Plants deficient in the IMMUTANS gene that encodes the oxidase are especially susceptible to photooxidative stress during early plastid development. The knockout plants exhibit a phenotype of variegated leaves with white patches that indicate a lack of pigmentation or photodamage. This effect is enhanced with increased light and temperature during plant development. The lack of plastid terminal oxidase indirectly causes photodamage during plastid development because protective carotenoids are not synthesized without the oxidase.
The enzyme is also thought to act as a safety valve for stress conditions in the photosynthetic apparatus. By providing an electron sink when the plastoquinone pool is over-reduced, the oxidase is thought to protect photosystem II from oxidative damage. Knockouts for Rubisco and photosystem II complexes, which would experience more photodamage than normal, exhibit an upregulation of plastid terminal oxidase. This effect is not universal because it requires plants to have additional PTOX regulation mechanisms. While many studies agree with the stress-protective role of the enzyme, one study showed that overexpression of PTOX increases the production of reactive oxygen species and causes more photodamage than normal. This finding suggests that an efficient antioxidant system is required for the oxidase to function as a safety valve for stress conditions and that it is more important during chloroplast biogenesis than in the regular functioning of the chloroplast.