Positive Health Online

Abstract

ASANO and colleagues, Department of Physiology, School of Medicine, Showa University, Tokyo, Japan investigated the antitumour action of the derivative of ascorbic acid (vitamin C), sodium 5,6-benzylidene-L-ascorbate (SBA), to determine whether it is mediated via oxidation-involved mechanisms .

Background

Methodology

The authors used 3 different systems in vivo 3-methyl-4-dimethylaminoazobenzene (DAB)-induced rat hepatocellular (liver) carcinoma, its homogenate (semi in vivo) and cultured cells (in vitro).

Results

Oral intake of DAB irreversibly caused liver cancer in rats; maximum cancer incid ence after 4 months. Intravenous administration of SBS induced vacuolar, eisinophilic degeneration and nuclear debris, producing greater amounts of ESR signal of ascorbate radical and hydrogen peroxide (H2O2)-derived chemiluminescence (CL) (H2O2)-CL) in the cancerous tissue than in the normal tissue. When SBA was added directly to the homogenates, higher amounts of ascorbate radical and H2O2-CL were generated in cancerous tissues. When SBA was added to the RPM medium supplemented with 10% foetal bovine serum, methionine was oxidised to methionine sulfoxide and H2O2 was produced in amounts to sufficiently induce apoptosis (cell death) in human promyelocytic leukaemic HL-60 cells. The cytotoxic activity of SBA was significantly reduced by catalase.

Conclusion

The results of this study suggest that antitumour activity of SBA in vivo may be due, at least in part, to H2O2, produced from SBA.

References

Asano K et al. Production of hydrogen peroxide in cancerous tissue by intravenous administration of sodium 5,6-benzylidene-L-ascorbate. Anticancer Research 19(1A): 229-36. Jan-Feb 1999.