Role of calcium in nitric oxide-induced programmed cell death in tobacco protoplasts

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 (Delta I(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+).