Global triazine herbicide pollution impairs marine phytoplankton nutrition through disruption of acetyl-CoA-related metabolism

Herbicide contamination impairs marine primary productivity, yet its subcellular impact on phytoplankton carbon allocation remains poorly understood. Global monitoring (1990–2023) revealed triazine herbicides as the dominant coastal pollutants, with atrazine and simazine exceeding 80% detection frequency; their combined toxicity corresponded to a median atrazine-equivalent concentration of 0.68 nmol L −1 . Exposure of the diatom Skeletonema costatum ( S. costatum ) at environmental concentration (5 nmol L −1 ) of atrazine (a typical triazine herbicide) significantly decreased the cell abundance, chlorophyll a (Chla) content, and photosynthetic efficiency. Crucially, total fatty acids decreased by 58.84%, with the nutritionally critical eicosapentaenoic acid (EPA) declining by 48.9%. Integrated transcriptomic and physiological analyses indicated that herbicide-induced photosynthetic inhibition limited ATP/NADPH supply, which, along with observed morphological alterations, suppressed the expression of genes involved in acetyl-CoA biosynthesis and utilization (e.g., ACSS1_2 , ACCase ) and those encoding fatty acid desaturases (e.g., SCD ) and elongases. This disruption preferentially depleted polyunsaturated fatty acids over biomass, compromising phytoplankton nutritional quality. Given the strong land-to-sea transfer of triazine herbicides, ongoing inputs may undermine the nutritional foundation of marine food webs, necessitating urgent cross-boundary management.