Figure 1.
Dose-dependent (A) and time course formation (B) of BPDE-N2-dGuo adducts in HepG2, A549 and T24 cell lines exposed 14 h to increasing concentrations from 0.2 to 5 µM of B[a]P (A) or incubated with 0.2 µM from 30 minutes to 24 h (B).
Figure 2.
Level of oxidative DNA damage measures by a calibrated Comet assay in cells exposed to B[a]P for 14 h.
Values for the strand breaks (A) were obtained from the standard version of the method while the level of 8-oxodGuo (B) was obtained with incubation of the slides with the Fpg repair enzyme. (Statistically significant (p<0.05) with respect to (*) DMSO control and (†) Fpg buffer control).
Figure 3.
Time-dependent formation of DNA strand breaks measured by the Comet assay in HepG2, A549 and T24 cell lines incubated with 0.2 µM for a time period ranged between 30 min to 24 h.
*: significantly different from t = 0 h (p<0.05).
Figure 4.
Expression of CYP1A1 (right) and CYP1B1 (left) genes in HepG2 and A549 cells exposed to increasing concentrations of B[a]P from 0.2 to 5 µM for 14 h.
Differences with respect to DMSO control were found statistically significant for both genes in both cell lines at all concentrations (p<0.05) except CYP1B1 in HepG2 at 0.2 and 2 µM B[a]P.
Figure 5.
Modulation of gene expression in T24 cells exposed for 14 h to increasing concentrations of B[a]P from 0.2 to 5 µM.
Statistically significant (p<0.05) with respect to (*) DMSO control).
Table 1.
Modulation of the expression of a series of phase I metabolization enzymes in HepG2 and A549 cells exposed for 14[a]P from 0.2 to 5 µM.
Figure 6.
Induction of CYP1A1 and 1B1 in A549 and HepG2 cells exposed to 0.2 µM B[a]P.
Data were found significantly different (p<0.05) with respect to DMSO control for both cell lines between 30 min and 6 h.
Table 2.
Modulation of phase I metabolism enzymes in HepG2 and A549 cells following exposure to 0.2 µM B[a]P.
Table 3.
Increase in EROD activitya measured in HepG2 and A549 cells exposed to B[a]P from 0.2 to 5 µM.
Figure 7.
Modulation of the expression of a series of GST genes in HepG2, A549 and T24 cells exposed to increasing concentrations of B[a]P from 0.2 to 5 µM.
*: significantly different from DMSO control (p<0.05). Expression of GSTA1 was not detected in T24.
Table 4.
GST activitya in HepG2 and A549 cells exposed to B[a]P from 0.2 to 5 µM.
Figure 8.
Modulation of the expression of the gene coding for AKRC1 and MRP4 in A549 and HepG2 cells exposed for 14 h to increasing concentrations of B[a]P from 0.2 to 5 µM.
Results were expressed with respect to untreated control.