**Background:** Polyphenol oxidase (PPO) is a copper-containing phenolase discovered in most animals, plants, and microorganisms. In plants, PPO is encoded by multiple nuclear genes, with the largest number (26 members) found in Salvia miltiorrhiza. PPO catalyzes two key reactions: hydroxylation of monophenols to o-diphenols and oxidation of o-diphenols to o-quinones, which further polymerize to form brown pigments. While enzymatic browning causes significant economic losses (approximately 50% of fruit and vegetable losses during processing), PPO also plays beneficial roles in plant defense and metabolite synthesis. This review aims to provide a comprehensive summary of recent advances in understanding plant PPOs.
**Methods:** The authors conducted a narrative review of classic and recent literature on plant PPOs, covering distribution, functional domains, optimal conditions (pH and temperature), substrate specificity, molecular weight, activation mechanisms, enzymatic browning, physiological functions, and gene regulation. Data were compiled from published studies on diverse plant species including tomato, potato, sweet potato, apple, tea, apricot, blueberry, and others.
**Key Results:** PPO contains three domains: an N-terminal plastid transit signal peptide, a highly conserved type-III copper center (with CuA and CuB bound to 6-7 histidine residues), and a C-terminal region that shields the active site. Optimal pH ranges from 4.0 to 7.0 depending on species and substrate, with most PPOs showing peak activity between pH 5.0-8.0. Optimal temperatures range from 15-50°C, with tropical plants like African bush mango showing higher optima (50°C) compared to cold-resistant species like lily (15°C). Molecular weights range from 21 kDa (kudzu) to 85 kDa (tea leaf PPO1). PPO exists in both latent (inactive) and active states; activation occurs via C-terminal cleavage by proteases. Substrate specificity favors diphenols and triphenols over monophenols, with catechol being the most commonly used substrate. PPO contributes to plant defense against pathogens (e.g., Pseudomonas syringae, Alternaria solani) and herbivores (e.g., Helicoverpa armigera, Spodoptera exigua) through protein alkylation, quinone toxicity, and melanin barrier formation. PPO also responds to abiotic stresses including drought, salt, heavy metals, and UV light. Gene regulation involves miRNAs (e.g., MIR1444 in Populus trichocarpa, smi-MIR12112 in Salvia miltiorrhiza) and transcription factors (e.g., CsMYB59 in Camellia sinensis, MnMYB3R1 in Morus notabilis).
**Clinical Implications:** While this review focuses on plant biology rather than clinical medicine, the findings have indirect implications for human health through food quality and nutrition. Understanding PPO-mediated browning can improve postharvest preservation of fruits and vegetables, reducing food waste and maintaining nutritional value. Natural inhibitors of PPO (e.g., flavonoids, curcumin, quercetin, strigolactone) offer safer alternatives to sulfites for browning control. Additionally, PPO's role in plant defense mechanisms may inform development of stress-resistant crops with enhanced nutritional profiles. The review notes that browning causes approximately 50% of fruit and vegetable losses during processing, highlighting the economic and nutritional significance of PPO research.