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We tried to determine the mechanisms by which Ca2+ 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 [Ca2+]cyt accumulation and decrease in mitochondrial membrane potential (ΔΨm) before the appearance of PCD. NO-induced PCD could be largely prevented not only by NO scavenger c-PTIO, but also by EGTA (Ca2+ chelator), LaCl3 (Ca2+-channel blocker) or CsA (a specific mitochondrial permeability transition pore inhibitor, which also inhibit Ca2+ cycling by mitochondria). All results suggested that NO-induced PCD is mediated through mitochondrial pathway and regulated by Ca2+.