Growth, ROS accumulation site, and photosynthesis inhibition mechanism of Chlorella vulgaris by triclosan.

Although the addition of triclosan (TCS) in consumer products has been strictly restricted, its continuous applications in hospitals and other medical facilities and its numerous residues still pose a potential risk to aquatic organisms and aquatic ecosystems. In this study, we investigated the growth, biochemical alterations, and physiological responses of Chlorella vulgaris exposed to different concentrations of TCS. The potential toxicity mechanisms associated with excessive production of reactive oxygen species (ROS) and disruption of photosynthetic system II (PSII) were also analyzed. The results indicated that the growth, cellular ultrastructure, and physiology of C. vulgaris were severely affected by TCS in a dose-effect dependent manner. TCS inhibited the growth of C. vulgaris, leading to mitochondria enlargement, the disordering of the arrangement of thylakoids, cell wall rupture, organelles loss, and the cytoplasm lysis. TCS induced severe oxidative damage characterized by ROS accumulation, elevated malondialdehyde (MDA), and up-regulation of antioxidant enzyme activities. Moreover, in TCS-induced algal cells, the main sites of ROS accumulation were chloroplasts, mitochondria, and cell membranes, with ROS accumulating most in the mitochondria. In addition, TCS caused damage to the reaction center (RC inactivation), donor side (OEC damage), and accepted side (electron transport from Q to Q) of PSII in C. vulgaris, leading to inhibition of photosynthetic activity. These results could provide novel insights into the mechanisms of TCS-induced ROS accumulation and photosynthetic inhibition in C. vulgaris, which would contribute to a deep understanding of TCS toxicity on algae.