"Anthraquinone compounds have been shown to induce apoptosis in different cancer cell
types. Effects of chrysophanol, an anthraquinone compound, on cancer cell death have not
been well studied. The goal of this study was to examine if chrysophanol had cytotoxic effects
and if such effects involved apoptosis or necrosis in J5 human liver cancer cells. Chrysophanol induced necrosis in J5 cells in a dose- and time-dependent manner. Non-apoptotic cell
death was induced by chrysophanol in J5 cells and was characterized by caspase independence, delayed externalization of phosphatidylserine and plasma membrane disruption.
Blockage of apoptotic induction by a general caspase inhibitor (z-VAD-fmk) failed to protect
cells against chrysophanol-induced cell death. The levels of reactive oxygen species production and loss of mitochondrial membrane potential (DCm) were also determined to assess the
effects of chrysophanol. However, reductions in adenosine triphosphate levels and increases
in lactate dehydrogenase activity indicated that chrysophanol stimulated necrotic cell death.
In summary, human liver cancer cells treated with chrysophanol exhibited a cellular pattern
associated with necrosis and not apoptosis."
