main Results:
- SBA prevented the induction of HIV antigen expression by TPA or TNF-α in a dose-dependent manner.
- Treatment with SBA in the presence of inducers led to U1 cell death, characterized by apoptosis.
- SBA showed minimal apoptotic effect on U1 cells without inducers or on parental U937 cells.
Conclusions:
- HIV-replicating U1 cells selectively undergo apoptosis upon treatment with SBA.
- SBA demonstrates potential as an agent to target and eliminate HIV-infected cells.