Dynamic Metabolomic Changes During Superficial Scald Development and 1-MCP Intervention in ‘Dangshansuli’ Pears

TL;DR

This study explores how 1-MCP prevents superficial scald in pears by altering metabolic pathways, reducing damage and improving fruit quality.

Contribution

The study reveals 1-MCP's role in reprogramming pear metabolism to prevent scald through detailed metabolomic analysis.

Findings

1-MCP inhibits ethylene and redirects metabolism away from scald-promoting compounds.

1-MCP promotes synthesis of protective alkaloids and flavonoids, enhancing antioxidant capacity.

Metabolic reprogramming by 1-MCP uncouples pears from oxidative damage pathways.

Abstract

Superficial scald, a postharvest physiological disorder of pears, leads to substantial economic losses. However, the dynamic metabolic shifts that underpin symptom development and the extent of metabolic reorganization triggered by the ethylene inhibitor 1-methylcyclopropene (1-MCP) remain poorly understood. We combined physiological assessments with untargeted metabolomics to track superficial scald development and 1-MCP’s inhibitory effect in ‘Dangshansuli’ pears (Pyrus bretschneideri). In control fruit, disorder progression followed a trajectory of escalating physiological disruption, initiated by an ethylene burst and early oxidative stress, which advanced to membrane lipid peroxidation, glutathione (GSH) depletion, and dysregulated phenolic metabolism. By contrast, 1-MCP fundamentally diverted this trajectory by acting both as an initial ethylene antagonist and a sustained broad-spectrum metabolic regulator. It time-dependently reconfigured secondary metabolism away from the production of scald-promoting compounds (e.g., α-farnesene and phenolic acids) and toward the sustained synthesis of protective alkaloids and flavonoids, thereby enhancing cellular homeostasis and antioxidant capacity. KEGG and correlation network analyses confirmed that 1-MCP uncoupled the metabolic network from oxidative damage. Our findings indicate that 1-MCP is associated with a comprehensive metabolic reprogramming that shifts the fruit away from the scald development trajectory, providing a mechanistic foundation for developing metabolism-targeted strategies to control postharvest losses.

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