Methylglyoxal triggers the heat tolerance in maize seedlings by driving AsA-GSH cycle and reactive oxygen species-/methylglyoxal-scavenging system.

Traditionally, methylglyoxal (MG) was looked upon as a toxic byproduct of cellular metabolism. Nowadays, MG has been found to be a novel signaling molecule. However, whether MG can trigger the heat tolerance in maize seedlings and the underlying mechanisms is still elusive. In this study, the maize seedlings irrigated with MG increased the survival percentage of seedlings under heat stress (HS), remitted a decrease in tissue vitality and an increase in electrolyte leakage, and reduced membrane lipid peroxidation, implying MG could trigger the heat tolerance of maize seedlings. The further experiments showed that MG drove the ascorbic acid (AsA)-glutathione (GSH) cycle by activating enzymes (glutathione reductase, monodehydroascorbate reductase, dehydroascorbate reductase, and ascorbate peroxidase) and increasing the contents of antioxidants (AsA and GSH) and the ratio of GSH/(GSH + oxidized glutathione) and AsA/(AsA + dehydroascorbate) under both non-HS and HS. Also, the reactive oxygen species (ROS)-scavenger system (catalase, guaiacol peroxidase, carotenoid, total phenols, and flavonoids) and MG-scavenger system (glyoxalase I and glyoxalas II) also were up-regulated in maize seedlings pretreated with MG under non-HS and HS. This work for the first time reported that MG could trigger the heat tolerance of maize seedlings by driving the AsA-GSH cycle and ROS-/MG-scavenging system.