Chrysophanol induces the necrosis of cancer cells via a reduction in ATP levels. Chrysophanol attentuates the effects of lead exposure in mice by reducing hippocampal neuronal cytoplasmic edema, enhancing mitochondrial crista fusion, significantly increasing memory and learning abilities, reducing lead content in blood, heart, brain, spleen, kidney and liver, promoting superoxide dismutase and glutathione peroxidase activities and reducing malondialdehyde level in the brain, kidney and liver. 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.