Methyl salicylate-improved mitochondrial stability obstructed cell death activation in preventing visible chilling injury in sweet basil under cold storage

Abstract

Mitochondrial stability plays an important part in compelling plant senescence and physiological disorders. The research aimed to investigate the role of mitochondrial reactive oxygen species (ROS) and oxidative damage in mediated cell death and chilling in sweet basil and to investigate the role of methyl salicylate (MeSA) immersion in retarding chilling injury development via activation of antioxidant defense systems to protect mitochondria-induced deterioration. Sweet basils were subjected to a 5-min immersion in 1 mM MeSA and stored at 6 °C for 8 d. In the control group, evident symptoms of chilling injury were observed on day 4, coinciding with a substantial accumulation of mitochondrial ROS and reduction in mitochondrial stability, particularly evident in cytochrome c dissipation. Concurrently, an increase in caspase-like enzyme activities, known to drive cell death, was observed following exposure to low temperatures. In contrast, chilling injury was mitigated in the MeSA-treated leaves. The MeSA treatment significantly enhanced the overall antioxidant capacity of the mitochondria and improved mitochondrial stability, thereby preventing the activation of caspase-like enzymes. Consequently, this treatment preserved membrane integrity and suppressed cell death activation, ultimately leading to a delay in the appearance of cold damage during storage.