Anti-browning action of melatonin is dependent on the type of tissue in minimally processed sweet potatoes

•Application of melatonin in sweet potatoes promotes increased levels of antioxidant.•Application of melatonin in sweet potatoes reduces damage to the cell membrane.•Application of melatonin in sweet potato contributes to cellular redox homeostasis.•Exogenous application of melatonia in sweet potato increases its bioactive compound. This study explored the impact of exogenous melatonin on oxidative damage, protective mechanisms against oxidation, and reactions leading to browning, as well as the accumulation of antioxidants in minimally processed white-fleshed and orange sweet potato roots. Sweet potato roots with white and orange pulp were subjected to minimal processing and immersion in melatonin solutions at concentrations of 0, 10, 100, and 1000 µmol L−1. Following packaging, these were stored at 5 ± 2 °C for 20 days. Results indicate that increasing melatonin concentrations significantly reduced browning symptoms in both white and orange sweet potato slices. This reduction was associated with decreased levels of hydrogen peroxide (H2O2), thiobarbituric acid-reactive substances (TBARs), and electrolyte leakage, indicating reduced cell membrane damage. Enhanced protection was observed through increased activity of antioxidant enzymes superoxide dismutase, catalase, and ascorbate peroxidase and higher levels of antioxidant metabolites, including vitamin C and phenolic compounds, as confirmed by in vitro assays for antioxidant capacity (FRAP and DPPH), however, the levels of total carotenoids, anthocyanins, and yellow flavonoids did not show a significant difference between the melatonin treatments. Notably, sweet potato slices treated with higher melatonin doses of 100 and 1000 µmol L−1 exhibited reduced phenylalanine ammonia-lyase activity and phenolic compound accumulation. This effect, coupled with lower polyphenol oxidase (PPO) and peroxidase (POD) activities, likely contributed to prolonged preservation quality by maintaining cellular redox homeostasis.