Disturbance of photosystem II-oxygen evolution complex induced the oxidative damage in Chlorella vulgaris under the stress of cetyltrimethylammonium chloride.

Oxygen evolution complex (OEC) in photosystem II (PSII) is sensitive to environmental stressors. However, oxidative damage mechanism in PSII-OEC is still unclear. Here, we investigated photosynthetic performance of PSII, oxidative stress and antioxidant reaction induced by reactive oxygen species (ROS) in a unicellular green alga Chlorella vulgaris (C. vulgaris) under the stress of cetyltrimethylammonium chloride (CTAC). From the changes of chlorophyll fluorescence parameters and PSII activity, it was proved that the electron transport, which occurred initially at the electron donor side of OEC, was disturbed by CTAC. Moreover, a significant decrease of the oxygen evolution rate in OEC (40.95%) while an increase of ROS (50.50%) was obtained after the exposure to 0.6 mg/L CTAC compared to the control (without CTAC), confirming that more oxygen transferred to ROS under the stress. Furthermore, the increased ROS in chloroplast and the structural destruction in thylakoid membrane were observed, respectively. These results proved that oxidative damage mechanism in PSII-OEC is mainly through the reduction of oxygen evolution and the production of excessive ROS, thus leading to the destruction of OEC performance and chloroplast structure.

Alleviating CTAC and Flu combined pollution damage in Chlorella vulgaris by exogenous nitric oxide.

This study investigates the effect of sodium nitroprussiate (SNP), an exogenous NO-donor, on the joint toxicity of binary mixtures of cetyltrimethylammonium chloride (CTAC) and fluoranthene (Flu) (CTAC/Flu), which are representatives for surfactants and polycyclic aromatic hydrocarbons (PAHs) respectively, in a unicellular green alga Chlorella vulgaris (C. vulgaris). The results showed that the addition of low SNP (20µM) alleviated the CTAC/Flu combined pollution damage in C. vulgaris. Supplement of low SNP significantly increased the algae biomass, chlorophyll content, soluble protein content and the activities of superoxide dismutase (SOD), peroxidase (POD) and catalase (CAT) as compared to CTAC/Flu treatment alone. SNP also reduced the content of malondialdehyde (MDA) and the reactive oxygen species (ROS), as compared with CTAC/Flu treated alone. On the contrary, the above phenomena were reversed when high concentration of SNP (100µM) was added. Our study indicated that the damage of the joint action of surfactants and PAHs on hydrobios can be alleviated through protecting against oxidant substances and increasing the activity of antioxidant enzymes with an exogenous supply of NO in certain concentration range.

Subcellular distribution of fluoranthene in Chlorella vulgaris with the presence of cetyltrimethylammonium chloride.

This study explored the possible mechanism of the joint toxicity of binary mixtures of cetyltrimethylammonium chloride (CTAC) and fluoranthene (Flu) to the green alga Chlorella vulgaris by examining the subcellular distribution of Flu within the alga. The joint action of CTAC (100 µg L(-1)) and Flu (0-200 µg L(-1)) on the algae changed from a synergetic effect (0-50 µg L(-1)) to an antagonistic effect (50-200 µg L(-1)) with an increase of the Flu concentration. The Flu uptake was enhanced by the presence of CTAC through the intracellular detection of Flu. Furthermore, the highest amount of Flu bound to the cytosol, whereas the least amount bound to the cellular debris when synergistic effect was observed at 2.5 µg L(-1) Flu. However, the highest amount of Flu bound to the cellular debris, whereas the least amount bound to the organelles when antagonistic effect was displayed at 200 µg L(-1) Flu. The different subcellular distribution of Flu may affect the uptake of the highly toxic CTAC by the algae in the binary mixture, and consequently lead to a different level of CTAC toxicity. The abovementioned results indicate that the subcellular distribution of chemicals can be used to elucidate possible mechanisms for the joint toxicity of their binary mixtures to aquatic organisms.