The effect of chloramphenicol, an often used protein synthesis inhibitor, in photosynthetic systems was studied on the rate of Photosystem II (PSII) photodamage in the cyanobacterium Synechocystis PCC 6803. Light-induced loss of PSII activity was compared in the presence of chloramphenicol and another protein synthesis inhibitor, lincomycin, by measuring the rate of oxygen evolution in Synechocystis 6803 cells. Our data show that the rate of PSII photodamage was significantly enhanced by chloramphenicol, at the usually applied 200 μg mL⁻¹ concentration, relative to that obtained in the presence of lincomycin. Chloramphenicol-induced enhancement of photodamage has been observed earlier in isolated PSII membrane particles, and has been assigned to the damaging effect of chloramphenicol-mediated superoxide production (Rehman et al. 2016, Front Plant Sci 7:479). This effect points to the involvement of superoxide as damaging agent in the presence of chloramphenicol also in Synechocystis cells. The chloramphenicol-induced enhancement of photodamage was observed not only in wild-type Synechocystis 6803, which contains both Photosystem I (PSI) and PSII, but also in a PSI-less mutant which contains only PSII. Importantly, the rate of PSII photodamage was also enhanced by the absence of PSI when compared to that in the wild-type strain under all conditions studied here, i.e., without addition and in the presence of protein synthesis inhibitors. We conclude that chloramphenicol enhances photodamage mostly by its interaction with PSII, leading probably to superoxide production. The presence of PSI is also an important regulatory factor of PSII photodamage most likely via decreasing excitation pressure on PSII.

氯霉素，经常使用的蛋白质合成抑制剂，在光合系统的影响进行了研究光系统上系统II（PSII）光损伤在蓝藻的速率集胞藻PCC 6803的光诱导的PSII活性的丧失在氯霉素和另一个的存在下进行了比较蛋白合成抑制剂林可霉素，通过测量拟藻囊藻6803细胞中的氧气释放速率来实现。我们的数据显示，在通常使用200μgmL ^{-1的条件下}，氯霉素显着提高了PSII的光损伤率。相对于林可霉素存在时的浓度。氯霉素诱导的光损伤增强在分离的PSII膜颗粒中得到了较早的观察，并被归因于氯霉素介导的超氧化物产生的破坏作用（Rehman等人2016，Front Plant Sci 7：479）。这种作用表明在球囊藻细胞中也存在氯霉素时，超氧化物作为破坏剂。不仅在野生型突囊藻中观察到氯霉素诱导的光损伤增强6803，既包含Photosystem I（PSI）和PSII，又包含无PSI的突变体，仅包含PSII。重要的是，在此处研究的所有条件下（即不添加蛋白质且存在蛋白质合成抑制剂的情况下），与野生型菌株相比，由于不存在PSI，PSII光损伤的速率也得以提高。我们得出的结论是，氯霉素主要通过与PSII的相互作用来增强光害，可能导致超氧化物的产生。PSI的存在也是PSII光损伤的重要调节因素，很可能是通过降低PSII的激发压力来实现的。