Chemistry Reference
In-Depth Information
Cr V H O
(
)
+
→
Cr VI
(
)
+
•
OH
(6.41)
2
2
Cr IV H O
(
)
+
→
Cr V
(
)
+
•
OH
.
(6.42)
2
2
In aerated solutions, there is consumption of oxygen in the reaction of
Cr(VI/V/IV). The possible reactions for such observations can be explained
by reactions (6.43) and (6.44):
R O
•
+ → +
2
R O
−
2
(6.43)
R
•
+ →
O
ROO
•
→
oxidized products
.
(6.44)
ox
2
Earlier studies have explored the formation of the chromate intermediate
and mode of reactive species
in vitro
and
in vivo
[44, 83, 86, 87, 92, 96, 98,
117-123, 125, 127-129, 137-139]. The primary reducing substrate(s) in the
reduction of Cr(VI) are determined by their cellular availabilities and reaction
rates with Cr(VI). In previous studies, the importance of both GSH and ascor-
bate has been emphasized [125, 140, 141]. GSH is abundantly intracellular and
its concentration has been determined at millimolar levels. The levels of ascor-
bate are also at millimolar
in vivo
. Most of the results have shown that ascor-
bate is more dominant and a kinetically favored biological reductant causing
∼90% of
in vivo
metabolism of Cr(VI) [125, 140]. GSH has been identified as
a modulator of cell stress in Cr(VI) cytotoxicity. When GSH is depleted, over-
expression of the heme-oxygenase 1 gene expression in human dermal fibro-
blasts by Cr(VI) has been detected [141]. Significantly, this can be considered
a marker in Cr(VI)-induced cell stress and cytotoxicity [141]. The stable Cr(III)
species cannot cross the cellular membrane, and hence, it detoxifies the cellular
membrane. However, if the reduction of Cr(VI) to Cr(III) occurs in the cell,
the weak permeability of Cr(III) intracellularly traps the molecule. This results
in the formation of a stable complex of Cr(III) with nucleic acid and proteins
that lead to DNA damage.
Several studies support the role of ROS in Cr(VI)-induced oxidative stress
[125, 137, 142-144], but a direct relationship between DNA-ROS and Cr(VI)-
induced DNA damage is not fully understood and is heavily debated [25, 27,
44, 98, 129, 138, 144-150]. One of the debate issues includes the identity of the
specific Cr(V) species responsible for the generation of
•
OH [117, 137]. A
tetraperoxochromate(V) species was suggested in the reduction of Cr(VI) and
H
2
O
2
, leading to the formation of
•
OH and singlet oxygen and resulting
in damage to DNA [117]. However, an independent study using the ESR
technique has shown that the reaction of Cr(VI) and H
2
O
2
did not result in
the generation of
•
OH. Furthermore, the reduction of Cr(VI) by ascorbate,
GSH, GSH reductase, and vitamin B
2
did not yield the formation of
tetraperoxochromate(V) [137]. Another example of the complexity of Cr(VI)-
mediated oxidative stress and damage is when Cr(VI) was reduced to Cr(V)
by vitamin B
2
(riboflavin) in Chinese hamster V79 cells, which resulted in an
increase in hydroxyl radicals, chromosomal aberrations, and mutations at the
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