Role of syringic acid in enhancing growth, photosynthesis, and antioxidant defense in lettuce exposed to arsenic stress.

Heavy metal pollution, especially arsenic toxicity, significantly impairs plant growth and development. Phenolic acids, known for their antioxidant properties and involvement in stress signaling, are gaining increased attention as plant secondary metabolites with the potential to enhance plant resistance to these stressors. This study aimed to investigate the effects of different concentrations of syringic acid (SA1, 10 μM; SA2, 250 μM; SA3, 500 μM) on growth, photosynthetic parameters, and antioxidant activity in lettuce seedlings subjected to arsenic stress (As, 100 μM). Arsenic stress reduced growth by 56.7%, water content by 7.39%, and osmotic potential by 26.2% in lettuce leaves compared to control. Conversely, SA1 and SA2 treatments mitigated the adverse effects of arsenic on growth and preserved the water balance in plants. However, the SA3 treatment led to a decrease in growth by 18.9% and 39.5% in the SA3 and As+SA3 groups, respectively, indicating that high-dose SA treatment adversely affected lettuce leaves under both control and stress conditions. Exogenous SA1 treatment significantly improved photosynthesis, whereas SA2 provided milder benefits and SA3 did not reduce the adverse effects of arsenic exposure. Arsenic stress increased H₂O₂ content by 47.3% and lipid peroxidation by 33.4% in lettuce seedlings. SA1 treatment effectively reduced oxidative stress by enhancing the activities of key antioxidant enzymes, such as superoxide dismutase (SOD) and peroxidase (POX). Moreover, SA1 was successful in maintaining the glutathione (GSH) pool, whereas SA2 primarily promoted ascorbate (AsA) regeneration. In conclusion, 10 μM of syringic acid (SA1) was identified as the optimal dose for reducing arsenic stress in lettuce by enhancing antioxidant activity and supporting growth. Overall, the findings underscore the potential of SA1 treatment in enhancing the resilience of lettuce to heavy metal toxicity.