Effect of butachlor on microcystis aeruginosa: cellular and molecular mechanisms of toxicity

The rapid development of agriculture increases the release of butachlor into aquatic environments. As a dominant species causing cyanobacterial blooms, Microcystis aeruginosa (M. aeruginosa) can produce microcystin and poses threats to aquatic ecosystems and human health. However, the impact of butachlor on M. aeruginosa remains unclarified. Therefore, the physiochemical responses of M. aeruginosa to butachlor were investigated, and the relevant underlying molecular mechanism was highlighted. There were no significant changes (P > 0.05) in the growth and physiology of M. aeruginosa at the low concentrations of butachlor (0-0.1 mg/L), which evidenced a high level of butachlor tolerance in Microcystis aeruginosa. For the high concentrations of butachlor (4-30 mg/L), the inhibition of photosynthetic activity, disruption of cell ultrastructure, and oxidative stress were dominant toxic effects on M. aeruginosa. Additionally, the impaired cellular integrity and lipid peroxidation may be attributed to the substantial elevations of extracellular microcystin-LR concentration. Downregulation of genes associated with photosynthesis, energy metabolism, and oxidative stress was inferred to be responsible for the growth suppression of M. aeruginosa in 30 mg/L butachlor treatment. The upregulation of gene sets involved in nitrogen metabolism may illustrate the specific effort to sustain the steady concentration of intracellular microcystin-LR. These findings dissect the response mechanism of M. aeruginosa to butachlor toxicity and provide valuable reference for the evaluation of potential risk caused by butachlor in aquatic environments.