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(a)
7
6
5
4
3
2
1
0
7
6
5
4
3
2
1
0
0-hour post-Cr
18-hour post-Cr
BSO
BSO
0
25
50
75
100
0
25
50
75
100
Cr(VI) (
µ
M)
Cr(VI) (
µ
M)
(b)
(c)
16
Asc
2000
Asc
Control
12
1500
8
1000
4
500
0
0
0
25
50
75
100
0
25
50
75
100
Cr(VI) (
µ
M)
Cr(VI) (
µ
M)
Figure 6.8.
Impact of Asc and GSH on DPC formation in A549 cells. All Cr(VI) expo-
sures were for 3 hours in a serum-free medium. Data are means ± SDs. (a) DPC levels
in cells with and without pretreatment with 0.1 mM BSO for 24 hours. DPCs were
measured either immediately (left panel) or 18 hours after Cr(VI) treatments (right
panel). (b) Formation of DPC in control and Asc-restored cells. (c) Cr accumulation
by A549 cells with and without Asc preloading (adapted from MacFie et al. [154] with
the permission of the American Chemical Society).
involved in stable protein-DNA association. It is likely that Cr(III) binds
favorably to His, Cys, and -COOH groups of Glu and Asp, which may be in
contact with the duplex in DNA-binding proteins [154]. Recently, the level of
DPCs in conjunction with levels of protein oxidation and lipid peroxidation
in Cr(VI) exposure to MOLT4 cells was determined [155].
The formation of protein carbonyls and DPCs are shown in Figure 6.9. Tiron
or α-tocopherol treated cells prior to the addition of Cr(VI) inhibited the
formation of the protein carbonyl by 63% and 56% and DPCs by 57% and
52%, respectively, compared to cells treated with Cr(VI) alone (Fig. 6.9). The
generation of H
2
O
2
and ultimately
•
OH radicals were provoked to explain the
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