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Genistein Induces Apoptosis of RPE-J Cells by Opening Mitochondrial PTP

2000; Elsevier BV; Volume: 276; Issue: 1 Linguagem: Inglês

10.1006/bbrc.2000.3445

1090-2104

Hee Seong Yoon, Seong Cheol Moon, Nam Deuk Kim, Bong-Soo Park, Min Ho Jeong, Young Hyun Yoo,

RNA Interference and Gene Delivery

Although previous studies demonstrated that genistein-induced apoptosis of various cell types including RPE-J cells, the involvement of mitochondrial events in such types of apoptosis has not been demonstrated to date. In this investigation of genistein-induced apoptosis of RPE-J cells, genistein induced the reduction of the mitochondrial membrane potential and the release of cytochrome c to cytosol. A mitochondrial permeability transition pore (PTP) blocker bongkrekic acid prevented the reduction of the mitochondrial membrane potential and cytochrome c release, and consequently abolished caspase-3 activation, nuclear condensation, and DNA fragmentation. On the other hand, zVAD-fmk did not inhibit the mitochondrial event such as the reduction of the mitochondrial membrane potential and cytochrome c release although it prevented caspase-3 activation, nuclear condensation, and DNA fragmentation. Taken together, genistein induces apoptosis of RPE-J cells by opening the mitochondrial PTP, and the mitochondrial event in this type of apoptosis is caused independently of caspase.