Spatially regulated oxidative stress responses during chlorotic symptom development in Pontederia crassipes exposed to clomazone
摘要
Clomazone is a pre-emergent herbicide with notable persistence and documented phytotoxicity to non-target aquatic plants. We evaluated oxidative stress responses in newly developed leaves of Pontederia crassipes during the green-to-chlorotic transition following exposure to 0, 0.1, and 0.3 mg L⁻¹ clomazone. Plants were assessed at 4, 8, and 11 days post-application via pigment quantification, reactive oxygen species (ROS) assays, lipid peroxidation, and key enzyme activities. Clomazone caused marked declines in chlorophyll a (87% at 0.1 mg L⁻¹; 90% at 0.3 mg L⁻¹), chlorophyll b (89% at 0.1 mg L⁻¹; 92% at 0.3 mg L⁻¹), and carotenoids (50% at 0.1 mg L⁻¹; 67% at 0.3 mg L⁻¹) relative to controls, most prominently in basal (chlorotic) regions of new leaves. Hydrogen peroxide peaked at 11 days (↑45% at 0.1 mg L⁻¹; ↑30% at 0.3 mg L⁻¹), while lipid peroxidation remained unchanged, consistent with the engagement of antioxidant defenses. Glycolate oxidase and glutathione S-transferase activities rose transiently, especially at 0.3 mg L⁻¹. Principal component analyses discriminated samples by leaf age (63.26% total variance), herbicide concentration (73.86%), and tissue region (81.07%), revealing greater ROS and enzymatic responsiveness in basal versus apical segments. Roots and mature leaves showed negligible alterations. Collectively, P. crassipes mounts spatially regulated oxidative defenses under clomazone, supporting its relevance as a sensitive bioindicator for monitoring herbicide contamination in aquatic ecosystems.