Physiological and molecular mechanisms of the inhibitory effects of artemisinin on Microcystis aeruginosa and Chlorella pyrenoidosa.

Artemisinin, a novel plant allelochemical, has attracted attention for its potential selective inhibitory effects on algae, yet to be fully explored. This study compares the sensitivity and action targets of Microcystis aeruginosa (M. aeruginosa) and Chlorella pyrenoidosa (C. pyrenoidosa) to artemisinin algaecide (AMA), highlighting their differences. Results indicate that at high concentrations, AMA displaces the natural PQ at the Q binding site within M. aeruginosa photosynthetic system, impairing the D1 protein repair function. Furthermore, AMA disrupts electron transfer from reduced ferredoxin (Fd) to NADP by interfering with the iron-sulfur clusters in the ferredoxin-NADP reductases (FNR) domain of Fd. Moreover, significant reactive oxygen species (ROS) accumulation triggers oxidative stress and interrupts the tricarboxylic acid cycle, hindering energy acquisition. Notably, AMA suppresses arginine synthesis in M. aeruginosa, leading to reduced microcystins (MCs) release. Conversely, C. pyrenoidosa counters ROS accumulation via photosynthesis protection, antioxidant defenses, and by regulating intracellular osmotic pressure, accelerating damaged protein degradation, and effectively repairing DNA for cellular detoxification. Additionally, AMA stimulates the expression of DNA replication-related genes, facilitating cell proliferation. Our finding offer a unique approach for selectively eradicating cyanobacteria while preserving beneficial algae, and shed new light on employing eco-friendly algicides with high specificity.