Abstract
Potato tubers are highly prone to postharvest quality deterioration due to enzymatic browning associated with physical injuries, which cause substantial economic losses and reduce marketability. This research investigated physiological and biochemical aspects, and postharvest management of blackspot and pressure bruise development and associated tissue browning in russet-type potato cultivars.,Postharvest management mitigation strategies included using 1-methylcyclopropene (1-MCP), nitric oxide (NO), and diphenylamine (DPA). The objectives were to (1) evaluate the progression of enzymatic browning and biochemical changes during long-term storage, (2) assess the efficacy of NO and 1-MCP in mitigating blackspot-induced browning, and (3) determine the effectiveness of NO, 1-MCP, and DPA in controlling pressure bruise-associated browning and enzyme activities.Chapter 1 of the thesis is a general introduction on postharvest browning in potatoes, its physiological and biochemical mechanisms, the impact of physical injuries such as pressure bruising and blackspot bruising, cultivar-specific susceptibility, and strategies including chemical treatments (NO, 1-MCP, and DPA) to mitigate browning and preserve tuber quality.
Chapter 2 addresses objective 1, presenting results from research conducted at the beginning and end of storage to evaluate the storage duration effect on the enzymatic browning susceptibility of four russet-type potato cultivars. Raw differences between the one- and six-month sampling periods were calculated to assess changes in biochemical and physiological parameters during storage. Enzymatic browning measured through ΔL increased over six months of storage (7.2°C and 95% RH) with Russet Burbank with ΔL 7.17 and Ranger Russet with ΔL 6.48 showed the highest susceptibility to enzymatic browning and Clearwater Russet the least with ΔL 4.82. Browning correlated positively with PPO activity (r=0.8), TPC (r=0.6), and amino acid precursors (r=0.8), and negatively with ascorbic acid content (r=-0.3).
Chapter 3 focuses on objective 2, aimed at assessing the effectiveness of NO and 1-1-MCP in controlling black spot enzymatic browning due to mechanical damage in Clearwater Russet, Russet Burbank, and Russet Norkotah cultivars. Tubers were treated with NO (98 ppm; 5 h), and 1-MCP (0.139 ppm; 24 h), in addition to the untreated control. Then tubers were mechanically injured to induce bruise and then held for 24 h at 23°C and 65% relative humidity to allow browning symptoms to develop. Enzymatic browning was evaluated based on a visual score (1-4), lightness (L*) of bruised surface after peeling, PPO activity, total phenolic content, phenolic profile, content of phenylalanine, tryptophan, tyrosine, and ascorbic acid. NO and 1-MCP treatments significantly reduced blackspot enzymatic browning score to 1.10 in 1-MCP and 1.31 in NO as compared to untreated controls 1.80. Treated tubers maintained higher L* values 70.47 in 1-MCP and 69.35 in NO. This study provided novel approaches to minimize bruise-associated discoloration in potatoes with the potential to reduce postharvest losses and enhance the marketable value of fresh potatoes.
Chapter 4 of the thesis addresses objective 3, to investigate the effectiveness of 1-MCP, NO, and DPA applications to reduce pressure flattened areas from cutting black development during simulated bulk storage. Russet Burbank potatoes were stored under two pressure conditions: a control (no pile pressure) and a constant downward force of 1,200 kg/m² (1,391 kg total), corresponding to a 1.8 m pile height. Curing occurred at 12.8 °C and 95% relative humidity (RH) for 14 days, followed by gradual cooling (0.3 °C day⁻¹) to 7.2 °C and subsequent storage for seven months. Treatments with 1-MCP (0.270 µL L⁻¹; 24 h) and NO (64 ppm; 5 h) were applied two weeks before unloading, while DPA (2.0 mL L⁻¹; dip for 1 min) was applied immediately after unloading. Tubers stored under pile pressure developed a significantly larger lesion area (7.66%) compared to the control (0.07%), Interestingly, weight loss was lower in tubers stored under pile pressure (2.7%) than without pile pressure (7.9%), possibly due to reduced transpiration under compression. Despite clear external flattening symptoms, no visible internal discoloration (cutting black) was detected within six days of unloading. This absence of discoloration corresponded to the lack of significant differences in electrolyte leakage and respiration rate between pressure and control treatments. However, activities of PPO and peroxidase (POD) were reduced by NO and DPA treatment compared to control treatments. Bruised area showed positive correlation with pressure bruise severity score (r=0.71), while lightness (L*) was negatively correlated with bruise severity (r=-0.6) and PPO activity (r=-0.45). PPO (r=0.57) and POD (r=0.31) activities exhibited positive correlations with electrolyte leakage, underscoring the role of membrane integrity loss in enabling enzymatic oxidation of phenolics. Although 1-MCP, NO, and DPA treatments showed some reduction in some enzymatic browning factors, further research is necessary to confirm the efficacy of these treatments under semi-commercial scale.
Together, the three chapters highlight the storage and cultivar-dependent nature of enzymatic browning susceptibility, the effectiveness of treatments in preventing discoloration and antioxidant compounds, and the complex interactions between mechanical stress, enzyme activity, and tissue physiology. Future research should focus on optimizing these treatment applications, such as timing and concentrations, and integrating non-destructive imaging and molecular tools to better predict and control bruise-associated browning in potatoes.