Abstract

Aluminum (Al) causes programmed cell death (PCD) in plants. Our previous studies have confirmed that nitric oxide (NO) inhibits Al-induced PCD in the root tips of peanut. However, the mechanism by which NO inhibits Al-induced PCD is unclear. Here the effects of NO on mitochondrial reactive oxygen species (ROS), malondialdehyde (MDA), activities of superoxide dismutase (SOD) and ascorbate peroxidase (APX), expression of alternative oxidase (AhAOX) and cytochrome oxidase (AhCOX) were investigated in peanut (Arachis hypogaea L.) root tips treated with Al. The results showed that Al stress induced rapid accumulation of H2O2 and MDA and increased the ratio of SOD/APX. The up-regulation of AhAOX and AhCOX expressions was not enough to inhibit PCD occurrence. Sodium nitroprusside (SNP, a NO donor) decreased the ratio of SOD/APX and eliminated excess H2O2 and MDA, thereby inhibiting Al-induced PCD in the root tips of peanut. The expression of AhAOX and AhCOX was significantly enhanced in Al-induced PCD treated with SNP. But cPTIO (a NO specific scavenger) supply had the opposite effect. Taken together, these results suggested that lipid peroxidation induced by higher levels of H2O2 was an important cause of Al-induced PCD. NO-mediated inhibition of Al-induced PCD was related to a significant elimination of H2O2 accumulation by decreasing the ratio of SOD/APX and up-regulating the expression of AhAOX and AhCOX.

Highlights

  • As a major factor, aluminum (Al) toxicity limits crop productivity in acid soil

  • To explore the mitochondrial pathway of Nitric oxide (NO) regulating Al-induced programmed cell death (PCD), the effects of treatment with NO donor and NO specific scavenger on mitochondrial reactive oxygen species (ROS), malondialdehyde (MDA), activities of superoxide dismutase (SOD) and ascorbate peroxidase (APX), expression of AhAOX and AhCOX under Al-induced PCD in the root tips of peanut were investigated. These results indicated that excess H2O2-induced lipid peroxidation was an important cause of Al-induced PCD

  • The results indicated that NO donor sodium nitroprusside (SNP) promoted the activities of SOD and APX (Fig. 7b-A), decreased the ratio of SOD and APX, up-regulated the expression of AhAOX and AhCOX (Fig. 7b-B), reduced the accumulation of H2O2 and O2.− (Fig. 7b-C), leading to inhibition of Al-induced PCD in the root tips of peanut. cPTIO supply had the opposite effects

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Summary

Introduction

Aluminum (Al) toxicity limits crop productivity in acid soil. Al inhibits root elongation growth and disrupts the uptake of nutrient and water in plants. To explore the mitochondrial pathway of NO regulating Al-induced PCD, the effects of treatment with NO donor and NO specific scavenger on mitochondrial ROS, malondialdehyde (MDA), activities of superoxide dismutase (SOD) and ascorbate peroxidase (APX), expression of AhAOX and AhCOX under Al-induced PCD in the root tips of peanut were investigated. These results indicated that excess H2O2-induced lipid peroxidation was an important cause of Al-induced PCD. NO-mediated inhibition of PCD induced by Al was related to a significant decrease in the ratio of SOD/APX and the up-regulation of AhAOX and AhCOX expressions

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