Mechanistic insights into hormesis induced by erythromycin in the marine alga Thalassiosira weissflogii.

Erythromycin (ERY) is a typical macrolide antibiotic with large production and extensive use on a global scale. Detection of ERY in both freshwaters and coaster seawaters, as well as relatively high ecotoxicity of ERY have been documented. Notably, hormesis has been reported on several freshwater algae under ERY stress, where growth was promoted at relatively lower exposures but inhibited at higher treatment levels. On the contrary, there is limited information of ERY toxicity in marine algae, hampering the risk assessment on ERY in the coaster waters. The presence of hormesis may challenge the current concept of dose-response adopted in chemical risk assessment. Whether and how exposure to ERY can induce dose-dependent toxicity in marine algae remain virtually unknown, especially at environmentally relevant concentrations. The present study used a model marine diatom Thalassiosira weissflogii (T. weissflogii) to reveal its toxicological responses to ERY at different biological levels and decipher the underlying mechanisms. Assessment of multiple apical endpoints shows an evident growth promotion following ERY exposure at an environmentally relevant concentration (1 µg/L), associated with increased contents reactive oxygen species (ROS) and chlorophyll-a (Chl-a), activated signaling pathways related to ribosome biosynthesis and translation, and production of total soluble protein. By contrast, growth inhibition in the 750 and 2500 µg/L treatments was attributed to reduced viability, increased ROS formation, reduced content of total soluble protein, inhibited photosynthesis, and perturbed signaling pathways involved in xenobiotic metabolism, ribosome, metabolism of amino acid, and nitrogen metabolism. Measurements of multiple apical endpoints coupled with de novo transcriptomics analysis applied in the present study, a systems biology approach, can generate detailed mechanistic information of chemical toxicity including dose-response and species sensitivity difference used in environmental risk assessment.

Triclosan toxicity in a model cyanobacterium (Anabaena flos-aquae): Growth, photosynthesis and transcriptomic response.

Exposure to triclosan (TCS) has been reported to reduce photosynthetic pigments, suppress photosynthesis, and inhibit growth in both prokaryotic and eukaryotic algae including Anabaena flos-aquae (a model cyanobacterium). In particular, cyanobacteria are more sensitive to TCS toxicity compared to eukaryotic algae possibly due to the structural similarity to bacteria (target organisms); however, whether TCS exerts its toxicity to cyanobacteria by targeting signaling pathways of fatty acid biosynthesis as in bacteria remains virtually unknown, particularly at environmental exposure levels. With the complete genome sequence of A. flos-aquae presented in this study, the transcriptomic alterations and potential toxic mechanisms in A. flos-aquae under TCS stress were revealed. The growth, pigments and photosynthetic activity of A. flos-aquae were markedly suppressed following a 7-day TCS exposure at 0.5 µg/L but not 0.1 µg/L (both concentrations applied are environmentally relevant). The transcriptomic sequencing analysis showed that signaling pathways, such as biofilm formation - Pseudomonas aeruginosa, two-component system, starch and sucrose metabolism, and photosynthesis were closely related to the TCS-induced growth inhibition in the 0.5 µg/L TCS treatment. Photosynthesis systems and potentially two-component system were identified to be sensitive targets of TCS toxicity in A. flos-aquae. The present study provides novel insights on TCS toxicity at the transcriptomic level in A. flos-aquae.