Organisms that perform oxygenic photosynthesis are subjected to inhibition of their photosynthetic functions when they are exposed to excessive illumination. Photoinhibition occurs mainly at the level of photosystem II, where a cyclic electron transport has often been proposed to be involved in photoprotection. However, a demonstration of direct protection by cyclic photosystem II against photoinhibitory damage has been lacking. In this report, we used the newly characterized compound 4-[methoxybis(trifluoromethyl)methyl]-2,6-dinitrophenylhydrazine methyl ketone (K-15), known to stimulate cyclic electron transport between the acceptor and donor sides of the photosystem [Klimov, V. V., Zharmukhamedov, S. K., Allakhverdiev, S. I., Kolobanova, L. P., & Baskakov, Y. A. (1993) Biol. Membr. 6, 715-732], to verify if photosystem II is significantly protected by cyclic electron transport against aerobic and anaerobic photoinhibitory damage. The photoinhibitory quenching of the maximal level of fluorescence and the decrease of the absorbance change at 685 nm related to pheophytin photoreduction observed during photoinhibitory illumination of untreated or Mn-depleted photosystem II submembrane fractions are significantly attenuated in the presence of K-15. The photodegradation of cytochrome b559 and the photobleaching of beta-carotene and chlorophyll-670 measured in Mn-depleted photosystem II preparations are also strongly retarded when K-15 is present. The detection, by photoacoustic spectroscopy, of the energy stored during the cyclic electron transport is also reported in Mn-depleted photosystem II submembrane fractions and in photosystem II reaction center complexes. This reaction is also gradually photoinhibited due to the progressive photodegradation of the required electron transport intermediates but is significantly more stable in the presence of K-15. It is deduced that cyclic electron transport around photosystem II constitutes an effective protective mechanism against photoinhibitory damage.