Integrating Physiological and Proteomic Analysis to Unravel the Ameliorating Mechanism of Nitric Oxide on Cadmium Toxicity in Ulva pertusa

Nitric oxide (NO) has been shown to alleviate cadmium (Cd) toxicity in plants. However, the molecular mechanisms by which NO mitigates Cd toxicity in algae are not yet fully understood. In this study, we systematically investigated the protective role of NO in Cd-stressed Ulva pertusa by integrating TMT-based proteomic analysis with physiological and biochemical data. Among the Cd concentrations tested (0, 25, 50, 100, 200, 400, and 800 μM), a nearly 50% reduction in Fv/Fm was observed at 50 μM Cd. The highest increase in Fv/Fm occurred at 150 μM sodium nitroprusside (SNP) under exposure to 50 μM Cd stress. Our findings also indicated that exogenous nitric oxide (NO) significantly mitigated the toxic effects of Cd in U. pertusa by regulating photosynthesis, as well as pigment and lipid synthesis. Through TMT-based proteomic analysis, we identified 579 proteins involved in modulating Cd-induced toxicity in U. pertusa under NO/Cd treatment. Notably, several metabolic pathways, including photosynthesis, chlorophyll and carotenoid metabolism, as well as lipid and amino acid synthesis, were significantly altered in response to NO treatment. Our results suggested that NO caused multiple molecular mechanisms to alleviate the toxicity of Cd in U. pertusa, which highlights its potential role as a protective agent in algae exposed to heavy metal stress.