ABSTRACT
Apoptosis is a term first used in 1972 by J. F. Kerr et al. to describe a tissue pathology known as “shrinking necrosis”. Apoptosis is regarded as an active and progressive response to physiologic and pathologic stimuli, and cells dying by apoptosis cause minimal disturbance to the surrounding tissue. It has been evident that most of cancer cytotoxic agents act primarily by inducing apoptosis in cancer cells. The chapter presents the mechanisms by which resveratrol appears to induce cell death, specifically apoptosis, with reference to its ability to act through cell death receptors, mitochondria pathway, nuclear factors and cell cycle arrest, and sensitization to drug-induced and free radical-associated apoptosis, in the context of its use as a cancer chemotherapeutic agent. Initial investigations of resveratrol at relatively high concentrations in human leukemia-60 cells showed a dose-dependent loss of membrane phospholipid asymmetry and DNA fragmentation. Resveratrol also has the ability to act as either an agonist or antagonist to nuclear steroid hormone receptors.
