No abstract

We tried to determine the mechanisms by which Ca 2+ mediated NO-induced programmed cell death (PCD) in tobacco protoplasts. Treatment of tobacco protoplasts with the NO donor sodium nitroprusside (SNP) resulted in a rapid [Ca 2+ ] cyt accumulation and decrease in mitochondrial membrane potential (ΔΨ m ) before the appearance of PCD. NO-induced PCD could be largely prevented not only by NO scavenger c-PTIO, but also by EGTA (Ca 2+ chelator), LaCl 3 (Ca 2+ -channel blocker) or CsA (a specific mitochondrial permeability transition pore inhibitor, which also inhibit Ca 2+ cycling by mitochondria). All results suggested that NO-induced PCD is mediated through mitochondrial pathway and regulated by Ca 2+ .