perchlorate stress. Physiological assessments revealed that perchlorate exposure significantly reduced the relative growth rate and induced severe ultrastructural damage, including thylakoid disorganisation and extensive vacuolisation. A massive reactive oxygen species burst and malondialdehyde accumulation coincided with marked decreases in photosynthetic pigments and photosynthetic efficiency. While primary antioxidant enzymes (SOD, POD, and CAT) were activated, the ascorbateglutathione cycle equilibrium was critically disrupted; specifically, the inhibition of MDHAR and DHAR activity blocked the recycling of reduced AsA, creating a metabolic bottleneck. Transcriptomic analysis identified thousands of differentially expressed genes (DEGs), revealing a near-universal transcriptional suppression of the "Ribosome" pathway and "Carbon fixation" machinery, along with significant increases in MAPK signalling and ABC transporters. Nontargeted metabolomic analysis revealed significant metabolic reprogramming, characterised by the depletion of essential amino acids and nucleotides and the accumulation of osmoprotectants. Multiomics analysis demonstrated a high degree of concordance between gene expression and metabolite accumulation, particularly within the purine metabolism and nucleotide salvage pathways. Notably, compared with male gametophytes, female gametophytes exhibited greater sensitivity and more complex regulatory fluctuations, suggesting sex-specific vulnerability to perchlorate. These findings provide a comprehensive molecular blueprint of perchlorate toxicity, identifying widespread transcriptional suppression of the ribosome pathway and the collapse of the antioxidant buffer as potential primary ecotoxicological mechanisms in marine macroalgae.
Li et al. (Tue,) studied this question.