Physiological and structural changes in cells of Synechocystis aquatilis f. aquatilis acclimated to grow in the presence of high zinc levels (2.20–3.30 mg·L−1) were investigated. Growth of these cells showed a decreased specific growth rate and final yield of about 60% and 50%, respectively, of the values found for cells grown in the presence of 0.21 mg zinc·L−1 (control culture). The higher the zinc concentration in the culture medium, the more pronounced the reduction in the chl a content. Regardless of zinc concentration, S. aquatilis possessed three distinct carotenoids. A decrease in carotenoid content accompanied the decrease of chl a, and the proportions of the pigments to each other were not affected by zinc. The photosynthetic performance of cells cultured in the presence of high zinc levels showed a decline in both the apparent photosynthetic efficiency and the photosynthetic maximal rate. In these cells the PSII reaction centers became partially closed, and the electron transport activity around PSII and PSI was reduced to 61% and 38% of the control values, respectively, which may indicate an altered PSII/PSI stoichiometry. In addition, electron micrographs revealed a reduced amount of thylakoid membranes, indicating that acclimation to high zinc levels led to a decrease in the overall number of photosynthetic units. On the other hand, light microscopic observation of negative‐stained cells revealed the presence of a thick mucilaginous layer surrounding the high zinc‐acclimated cells. This extracellular material could retain high amounts of metal ions from the medium, thus providing the Synechocystis cells a mechanism to circumvent toxic levels of zinc.

Zinc toxicity on photosynthetic activity in cells of Synechocystis aquatilis f. aquatilis Sauvageau was investigated by monitoring Hill activity and fluorescence. The oxygen-evolving activity decreased to about 80% of the initial value after exposure to 0.1 mM ZnSO 4 for 1 h. The PSII activity was inhibited by 40% in the presence of zinc concentrations ranging from 0.5 to 5.0 mM, suggesting that the metal effect is limited by zinc uptake. The fluorescence capacity (F max -F/F max ) decreased from 0.57 to 0.35 and 0.20 in Zn-treated cells for 15 and 60 min, respectively, thus providing evidence for rapid inactivation of electron transport at PSII. Zinc treatment promoted a rapid increase in PSII fluorescence that was counteracted by addition of 1,4-benzoquinone, indicating that electron transfer at the reducing side of the PSII reaction center is arrested by zinc. Furthermore, a decline in the fluorescence yield could be observed after 1 h of zinc treatment as well as when Zn-treated cells were excited in presence of 3-(3 0 ,4 0 -dichlorophenyl)-1,1-dimethylurea. Under these conditions, zinc did not affect energy transfer from phycobilisomes to PSII, and the gradual quenching of PSII fluorescence may be due to a decrease in electron flow on the donor side of PSII. However, the 20% increase in the minimal fluorescence intensity (F o ) in parallel to the absence of changes in the maximal fluorescence intensity (F max ), observed in the first hour of zinc treatment, could also suggest a metal-induced decline in the energy transfer from PSII-chl a antenna to the PSII reaction center.

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