Cyclic electron flow (CEF) around photosystem I has a role in avoiding photoinhibition of photosystem II (PSII), which occurs under conditions in which the rate of photodamage to PSII exceeds the rate of its repair. However, the molecular mechanism underlying how CEF contributes to photoprotection is not yet well understood. We examined the effect of impairment of CEF and thermal energy dissipation (qE) on photoinhibition using CEF (pgr5) and qE (npq1 and npq4) mutants of Arabidopsis (Arabidopsis thaliana) exposed to strong light. Impairment of CEF by mutation of pgr5 suppressed qE and accelerated photoinhibition. We found that impairment of qE, by mutations of pgr5, npq1, and npq4, caused inhibition of the repair of photodamaged PSII at the step of the de novo synthesis of the D1 protein. In the presence of the chloroplast protein synthesis inhibitor chloramphenicol, impairment of CEF, but not impairment of qE, accelerated photoinhibition, and a similar effect was obtained when leaves were infiltrated with the protonophore nigericin. These results suggest that CEF-dependent generation of DeltapH across the thylakoid membrane helps to alleviate photoinhibition by at least two different photoprotection mechanisms: one is linked to qE generation and prevents the inhibition of the repair of photodamaged PSII at the step of protein synthesis, and the other is independent of qE and suppresses photodamage to PSII.