The harmful raphidophyte Chattonella marina complex causes severe ecological impacts and massive fish kills worldwide through potent hemolytic toxicity. Increasing evidence suggests that its ichthyotoxicity is light-dependent and closely associated with chlorophyll-mediated photosynthetic pathways. To elucidate the underlying toxigenic and toxic mechanisms, C. marina was cultured under various spectral conditions, white (440 + 543 nm), red (630 nm), green (520 nm), and blue (460 nm), all at a constant intensity of 50 μmol m^-2 s^-1. The results indicate that while red light promotes growth and photosynthetic performance, green and blue light induce significant physiological stress, characterized by depressed maximum quantum yield (F_v/F_m), reduced effective quantum yield (Y_II), decreased electron transport (rETR_max), and lower chlorophyll a content, alongside elevated non-regulated energy loss (Y_NO). Integrated transcriptomic and proteomic analyses revealed that high-toxicity phenotypes were associated with upregulation of glutathione-related enzymes (GSS and GR) and metabolic shifts in the porphyrin biosynthetic pathway. Notably, although green and blue light stimulated the biosynthesis and accumulation of hemolytic potential, actual lytic activity was wavelength-specific, primarily triggered by red and blue light, but remained inactive under green light or in darkness. While toxicity did not correlate with baseline intracellular ROS levels, the antioxidant N-acetyl-L-cysteine (NAC) significantly attenuated hemolysis, suggesting that the mechanism involves photosensitive metabolites (e.g., pheophorbide a) acting synergistically with ROS. These findings suggest that spectral manipulation and antioxidant interventions could serve as viable strategies to mitigate the impacts of ichthyotoxic C. marina blooms.

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