Insights into the regulation mechanisms of algal extracellular polymeric substances secretion upon the exposures to anatase and rutile TiO2 nanoparticles

Abstract

As an important part of extracellular secondary metabolites, extracellular polymeric substances (EPS) can play a significant role in protecting cells from the threat of exogenous substances, including nanoparticles (NPs). However, the regulation mechanisms of EPS secretion under NPs exposure remain largely unknown. This study investigated the signaling pathways and molecular responses related to EPS secretion of algae (Chlorella pyrenoidosa) upon the exposures to anatase and rutile TiO2 NPs (nTiO2-A and nTiO2-R, respectively) at two similar toxic (20% and 50% of algal growth inhibition) concentrations. The results showed that EPS responded to nTiO2 stress via excess secretion and compositional variation, and nTiO2-A induced more EPS secretion than nTiO2-R at similar toxicity concentrations. The up-regulation of the Ca2+ signaling pathway might play a greater role in promoting EPS secretion under nTiO2-R exposure compared with nTiO2-A exposure, while the significantly increased intracellular ROS could mainly account for the increased EPS secretion under nTiO2-A exposure. The up-regulated genes related to biological synthesis and protein metabolism and the enhanced biosynthetic metabolism might be the direct causes of the increased EPS secretion. The increased ROS could have a greater effect on the amino acid metabolism and related genes upon the exposure to nTiO2-A than nTiO2-R to induce more EPS secretion. More serious membrane damage caused by nTiO2-R than nTiO2-A would affect the intracellular inositol phospholipid metabolism more severely, while the inositol phospholipid pathway and Ca2+ signaling pathway might agree and communicate with each other inherently to regulate EPS secretion upon nTiO2-R exposure. The findings address the regulation mechanisms of algal EPS secretion under nTiO2 exposure and provide new insights into algal bio-responses to nTiO2 exposure.