The contents of six heavy metals (HMs: Cr, Cu, As, Pb, Cd, and Zn) in sediments from the upper reaches of Liangtan River (LTR) were determined. The geo-accumulation index (Igeo), pollution load index (PLI), and potential ecological risk index (RI) were employed to assess the HM contamination in the sediments. Pearson’s correlation coefficient analysis (PCC), principal component analysis (PCA), and cluster analysis (CA) were used to infer the sources of HMs. The average concentrations of Cr, Cu, As, Pb, Cd, and Zn were 44.63 ± 25.36, 31.40 ± 22.56, 4.66 ± 2.07, 29.20 ± 27.73, 0.25 ± 0.06, and 68.87 ± 104.62 μg/g, respectively. The Igeo indicated that the Cd contamination level was unpolluted to moderately polluted. The mean PLI was 0.97 ± 0.53, suggesting that the sediments were unpolluted, but close to moderately contaminated. The RI values indicated that the potential environmental risk of HMs in the sediments of the LTR was low. The results of PCC, PCA, and CA suggested that the Cr, Cu, As, and Zn in the sediment may mainly originate from natural processes; Pb mainly comes from human industrial and agricultural production activities as well as natural processes; and the main source of Cd may be the production activities of the surrounding chemical enterprises and chemical fertilizer application in farmland.

Pefloxacin (PFLX) is a type of fluoroquinolone (FQ) that has been widely used in aquaculture and animal husbandry. It is also a new kind of pseudo-persistent pollutant, which has some toxic effects. In this study, zebrafish (Danio rerio) embryos were used as exposure models to analyze the toxicity of PFLX. The results showed that PFLX was absorbed on the outer membrane surface at the beginning, and then a few PFLX slowly entered the cytoplasm. The adsorption complied with the Langmuir isotherm adsorption model. The surface morphology of the embryonic membrane was changed. PFLX exposure had no effect on fetal autonomous movement, but it significantly inhibited the embryo hatching rate. After PFLX exposure, the embryo and larval survival rates showed a clear dose–effect relationship. Though PFLX exposure did not cause teratogenic toxicity, it still affected cardiovascular function. The potential toxicity mechanism and developmental toxicity of PFLX to zebrafish were revealed. These results could be important for studies concerning FQ toxicology.

Engineered nano-ZnO is extensively utilized in both production and daily life, leading to its inevitable entry into the wastewater treatment system through various pathways. Nitrogen removal microorganisms in wastewater treatment systems are highly susceptible to environmental impacts. The antibacterial properties of nano-ZnO can impede the biological nitrogen removal (BNR) process and adversely affect the nitrogen removal performance. A comprehensive understanding of the inhibitory effect and mechanism of nano-ZnO on the BNR process is crucial in devising appropriate countermeasures to ensure optimal nitrogen removal performance. This review provides an overview of the sources of nano-ZnO in the environment, its impact on the BNR process, and the inhibition mechanism, and proposes potential methods that can mitigate the inhibitory effect of nano-ZnO. Additionally, future prospects are also discussed. This review serves as a foundation for a deeper understanding of the inhibition of engineered nano-ZnO on the BNR process and aids in guiding efforts to maintain the nitrogen removal performance in the presence of engineered nano-ZnO.

Gatifloxacin (GTFX), a fourth-generation fluoroquinolone, causes metabolic disturbances in mammals, but its hepatotoxic mechanisms in aquatic vertebrates remain unclear. This study investigated whether GTFX induces liver injury in zebrafish larvae through oxidative stress or alternative pathways. Larvae at 3 days post-fertilization were exposed to 0.2–2.3 mg/mL GTFX for 48 h. Liver morphology, histopathology, intracellular reactive oxygen species (ROS), and expression of lipid metabolism (pparg) and xenobiotic biotransformation genes (cyp1a, cyp1b1) were assessed. GTFX exposure caused concentration-dependent reductions in liver area, increased hepatic opacity, delayed yolk sac absorption, and hepatocyte swelling with cytoplasmic vacuolization. Despite these structural changes, ROS levels did not differ significantly from those of controls. In contrast, transcriptional analysis revealed significant upregulation of pparg, cyp1a, and cyp1b1, indicating disrupted lipid homeostasis and enhanced detoxification responses. Acute high-dose GTFX exposure induced a metabolism-associated hepatotoxic response in zebrafish larvae, which occurred without a statistically significant change in bulk ROS levels. Together, these findings offer mechanistic insight into fluoroquinolone-associated liver injury.