Zheng_2026_Pestic.Biochem.Physiol_219_107009

Imazapyr (IMA) is a broad-spectrum imidazolinone herbicide increasingly applied in coastal wetlands and other aquatic-adjacent systems, raising concerns about its risks to non-target aquatic organisms. This study evaluated the developmental toxicity of IMA and the associated biochemical and molecular responses in Takifugu obscurus (a brackish-water model) and Danio rerio (a freshwater model). Fertilized embryos were exposed throughout embryogenesis to a gradient of nominal IMA concentrations (0-10 mg/L for pufferfish; 0-1 mg/L for zebrafish), encompassing environmentally relevant levels to stress-inducing levels. Survival, hatching, body length, cardiac function, and locomotor behavior were assessed during early development. Oxidative status was evaluated by measuring antioxidant defenses: superoxide dismutase (SOD), catalase (CAT), total anti-oxidant capacity (T-AOC); reactive oxygen species indicators: hydrogen peroxide (H(2)O(2)), superoxide anion (.O(2)(-)), hydroxyl radical (.OH); oxidative damage: malondialdehyde (MDA), while acetylcholinesterase (AChE) activity was measured as a neurotoxicity-related biomarker. Biochemical biomarkers were further integrated using the integrated biomarker response v2 (IBRv2) approach. The results showed that IMA delayed early hatching and altered locomotor behavior in both species, with species-specific sensitivities in survival and body length, and non-monotonic response patterns at low doses. Biochemical assays and apoptosis staining indicated that IMA disrupted redox homeostasis, promoting oxidative damage and apoptotic responses. Immune- and stress-related transcripts were also perturbed, albeit in species- and dose-dependent manners. Overall, these findings indicate that IMA can induce developmental and sublethal toxicity in early-life-stages fish via oxidative stress-associated pathways, highlighting the need to consider both water-column exposures and localized hotspot scenarios in ecological risk assessment.