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

Abstract

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.