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. 2023 Nov 13;15(11):653. doi: 10.3390/toxins15110653

Table 1.

In vitro toxic effects of aflatoxin B1 (AFB1) in different cell lines after short-term exposure.

Organs Cells Exposure Time (Hour) Concentration (μM) Effects References
Liver HepG2 cells 24 32.0 Inducing cell death, DNA strand breaks, ROS generation, nuclear changes, cell cycle arrests, and apoptotic body formation [33]
HepG2 cells 24 13.0 Promoting MDA release, inhibiting cell growth, causing DNA migration, and increasing the level of ERK1/2-P (A) in the MAPK pathway [41]
HepG2 cells 24 100.0 Decreasing the expression of the p53 protein [43]
HepG2 cells 24 105.0 Suppressing p53 protein expression, and causing mitochondrial damage, nuclear condensation, and a loss of cell-to-cell contact [45]
HepG2 cells 24 16.9 Increasing ROS and ΔΨm damage, and the expression of p53 [44]
HepG2 cells 24 10.0 Inducing ROS production and DNA oxidation [50]
HepG2 cells 24 30.0 Increasing GST activity, to induce ROS [36]
L-O2 cell 24 192.0 Reducing ΔΨm, and increasing ROS generation [51]
HepG2 cells 24 5.0 Causing oxidative stress, and increasing GST activities [52]
HepG2 cells 24 30.0 Inducing DNA damage and more significant amounts of ROS [37]
HepG2 cells 24 32.0 Inducing oxidative stress, energy metabolism, DNA damage, and cell apoptosis [34]
HepG2 cells 24 50.0 Inducing DNA fragmentation and ROS [53]
HepG2 cells 24 10.0 Ameliorating DNA damage and p53-mediated apoptosis [42]
HepG2 cells 24 10.0 Causing ROS production and DNA damage [54]
HepG2 cells 24 10.0 Inducing oxidative lipid damage [55]
HL7702 cells 24 10.0 Inducing oxidative stress and DNA damage [56]
HepG2 cells 24 10.0 Inducing ROS and DNA strand break, downregulating the Nrf2/HO-1 pathway [57]
HepG2 cells 24 4.0 Altering the GSH content, GPx, and SOD activity [58]
HepG2 cells 24 3.0 Inducing P450 activities and DNA damage [46]
HepG2 cells 24 48.4 Increasing ROS generation and MMP disruption, inducing mitochondrial dysfunction, and inhibiting ATP production [31]
L-O2 cell 36 40.0 Inducing autophagy by regulating the EGFR/PI3K-AKT/mTOR signaling pathway [32]
HepG2 cells 48 10.0 Decreasing the activity of GST, increasing the P450 3A4 activity, and inducing oxidative stress [59]
L-O2 cell 48 8.0 Inducing the expression of P450 and the nuclear translocation of AHR [48]
BFH12 cells 48 0.1 Causing lipid peroxidation, reducing the antioxidant activity of the NAD(H): quinone oxidoreductase 1, and increasing the cytochrome P450 3A activity [47]
HepG2 cells 72 2.0 Inducing apoptosis and cytochrome P450 1A/1B activity [60]
Intestine Caco-2 cells 24 13.0 Promoting MDA release, inhibiting cell growth, causing DNA migration, and increasing the level of ERK1/2-P (A) in the MAPK pathway [41]
Caco-2 cells 24 20.0 Leading to cellular apoptosis or necrosis: downregulating the Bcl-2 gene and upregulating the Bax, p53, caspase-3, caspase-8, and caspase- 9 genes, and seriously affecting glycine, serine, threonine, and pyruvate metabolism. [39]
Caco-2 cells 24 50.0 Inducing DNA fragmentation and ROS [53]
Caco-2 cells 24 10.0 Inducing oxidative lipid damage [55]
Caco-2 cells 24 80.6 Increasing ROS and MMP damage, disrupting the ETC, and inhibiting ATP production [31]
Caco-2 cells 72 3.0 Increasing intracellular ROS generation, and leading to membrane damage and DNA strand break. [61]
Kidney Vero cells 24 40.0 Inducing DNA fragmentation, increasing the level of p53, and decreasing the level of bcl-2 protein [62]
HEK cells 24 13.0 Promoting MDA release, inhibiting cell growth, and causing DNA migration [41]
PK-15 cells 24 1.0 Inducing ROS production and apoptosis [63]
MDCK cells 24 0.8 Inducing oxidative stress: MDA level increased, GSH level and GPX1 activity decreased. [64]
HEK 293 cells 48 1.6 Activating oxidative stress [65]
Bronchial epithelial BEAS-2B cells 12 1.5 Inducing mutation by the attenuation of DNA adduct and p53-mediated [66]
BEAS-2B cells 24 0.1 Inducing apoptosis by inhibiting the CYP enzyme, and increasing DNA adduct [67]
BEAS-2B cells 24 1.5 Decreasing both 1A2-expressing and 3A4-expressing CYPs [68]
Genital system sperm cells 4 1.0 Decreasing MMP, and inducing fragmented DNA [69]
Bone marrow SK-N-SH cells 24 12.8 Promoting MDA release, inhibiting cell growth, and causing DNA migration [41]
Mammary gland MAC-T cells 24 12.8 Increasing ROS production, decreasing MMP, and inducing apoptosis, by reducing three anti-stress genes (Nrf2, SOD2, and HSP70) of the Nrf2 pathway [70]
Bone MSCs and CD34+ cells 24 10.0 Inducing DNA damage [71]
Colon HCT-116 cells 24 10.0 Increasing the expression of p53 [72]
Brain NHA-SV40LT cells 48 50.0 Inducing cytosolic and mitochondrial calcium changes and ROS generation, and changes in AKT and ERK1/2 MAPK signaling [40]

ΔΨm: mitochondria membrane permeability; ROS: reactive oxygen species; GST: glutathione S-transferase; DNA: deoxyribonucleic acid; MDA: malondialdehyde; ERK: extracellular signal-regulated protein kinase; MAPK: mitogen-activated protein kinase; GST: glutathione S-transferase; GSH: glutathione; GPx: glutathione peroxidase; CYPs: cytochromes P450; MMP: mitochondrial membrane potential; Nrf: nuclear factor erythroid 2-related factor; HSP: heat shock protein; AKT: protein kinase B; AHR: aryl hydrocarbon receptor; ETC: electron transport chain.