Delay of Postharvest Browning in Litchi Fruit by Melatonin via the Enhancing of Antioxidative Processes and Oxidation Repair
文献类型: 外文期刊
第一作者: Zhang, Yueying
作者: Zhang, Yueying;Xu, Xiangbin;Zhang, Zhengke;Huber, Donald J.;Hu, Meijiao;Gao, Zhaoyin;Jiang, Guoxiang;Jiang, Yueming
作者机构:
关键词: litchi fruit; browning; melatonin treatment; antioxidation; Msrs expression
期刊名称:JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY ( 影响因子:5.279; 五年影响因子:5.269 )
ISSN: 0021-8561
年卷期: 2018 年 66 卷 28 期
页码:
收录情况: SCI
摘要: Melatonin acts as a crucial signaling and antioxidant molecule with multiple physiological functions in organisms. To explore effects of exogenous melatonin on postharvest browning and its possible mechanisms in litchi fruit, 'Ziniangxi' litchi fruits were treated with an aqueous solution of melatonin at 0.4 mM and then stored at 25 degrees C for 8 days. The results revealed that melatonin strongly suppressed pericarp browning and delayed discoloration during storage. Melatonin treatment reduced relative membrane-leakage rate and inhibited the generation of superoxide radicals (O-2(-center dot)), hydrogen peroxide (H2O2), and malondialdehyde (MDA). Melatonin treatment markedly promoted the accumulation of endogenous melatonin; delayed loss of total phenolics, flavonoids, and anthocyanins; and enhanced the activities of antioxidant enzymes, including superoxide dismutase (SOD, EC 1.15.1.1), catalase (CAT, EC 1.11.1.6), ascorbate peroxidase (APX, EC 1.11.1.11), and glutathione reductase (GR, EC 1.6.4.2). By contrast, the activities of browning-related enzymes including polyphenoloxidase (PPO, EC 1.10.3.1) and peroxidase (POD, EC 1.11.1.7) were reduced. In addition, melatonin treatment up-regulated the expression of four genes encoding enzymes for repair of oxidized proteins, including LcMsrA1, LcMsrA2, LcMsrB1, and LcMsB2. These findings indicate that the delay of pericarp browning and senescence by melatonin in harvested litchi fruit could be attributed to the maintenance of redox homeostasis by the improvement of the antioxidant capacity and modulation of the repair of oxidatively damaged proteins.
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