Table 3.
Reported biological effects provoked by LCMs.
| Study Type | Result | Reference | |
|---|---|---|---|
| In vivo (mice) | No difference in body weight and food intake; No indication of cell damage in the stomach, spleen, liver, or kidney; LCMs were greatly absorbed by the intestinal tract. |
[97] | |
| In vivo (catfish) | Significant upregulation of antioxidant enzymes (CAT, SOD, and Se-GPx); Global oxidative stress exhibited when the dosage level exceeded 20 μg LCM/g fish. |
[19] | |
| In vitro (fluorescent staining assays) | LCMs exposure induced cell death in 3T3 fibroblast and HCEC; LCM with fluorophenyl group showed minimal acute toxicity; Cholesteric LCM posed a lethal threat to HCEC only. |
[95] | |
| In vitro (PCR array) | Upregulation FC | CYP1A4: 2.38–14.4 | [6] |
| FGF19: 2.68–4.47 | |||
| LBFABP: 1.77–5.94 | |||
| Downregulation FC | PDK4:1.56–2.68 | ||
| CRYAB: −1.71 to −3.63 | |||
| IGF1: −1.57 to −3.32 | |||
| In vitro (bacterial viability assay) | LCMs mixture’s viability ratio | THRSP: −1.57 to −2.85 | [99] |
| E. coli: 1.01 ± 0.02 | |||
| S. aureus: 0.97 ± 0.02 | |||
| E. coli death ratio | B. atrophaeus: 0.94 ± 0.03 | ||
| CPCI: 0.913 | |||
| CsPFO: 0.854 | |||
FC, fold change; CAT, catalase; SOD, superoxide dismutase; Se-GPx, selenium-dependent glutathione peroxidase; CPCI, cetylpyridinium chloride; CsPFO, cesium pentadecafluorooctanoate; HCEC, human corneal epithelial.