Elevated pCO2 promotes growth but compromises PSII repair and antioxidant balance in the bloom-forming diatom Skeletonema costatum under ultraviolet radiation.

Diatoms serve as key marine primary producers, driving global biogeochemical cycles, but their physiological performance is increasingly challenged by ocean acidification (OA) and enhanced ultraviolet radiation (UVR). This study investigated how OA caused by elevated pCO2 (1000μatm) modulates the UVR sensitivity of the bloom-forming diatom Skeletonema costatum. Elevated pCO2 significantly enhanced the specific growth rate by ~11.6%; it did not significantly aggravate the UVR-induced decline in Fv/Fm, but it constrained PSII repair and PsbA turnover, as indicated by lower rate constants for PSII repair (Krec, s-1) and PsbA removal (KPsbA, s-1), and was associated with a greater net decline in total PsbA content under PAR + UVR. Although elevated pCO2 upregulated the relative maximal electron transport rate (rETRmax) and light-saturation parameter (Ik), and maintained a higher RbcL/PsbA ratio consistent with a possible role of carbon assimilation as a downstream sink, it did not enhance the sustained non-photochemical quenching (NPQs). Furthermore, under elevated pCO2, CAT activity had a lower baseline; although CAT increased under UVR relative to PAR, its absolute activity remained lower, indicating an imbalanced antioxidant response. Collectively, these findings reveal a physiological trade-off: elevated pCO2 promotes growth and carbon-sequestration capacity but simultaneously compromises photoprotective mechanisms. Consequently, S. costatum grown under elevated pCO2 becomes more susceptible to UVR-induced photoinhibition, potentially suppressing photosynthetic production during surface blooms and influencing bloom persistence and carbon export.