September 8, 2006
Tocotrienols induce apoptosis in prostate cancer cells
The July 28, 2006 issue of the journal Biochemical and Biophysical Research Communications published the findings of Janmejai K. Srivastava and Sanjay Gupta of Case Western Reserve University in Cleveland, Ohio, that the application of a tocotrienol-rich fraction (TRF) of palm oil resulted in the programmed self-destruction (apoptosis) and growth arrest of prostate cancer cells, while not significantly affecting normal prostate cells. Tocotrienols are four of the eight fractions of vitamin E that may have cancer preventive properties along with other benefits.
The duo used cultures of normal human prostate epithelial cells, virally transformed normal cells, and three types of human prostate cancer cells for the current study. Tocotrienols were administered in concentrations of 5, 10, 20, 40 and 80 micrograms per milliliter. Control groups of cells received an inert solution.
While minimal growth inhibition occurred in the normal and virally transformed normal cells following the addition of the highest concentration of tocotrienols, there was a significant decrease in cell viability and colony formation in all of the prostate cancer cell lines beginning at lower concentrations. Prostate cancer cells treated with tocotrienols underwent significant apoptosis that increased with higher concentrations, while normal cells did not undergo apoptosis. Cell cycle analysis also showed a dose-dependent effect at a particular phase of the cell cycle only in the three prostate cancer lines. "These observations suggest that prostate cancer cells respond differentially to TRF exposure than their normal counterparts," the authors observed.
According to Drs Srivastava and Gupta, the prevalence and long latency period of prostate cancer make it an ideal candidate for chemopreventive measures. To their knowledge this is the first study to demonstrate that tocotrienol-rich fraction of palm oil causes cell cycle arrest and apoptosis in prostate cancer cells while leaving normal cells unaffected.
Tocotrienols induce apoptosis in prostate cancer cells
The July 28, 2006 issue of the journal Biochemical and Biophysical Research Communications published the findings of Janmejai K. Srivastava and Sanjay Gupta of Case Western Reserve University in Cleveland, Ohio, that the application of a tocotrienol-rich fraction (TRF) of palm oil resulted in the programmed self-destruction (apoptosis) and growth arrest of prostate cancer cells, while not significantly affecting normal prostate cells. Tocotrienols are four of the eight fractions of vitamin E that may have cancer preventive properties along with other benefits.
The duo used cultures of normal human prostate epithelial cells, virally transformed normal cells, and three types of human prostate cancer cells for the current study. Tocotrienols were administered in concentrations of 5, 10, 20, 40 and 80 micrograms per milliliter. Control groups of cells received an inert solution.
While minimal growth inhibition occurred in the normal and virally transformed normal cells following the addition of the highest concentration of tocotrienols, there was a significant decrease in cell viability and colony formation in all of the prostate cancer cell lines beginning at lower concentrations. Prostate cancer cells treated with tocotrienols underwent significant apoptosis that increased with higher concentrations, while normal cells did not undergo apoptosis. Cell cycle analysis also showed a dose-dependent effect at a particular phase of the cell cycle only in the three prostate cancer lines. "These observations suggest that prostate cancer cells respond differentially to TRF exposure than their normal counterparts," the authors observed.
According to Drs Srivastava and Gupta, the prevalence and long latency period of prostate cancer make it an ideal candidate for chemopreventive measures. To their knowledge this is the first study to demonstrate that tocotrienol-rich fraction of palm oil causes cell cycle arrest and apoptosis in prostate cancer cells while leaving normal cells unaffected.