Nitric oxide is a suppressor of aluminum-induced mitochondria and caspase-like protease-dependent programmed cell death in plants.

Aluminum (Al) promotes programmed cell death (PCD) in plants. Although a lot of knowledge about the mechanisms of Al tolerance has been learned, how Al-induced PCD is regulated by nitric oxide (NO) is poorly understood. Mitochondrion is the regulatory center for PCD. We found that Al reduced the level of mitochondrial NO/HO, promoted the opening of mitochondrial permeability transition pore, decreased mitochondrial inner membrane potential (∆ψ), and increased caspase-like protease activity. NO-specific scavenger cPTIO enhanced these effects that were reversed by NO donor sodium nitroprusside. Our data suggest that NO suppresses Al-induced PCD by improving mitochondrial physiological properties.