Effects of SNP and cPTIO on oxidative membrane damage and pericarp browning of harvested longan fruits

Abstract

Nitric oxide (NO) induces the production of other reactive nitrogen species (RNS), progressive cellular damage and associated disorders due to oxidative stress. Here, we investigated the effects of sodium nitroprusside (SNP; NO donor) or 2-(4- carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (cPTIO; NO scavenger) on reactive oxygen species (ROS) contents, oxidative membrane damage and pericarp browning of longan during storage. Longan fruits were dipped in distilled water (control), SNP (50 and 100 mM) or cPTIO (100 and 500 μM) for 10 min, then stored at 25±1°C for 7 days. SNP-treated fruit exhibited higher ROS contents (superoxide radical, hydrogen peroxide and hydroxyl radical), oxidative membrane damage (malondialdehyde, protein carbonyl and electrolyte leakage) as well as pericarp browning (browning index and polyphenol oxidase activity), compared with control fruits. In contrast, exposure to cPTIO attenuated ROS content, oxidative membrane damage and pericarp browning of longan pericarp during storage. The severity of pericarp browning, ROS production and oxidative damage depend on SNP or cPTIO concentrations. These findings suggest that NO might be involved in oxidative stress which contributes to pericarp browning in harvested longan by alteration of the balance between ROS generation and scavenging.