Photochemical changes and oxidative damage in the aquatic macrophyte Cymodocea nodosa exposed to paraquat-induced oxidative stress.

The non-selective herbicide paraquat (Pq) is being extensively used for broad-spectrum weed control. Through water runoff and due to its high water solubility it contaminates aquatic environments. Thus, the present study was carried out to investigate the photochemical changes and oxidative damage in the aquatic macrophyte Cymodocea nodosa to short- (2h) and long-term (24h) exposure to 2, 20, 200 and 1000μM paraquat (Pq) toxicity by using chlorophyll fluorescence imaging and H2O2 real-time imaging. The effective quantum yield of PSII (ΦPSII) show a tendency to increase at 2μM Pq after 2h exposure, and increased significantly at 20 and 200μM Pq. Τhe maximum oxidative effect on C. nodosa leaves was observed 2h after exposure to 200μM Pq concentration when the highest increases of ΦPSII due to high electron transport rate (ETR) resulted in a significant increase of H2O2 production due to the lowest non-photochemical quenching (NPQ) that was not efficient to serve as a protective mechanism, resulting in photooxidation. Prolonged exposure (24h) to 200μM Pq resulted in a decreased ΦPSII not due to an increase of the photoprotective mechanism NPQ, but due to high quantum yield of non-regulated energy loss in PSII (ΦNO), resulting to the lowest fraction of open PSII reaction centers (qp). This decreased ΦPSII has resulted to less Pq radicals to be formed, with a consequence of a small increase of H2O2 production compared to control C. nodosa leaves, but substantial lower than that of 2h exposure to 200μM Pq. Exposure of C. nodosa leaves to 1000μM Pq toxicity had lower effects on the efficiency of photochemical reactions of photosynthesis under both short- (2h) and long-term (24h) exposure than 200μM Pq. This was evident by an almost unchanged ΦPSII and qp, that remained unchanged even at a longer exposure time (48h), compared to control C. nodosa leaves. Thus, the response of C. nodosa leaves to Pq toxicity fits the "Threshold for Tolerance Model", with a threshold concentration of 200μM Pq required for initiation of a tolerance mechanism, by increasing H2O2 production for the induction of genes encoding protective processes in response to Pq-induced oxidative stress. Overall, it is concluded that chlorophyll fluorescence imaging constitutes a promising basis for investigating herbicide mode of action in aquatic plants and for detecting their protective mechanisms.