Why Do Apples Turn Brown When Cut?

The familiar brown discoloration of cut apples—often called "enzymatic browning"—is one of the most studied post-harvest reactions in fruits, driven by three key components: an enzyme called polyphenol oxidase (PPO), naturally occurring plant compounds called polyphenols, and molecular oxygen from the air. Apple Browning Illustration 1

According to a landmark review by Nicolas et al. (1994) in Trends in Food Science & Technology, enzymatic browning is defined as "the PPO-catalyzed oxidation of phenolic compounds to quinones, which then undergo non-enzymatic polymerization to form brown, red, or black pigments called melanins." This process is not unique to apples—it occurs in bananas, potatoes, and avocados too—but apples are a model system due to their high PPO and polyphenol content.

To break down the chemistry: PPO acts as a biological catalyst, speeding up the oxidation (electron loss) of polyphenols—specifically o-diphenols, which have two hydroxyl groups attached to adjacent carbon atoms on a benzene ring. The first step converts o-diphenols to o-quinones, a highly reactive class of molecules. Apple Browning Illustration 2

Quinones are unstable and quickly undergo non-enzymatic polymerization, linking together into long chains of molecules called melanins. As noted in Owen R. Fennema’s Food Chemistry (1996), a foundational textbook, melanins are large, insoluble polymers with conjugated double bonds that absorb blue-green light—this is why they appear brown to the human eye. Crucially, the reaction only proceeds if all three components (PPO, polyphenols, oxygen) are present; remove any one, and browning stops.

So why does an apple only turn brown when cut or bruised? The answer lies in cellular compartmentalization—a key feature of plant cell structure that keeps reactive molecules separate. In intact apple cells, PPO is sequestered inside plastids (organelles like chloroplasts or chromoplasts), while polyphenols are stored in the vacuole (a membrane-bound sac acting as the cell’s "storage closet"). Apple Browning Illustration 3

Oxygen is mostly excluded from the cell’s interior. When you cut an apple, you rupture cell membranes and walls, mixing PPO from plastids with polyphenols from the vacuole—while air rushes in to provide oxygen. A classic study by Mathew and Parpia (1971) in Phytochemistry confirmed this: using centrifugation to isolate apple cell organelles, they found 90% of PPO activity in the plastid fraction, with polyphenols concentrated in the vacuole. This separation is nature’s way of preventing premature browning in intact fruits.

Several factors can speed up or slow down enzymatic browning—a fact food scientists have exploited for decades. First, pH: PPO works best at a neutral-to-slightly-acidic pH (around 6 for apples) but denatures (loses function) in highly acidic conditions. This is why lemon juice (pH ~2) stops browning—citric acid lowers the pH below PPO’s optimal range. Apple Browning Illustration 4

Second, temperature: High heat (above 70°C) denatures PPO permanently (why cooked apples stay pale), while cold temperatures (4°C, or fridge temperature) slow its activity by reducing molecular motion. Third, oxygen availability: Wrapping cut apples in plastic or storing them airtight limits oxygen, halting the reaction. A review by Whitaker and Lee (1995) in Critical Reviews in Food Science and Nutrition summarizes these strategies, noting that "inhibiting PPO activity or blocking access to substrates/oxygen is the basis of all commercial anti-browning techniques."

But why do apples have PPO at all? The process isn’t just a nuisance—it serves a critical defense function against pathogens and herbivores. When a plant is wounded (by insects, knives, or fungi), enzymatic browning produces melanins, which are toxic to bacteria, fungi, and insects. Apple Browning Illustration 5

Melanins also form a physical barrier, sealing wounds to prevent further infection. A study by Constabel and Ryan (1995) in Phytochemistry supports this: they found tomato plants with higher PPO activity were more resistant to the bacterial pathogen Pseudomonas syringae, and PPO expression spiked in wounded leaves. For apples, this defense evolved to protect the fruit— the plant’s "seed dispersal package"—from damage during ripening or after falling from the tree.

In short, apple browning is a perfect example of compartmentalized biochemistry gone visible: a defense mechanism that backfires (for us) when we break open the cell’s "safety locks." The next time you squeeze lemon juice on apple slices, you’re not just preventing browning—you’re hijacking a plant’s evolutionary defense system, one enzyme at a time. Apple Browning Illustration 6

References

- Nicolas, J., Richard-Forget, F., Goupy, P., Amiot, M. J., & Aubert, S. (1994). Enzymatic browning and its prevention in fruits and vegetables. Trends in Food Science & Technology, 5(5), 137–143.

- Fennema, O. R. (1996). Food Chemistry (3rd ed.). Marcel Dekker.

- Mathew, S. K., & Parpia, H. A. B. (1971). Subcellular localization of polyphenol oxidase in apple tissue. Phytochemistry, 10(12), 2867–2872.

- Whitaker, J. R., & Lee, C. Y. (1995). Polyphenol oxidase and peroxidase in fruits and vegetables. Critical Reviews in Food Science and Nutrition, 35(2), 143–187.

- Constabel, C. P., & Ryan, C. A. (1995). Polyphenol oxidase in plant defense against pathogens and herbivores. Phytochemistry, 39(3), 485–495.