Table 2.
The effect of PFHxS exposure in different zebrafish studies.
| Study | PFHxS Concentration |
Major Findings | ||
|---|---|---|---|---|
| Developmental and Behavioral Toxicities |
Liver Function | Endocrine/Metabolic Problems |
||
| Ulhaq and Tse, 2023 [11]; Ulhaq et al., 2023 [22] | 0.1–10 µM | Developmental toxicity can be observed to have started at 5 µM | Lipid accumulation was not assessed in the liver; however, it was observed in the GIT. | Hyperglycemia, hyperactivation of glucose uptake, |
| Annunziato et al., 2020 [23]; Annunziato et al., 2019 [24] | 100–1000 µM 0.011–0.22 ng/mL |
LC50 = 340 µM PFHxS up to 22.5 mg/L did not show any morphological defect |
Aqueous film-forming foam (AFF) exposure reduced liver size | AFF leads to the disruption of β cells, resulting in their fragmentation, and negatively impacting the growth and development of the pancreas |
| Gaballah et al., 2020 [25] | 0.4–80 µM | EC50 = 92.7 µM Hyperactivity at 14–25.1 µM |
NA | NA |
| Huang et al., 2022 [26] | 1–100 ng/mL | NA | PFHxS tightly bind to the active pocket of ZSA and ZL-FABP, lipid accumulation in the liver possibly due to hepatocyte vacuolation | NA |
| Menger et al., 2020 [27] | 12–60 µM | Reduction in swimming activity in dark environments and increased burst swimming activity | NA | NA |
| Phelps et al., 2023 [28] | 0.03–80 µM | AC50 = 28.63 µM Suppression of respiratory burst |
NA | NA |
| Vogs et al., 2019 [29] | 0.4–330 µM | EC50 = 84.5 µM | NA | NA |
| Xu et al., 2023 [30]; Xu et al., 2022 [31] | 0.3–10 µM | NA | Dysregulation of FAO | A glucose metabolism defect marked by the inhibition of the hydrolysis of large-molecular sugar |
FAO, fatty acid β-oxidation; NA, not available; GIT, gastrointestinal tract; LC50, median lethal dose; EC50, half-maximal response dose; AC50, the concentration for half-maximal activity derived from the Hill equation model; ZSA, zebrafish serum albumin; ZL-FABP, zebrafish liver fatty acid-binding protein.