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Mitochondrial control of cell death induction by sodium 5,6-benzylidene-L-ascorbate
Hiroko Fujii1, Osamu Amano, Mutsuyuki Kochi
1Department of Oral Anatomy II, Meikai University School of Dentistry, Sakado Saitama, 350-0283, Japan.
Abstract:
Previous studies have demonstrated the dramatic antitumor activity of sodium 5,6-benzylidene-L-ascorbate (SBA). However, the molecular mechanism of this antitumor action is unclear. We investigated the changes in the fine structures of a human submandibular gland carcinoma cell line, HSG, during the cell death induced by SBA. When HSG cells were incubated for 6 hours with non-cytotoxic concentrations of SBA, changes in the mitochondria, such as the disassembly of cristae and decrease in the electron density, were discrenible. At cytotoxic concentrations, the swelling and vacuolization of the mitochondria became apparent, while the nuclear architecture including the profile and ratio of heterochromatin and euchromatin and thickness of the nuclear membrane were intact. These data suggest that the mitochondria, not the nucleus, may be the target organelle of SBA, and support the ability of SBA to induce non-apoptotic cell death in HSG cells.
Insights
Sodium 5,6-benzylidene-L-ascorbate (SBA) shows antitumor activity by damaging mitochondria, not the nucleus. This suggests SBA induces non-apoptotic cell death in HSG carcinoma cells.
Area of Science:
- Biochemistry
- Cell Biology
- Oncology
Background:
- Sodium 5,6-benzylidene-L-ascorbate (SBA) exhibits significant antitumor effects.
- The precise molecular mechanisms underlying SBA's anticancer activity remain largely unknown.
Purpose of the Study:
- To investigate the ultrastructural changes in human submandibular gland carcinoma (HSG) cells induced by SBA.
- To elucidate the molecular targets and cell death pathways affected by SBA.
Main Methods:
- Human submandibular gland carcinoma (HSG) cells were treated with varying concentrations of SBA.
- Cellular fine structures, particularly mitochondria and nuclei, were examined using electron microscopy.
Main Results:
- Non-cytotoxic SBA concentrations induced mitochondrial changes like cristae disassembly and decreased electron density.
- Cytotoxic SBA concentrations led to mitochondrial swelling and vacuolization.
- Nuclear architecture, including chromatin and nuclear membrane, remained unaffected by SBA treatment.
Conclusions:
- Mitochondria appear to be the primary target organelle for SBA in HSG cells.
- SBA-induced cell death in HSG cells is likely a non-apoptotic form of cell death.
- These findings provide insight into the molecular mechanism of SBA's antitumor activity.