Arginase induction by heat treatment contributes to amelioration of chilling injury and activation of antioxidant enzymes in tomato fruit

Treatment of tomato (Solanum lycopersicum L. cv. Messina) fruit with hot air (HA) at 38 °C enhanced the transcript levels of LeARG1 and LeARG2, the two genes encoding arginase, and arginase activity. The strongest induction of LeARG1 and LeARG2 transcripts was observed after fruit treated with 38 °C HA for 12 h, which also effectively alleviated chilling injury (CI) of tomato fruit, manifested as decreased CI index, electrolyte leakage and malondialdehyde content during cold storage. To investigate the potential role of arginase in HA-induced chilling tolerance, fruit were treated with HA, or arginase inhibitor Nω-hydroxy-nor-l-arginine (nor-NOHA) combined with HA and then stored at 2 °C for up to 28 d. The results showed that HA-induced arginase activity was strongly inhibited by pretreatment with nor-NOHA and the reduction of CI by HA was nearly abolished by the arginase inhibitor. In addition, HA treatment increased activities of superoxide dismutase, catalase and ascorbate peroxidase, inhibited peroxidase activities, and promoted the accumulation of arginine, proline and putrescine. These effects were partially counteracted by nor-NOHA except that arginine and putrescine accumulation was unaffected. Our results indicate that arginase induction may be partly involved in HA-induced chilling tolerance in tomato fruit, possibly by a mechanism involving activation of antioxidant enzymes and an increase in proline levels.

► Hot air (HA) treatment induced gene expression and activity of arginase in tomato fruit.
► HA-induced chilling tolerance was almost abolished by an arginase inhibitor nor-NOHA.
► The changes in activities of antioxidant enzymes in HA-treated fruit was diminished by nor-NOHA.
► Inhibition of arginase activity by nor-NOHA reduced HA-induced proline accumulation.
► Arginase induction is involved in HA-induced chilling tolerance in tomato fruit.