Table 14.
Cell Type | Dose and Duration | Findings | Mechanisms | Reference |
---|---|---|---|---|
HepG2 (Hepatocellular carcinoma) | 25–250 μM RA (24 h) | ↓ OTA- and AFB-induced cell damage and apoptosis ↓ DNA and protein synthesis inhibition induced by OTA- and AFB- |
↓ ROS production ↓ capase-3 activation |
[98] |
HepG2 (Hepatocellular carcinoma) | 5–10 μg/mL (13.9–27.8 µM) RA (72 h) | ↑ apoptosis | ↑ casp 8, NFBIA, TNFSF9 and Jun mRNA ↓ Bcl-2 mRNA expression |
[99] |
HepG2 (Hepatocellular carcinoma) | 60 μM RA (24 h) | ↓ cell viability | [92] | |
Hep-3B (Hepatocellular carcinoma) | 6.25–50 µg/mL (17.3–138.8 µM) RA (48 h) | ↓ cell viability | [30] | |
HepG2 (Hepatocellular carcinoma) | 20–80 μM RA (24 h or 4 days) | ↔cell viability | ↑ translocation of Nrf2 ↑ ARE-luciferin activity ↑ efflux of p-glycoprotein ↑ MRP2 ↑ intracellular ATP |
[100] |
NCI-H82 (Lung carcinoma; SCLC) | 6.25–50 µg/mL (17.3–138.8 µM) RA (48 h) | ↓ cell viability | [30] | |
A549 (Lung adenocarcinoma) | 10–500 μM RA (48 h) IC50 198.12 | ↓ cell proliferation | ↓ hCOX2 activity | [101] |
OTA (ochratoxin), AFB (Aflatoxin), ROS (reactive oxygen species), casp (caspase), NFBIA (nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor-alpha), TNFSF9 (tumor necrosis factor ligand superfamily-member 9), Jun (v-jun sarcoma virus 17 oncogene), Bcl-2 (B-cell CLL/lymphoma 2), Nrf2 (nuclear factor E2-related factor-2), ARE (antioxidant response element), MRP2 (multidrug resistance-associated protein 2), ATP (adenosine triphosphate), hCOX2 (human cyclooxygenase 2).