<p>Enzymatic browning affects the quality of fresh-cut products. This study aimed to evaluate the inhibitory effect of β-sitosterol on enzymatic browning in fresh-cut potatoes using physiological, biochemical, and molecular approaches. Pre-cutting β-sitosterol treatment at 10 mg L<sup>− 1</sup> enhanced the overall visual quality and alleviated browning. β-sitosterol treatment reduced polyphenol oxidase (PPO) activity and downregulated the relative expression levels (Rel) of <i>StPOT32</i> and <i>StPOT33</i>. Additionally, β-sitosterol treatment decreased tyrosine content and the Rel of <i>StCM1</i> and <i>StCM2</i>. β-sitosterol treatment enhanced DPPH radical scavenging rate while reducing the accumulation of H<sub>2</sub>O<sub>2</sub>, O<sub>2</sub><sup>•−</sup>, and malondialdehyde (MDA). β-sitosterol treatment also improved the enzyme activities of succinate dehydrogenase (SDH) and cytochrome c oxidase (CCO), indicating enhanced mitochondrial function. Furthermore, β-sitosterol treatment improved the activities and gene expression of superoxide dismutase (SOD), catalase (CAT), and ascorbate peroxidase (APX). Combined with correlation analysis, our results indicated that β-sitosterol treatment inhibited browning by suppression of phenolic substrate oxidation and ROS accumulation, as well as modulation of mitochondrial function. Importantly, compared with the control, β-sitosterol treatment extended the shelf life of fresh-cut potatoes from 1 d to 5 d, significantly enhancing its commercial acceptability.</p>

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Anti-browning effects of β-sitosterol in fresh-cut potatoes through modulation of PPO activity, ROS metabolism, and mitochondrial function

  • Zan Meng,
  • Qingguo Wang,
  • Yanyan Feng

摘要

Enzymatic browning affects the quality of fresh-cut products. This study aimed to evaluate the inhibitory effect of β-sitosterol on enzymatic browning in fresh-cut potatoes using physiological, biochemical, and molecular approaches. Pre-cutting β-sitosterol treatment at 10 mg L− 1 enhanced the overall visual quality and alleviated browning. β-sitosterol treatment reduced polyphenol oxidase (PPO) activity and downregulated the relative expression levels (Rel) of StPOT32 and StPOT33. Additionally, β-sitosterol treatment decreased tyrosine content and the Rel of StCM1 and StCM2. β-sitosterol treatment enhanced DPPH radical scavenging rate while reducing the accumulation of H2O2, O2•−, and malondialdehyde (MDA). β-sitosterol treatment also improved the enzyme activities of succinate dehydrogenase (SDH) and cytochrome c oxidase (CCO), indicating enhanced mitochondrial function. Furthermore, β-sitosterol treatment improved the activities and gene expression of superoxide dismutase (SOD), catalase (CAT), and ascorbate peroxidase (APX). Combined with correlation analysis, our results indicated that β-sitosterol treatment inhibited browning by suppression of phenolic substrate oxidation and ROS accumulation, as well as modulation of mitochondrial function. Importantly, compared with the control, β-sitosterol treatment extended the shelf life of fresh-cut potatoes from 1 d to 5 d, significantly enhancing its commercial acceptability.