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The oxygen-evolving complex (OEC) of Zostera marina is prone to deactivation under visible light, which results in a formation of the long-lived radical P680+. The mechanism to prevent damage caused by P680+ remains unclear. In this study, following light exposure, the upregulation in ascorbate (AsA) content and the presence of PSII cyclic electron flow (PSII-CEF) provide evidence that AsA and PSII-CEF donate electrons to PSII. Furthermore, a factorial design experiment with different combinations of inhibition of AsA and PSII-CEF demonstrates that both inhibition treatments lead to decreases in maximal photochemical yield of PSII, increases in relative variable fluorescence at the K-step, as well as the net loss of PSII reaction center proteins and further degradation of OEC peripheral proteins. These results suggest that AsA and PSII-CEF play photoprotective roles by providing electrons to efficiently prevent damage to PSII from the highly oxidizing radical P680+ in Z. marina.