Glucosinolate Metabolism During Postharvest Storage of Broccoli Heads Treated with Ethylene, Cytokinins and 1-MCP

Broccoli (Brassica oleracea L. var. Italica) is a rich source of glucosinolates, bioactive compounds whose levels are markedly affected by postharvest senescence. The present study evaluated the effects of hormonal regulators associated with senescence—cytokinins, ethylene, and the ethylene-action inhibitor 1-methylcyclopropene (1-MCP)—on glucosinolate metabolism during postharvest storage of broccoli heads. Broccoli heads were treated with 6-benzylaminopurine (BAP), ethephon, or 1-MCP and stored at 20 °C for five days in darkness. Senescence progression was evaluated through superficial color and chlorophyll content. Glucosinolate pattern and gene expression involved in glucosinolate biosynthesis and degradation was also analyzed. Postharvest storage induced rapid yellowing, chlorophyll loss, and a general decline in glucosinolate content in control samples. BAP and 1-MCP treatments significantly delayed senescence, preserved chlorophyll levels, and reduced glucosinolate losses, particularly for indolic glucosinolates such as glucobrassicin and neoglucobrassicin. In the case of BAP-treated samples, glucobrassicin and neoglucobrassicin contents were 117% and 93% higher, respectively, compared to the controls on day 5. In the case of 1-MCP-treated samples, greater differences were detected on day 3, with glucobrassicin and neoglucobrassicin levels 69% and 66% higher, respectively. In contrast, ethephon accelerated senescence and promoted a more pronounced decrease in both aliphatic and indolic glucosinolates. Gene expression analyses showed a general downregulation of aliphatic glucosinolate biosynthetic genes during storage, whereas indolic pathway genes exhibited hormone-dependent responses. Overall, the results indicate that senescence-associated hormonal regulation plays a central role in glucosinolate metabolism during broccoli postharvest storage, and that BAP and 1-MCP treatments are effective strategies to maintain nutritional quality by delaying senescence and glucosinolate degradation.