Toxicity of the Covalent Organic Framework Material TpPa to Zebrafish

Simple SummaryCovalent organic frameworks (COFs) are promising materials for environmental cleanup due to their unique structures. However, little is known about their safety for aquatic life once they are released into water. This study used zebrafish (Danio rerio), a small freshwater fish commonly used in toxicity testing, to evaluate the harmful effects of a typical COF material called TpPa (Tp = 1,3,5-triformylphloroglucinol, Pa =p-phenylenediamine). Zebrafish embryos and larvae were exposed to different concentrations of TpPa for 120 h. The results showed that TpPa caused damage in a dose-dependent manner, with obvious developmental effects observed, including delayed hatching, physical deformities, reduced growth, abnormal heart rates, and altered swimming behavior. Further investigation revealed that TpPa induced oxidative stress and activated cell death pathways, ultimately disrupting normal development through a cascade mechanism. These findings provide important information for setting safety limits and assessing the ecological risks of TpPa and similar COF materials in aquatic environments.Covalent organic frameworks (COFs) show great potential in environmental remediation, yet the aquatic safety of TpPa (Tp = 1,3,5-triformylphloroglucinol, Pa =p-phenylenediamine), a typical COF, remains unclear. This study employed zebrafish (Danio rerio) to evaluate the environmental toxicity of TpPa and elucidate molecular mechanisms. Zebrafish embryos were exposed to 0–50 mg/L TpPa for 120 h, and developmental toxicity, oxidative stress, and physiological and molecular responses were investigated. Results demonstrated that TpPa exposure exerted concentration- and time-dependent effects. Mortality and malformation rates increased significantly from 5 mg/L, accompanied by reduced body length. The hatching rate showed a biphasic pattern, increasing with concentration at 48 h and decreasing with concentration at 120 h. Spontaneous movement was elevated at 50 mg/L, while heart rate increased dose-dependently starting from 5 mg/L at 48 h and from 1 mg/L at 72 h. Mechanistically, TpPa induced oxidative stress via reactive oxygen species accumulation and impaired the activities of both superoxide dismutase and catalase. These effects activated thep53-mediated apoptotic pathway, reduced theBcl2/Baxratio, and disrupted theGH/IGFgrowth axis and neuromotor regulatory pathways, ultimately causing developmental abnormalities. These findings provide critical data for the environmental safety assessment of TpPa, with direct relevance to establishing health monitoring protocols for COF-exposed aquaculture species.