Numerous studies demonstrated that genistein induced the decrease of proliferation and apoptosis in a variety of cells. However, there is no report about the effect of genistein on proliferation and demise of mast cells.

This study was conducted to investigate genistein-induced aoptosis of mast cells as it pertains to both its basic drug mechanism and the potential therapeutics of the pathologic conditions accompanying mast cell proliferation.

p815 murine mastcytoma cell line was used to assess the effects of genistein treatment including viability and proliferation, morphlolgic study, DNA electrophoresis, the effect of caspase inhibitor, western blotting, and mitochondrial event.

Genistein indeced many apoptotic manifestations as evidenced by changes in cell morphology, generation of DNA fragmentation, activation of caspase 3, and DNA hypoploidy. The reduction of mitochondrial membrae potential and the release of cytochrome c to cytosol were also demonstrated. However, reduction of mitochondrial membrane potential and cytochrome c release were not prevented by caspase inhibitors zVAD-fmk and BocD.fmk, or PTP(permeability transition pore) blockers such as bongkrekic acid and cyclosporin A.

This in vitro study suggests that pathologic increases in mast cell number possibly be regulated in vivo by therapeutic strategy enhancing apoptosis by treatment of genistein.