Biological responses of alga Euglena gracilis to triclosan and galaxolide and the regulation of humic acid

Although the toxicity of triclosan (TCS) and galaxolide (HHCB) in freshwater has been reported, little study is shed light on their molecular toxicity mechanism and the regulation of humic acid (HA). In this work, freshwater algae E. gracilis was selected to explore these processes, and the molecular toxicity mechanism was analyzed by metabolomics. TCS was more toxic to E. gracilis than HHCB at 1 d exposure with the EC50 value of 0.76 mg L-1, but HHCB showed a higher toxicity as the exposure time prolonged. HA could alleviate the toxicity of TCS and HHCB, mainly due to the inhibition of TCS uptake and oxidative stress, respectively. The perturbations on a number of antioxidant defense-related metabolites in response to TCS or HHCB also indicated oxidative stress was a main toxicity mechanism. However, the exposure to HHCB resulted in more pronounced perturbations in the purine metabolism than TCS, implying that HHCB may pose a genetic toxicity on algae. It may explain the higher toxicity of HHCB to algae as the exposure time increased. These findings provide a comprehensive understanding on the ecological risks of TCS or HHCB in natural waters.

Automated summary

This study investigated the molecular toxicity mechanism and regulation of humic acid (HA) on the toxicity of triclosan (TCS) and galaxolide (HHCB) in freshwater using the freshwater algae E. gracilis. The results showed that HA could alleviate the toxicity of TCS and HHCB by inhibiting TCS uptake and reducing oxidative stress, respectively. Additionally, HHCB exposure resulted in more pronounced perturbations in the purine metabolism, indicating genetic toxicity on algae. These findings provide a comprehensive understanding of the ecological risks of TCS and HHCB in natural waters.