Mechanism of capsaicin-induced apoptosis

Abstract

Capsaicin(CAP : 8-methyl-N-vanillyl-6-noneamide) is a major pungent component of hot peppers. The vanilloid compounds, capsaicin is a quinone analogue that inhibit the NADH-plasma membrane electron transport system. We previously reported that CAP induces apoptosis in Korean stomach cancer cell line, SNU-1. In the present study, the mechanism of CAP-induced apoptotic cell death was investigated. Because disruption of the mitochondrial transmembrane potential(A U' m) is a common metabolic alteration in all apoptotic processes, we have evaluated the role of mitochondrial permeability transition in CAP-induced apoptosis. Using a cytofluorimetric approach, we have determined that DNA nuclear loss is proceeded by an increase of the production of reactive oxygen species(R0S) and by a subsequent A U' m dissipation in stomach cell line. We suggest that ROS generation by inhibition of the NADH-dependent plasma membrane electron transport system resulted in the oxidation of mitochondrial megachannel pores that allows for the disruption of A U' m.