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

Authors:	Y Wang J S Lin G X Wang

Institution:	(1) Center of Neurosciences and Cell Biology, Department of Zoology, University of Coimbra, 3004-517 Coimbra, Portugal;(2) Department of Biochemistry, University of Coimbra, Coimbra, Portugal;

Abstract:	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 (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 (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⁺.

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