Fluorine (F) and Cadmium (Cd) have given rise to public concern regarding their adverse impacts on the environment and human beings. Yet, the toxic interplay between F and Cd on the intestine is still vague. Aiming to investigate the role of F on Cd-damaged intestine, a total of five groups of 30 SD rats were picked at random to be gavaged for 90 days: Control group (Ultra-pure water), Cd (Cd 1 mg/kg), Cd+LF (Cd 1 mg/kg+F 15 mg/kg), Cd+MF (Cd 1 mg/kg+F 45 mg/kg), and Cd+HF (Cd 1 mg/kg+F 75 mg/kg). It demonstrated that Cd enriched in the intestine and disordered intestinal barrier of rats. Interestingly, two side effects of F were observed resisting to the Cd toxicity. The Cd levels in colon contents were attenuated by 45.45 %, 28.11 %, and 19.54 % by F supplement, respectively. In the Cd+LF group, SOD, GSH-Px, and CAT activities elevated by 0.93, 1.76, and 1.78 times, respectively, and the MDA content reduced 0.67 times; the expressions of NQO1, SOD2, and GSH-Px mRNA markedly enhanced, as well as the Keap1 mRNA significantly decreased. Nevertheless, all indexes above in the Cd+HF group showed the opposite trends. Furthermore, LPS levels decreased by 45.93 % for the Cd+LF group and increased by 12.70 % in that the Cd+HF group. The ZO-1 expression in the Cd+LF group increased, whereas the Cd+HF group's expressions of Claudin-1, Occludin, and ZO-1 were all diminished by 35.46 %, 27.23 %, and 16.32 %, respectively. Moreover, the levels of TNF-α, IL-1β and TLR-4 decreased and IL-10 level promoted, while all showed opposite trends in the Cd+HF group. Collectively, it indicated there is a twofold interplay between F and Cd on intestinal damage and mainly depends on F dosages.

Predicting the sorption coefficients of pesticides in the real environment is a complex and challenging task. This complexity arises from the fact that multiple factors, including the characteristics of the contaminants, the composition of the sediment and the prevailing environmental conditions, can exert a significant influence on the sediment-water partition coefficient. Here, 54 commonly-used pesticides were detected in a river. Subsequently, the performance of the extended connectivity fingerprint model and the energy lattice points model in predicting sediment-water partition coefficients was compared. The results indicated that the concentration levels of pesticides in the research region followed a specific order: herbicide concentration (126.35 ± 65.68 ng/L in water and 93.02 ± 39.21 ng/g in sediment) > fungicide concentration (51.88 ± 19.91 ng/L in water and 55.26 ± 18.21 ng/g in sediment) > insecticide concentration (9.25 ± 5.24 ng/L in water and 8.18 ± 4.85 ng/g in sediment) > plant growth regulator concentration (5.68 ± 1.05 ng/L in water and 5.90 ± 2.70 ng/g in sediment). The quantitative structure-property relationship model demonstrated that, in comparison to the traditional extended connectivity fingerprint model, the accuracy of the energy lattice points model in prediction was significantly improved (r² = 0.85 vs. 0.60). This finding suggests that the energy lattice points, when used as a descriptor, can more effectively reflect the non-binding interaction characteristics between small-molecule contaminants and sediments compared to traditional model. And the energy lattice point model can be well applied to the prediction of pollutant adsorption factors in real environments.

The combined pollution of cadmium (Cd) and enrofloxacin (ENR) in aquatic environments represents a critical issue in environmental toxicology. Using zebrafish as model organisms, we systematically investigated the combined toxicity of Cd and ENR through both acute (96-h) and chronic (20-d) exposure experiments. Our results demonstrated significant synergistic effects: co-exposure reduced the 96-h LC50 values from 89.12 mg/L (Cd alone) and 190.11 mg/L (ENR alone) to 46.35 mg/L and 99.39 mg/L, respectively (combined effect index = 0.96). Chronic exposure revealed that ENR enhanced Cd accumulation in the liver, intestine, and muscle tissues by 1.11–2.33-fold compared to single Cd exposure. Oxidative stress markers showed dynamic temporal changes, with superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) activities initially increasing by 1.34–7.06-fold, 0.98–3.28-fold, and 1.53–3.65-fold at 8 d, respectively, followed by 9.9–48.98% reductions after 20 d of exposure. Malondialdehyde (MDA) levels progressively accumulated, reaching up to 4.06-fold higher than controls. Notably, co-exposure elevated oxidative stress by 11.24–34.48% relative to single exposures. The 16S rDNA sequencing analysis indicated that Cd exposure significantly reduced the α-diversity of zebrafish gut microbiota (57–63% decrease in Shannon index), characterized by a 16–20% reduction in beneficial Cetobacterium and a 44–114% increase in pathogenic Aeromonas abundance. The combined exposure further exacerbated these gut microbiota dysbiosis patterns. These findings provide crucial evidence for ecological risk assessment, suggesting that current environmental standards based on single-pollutant evaluations may substantially underestimate the actual risks of heavy metal-antibiotic co-contamination in aquatic ecosystems.