Chemistry Reference
In-Depth Information
Table 18.1 Genotoxicity in humans after exposure towards elevated arsenic drinking water
levels
Individuals (exposed,
controls) Country
Arsenic in drinking
water
Effects in exposed individuals
Ref.
24 (11, 13)
53
controls: 26
µ
g/l
L: CA (
), SCE (-),
mutations in HPRT-locus
Mexico
exposed: 390
µ
g/l
437 (282, 155)
54
controls: 20
µ
g/l
L: SCE
Argentina
exposed: 130
µ
g/l
36 (18, 18)
controls: 16
g/l
UC: MN (
)
55
µ
Nevada, USA
exposed: 1313
g/l
µ
44 (22, 22)
controls: 8.4
g/l
L: MN
, trisomy,
56
µ
Argentina
exposed: 205
g/l
SCE (-)
µ
69 (35, 34)
controls: 30
g/l
L: CA (
),
OC,BC: MN (
57
µ
Mexico
exposed: 408
µ
g/l
)
125 (70, 55)
controls: 15
µ
g/l
UC: MN (
)
58
Chile
exposed: 600
µ
g/l
74 (42, 32)
controls: 7
µ
g/l
L: CA
59
Finland
exposed: 410
µ
g/l
32 (19, 13)
controls: 4.5
µ
g/l
OC,UC: MN
60
Inner Mongolia, China
exposed: 527.5
µ
g/l
66 (45, 21)
controls: 5.5
µ
g/l
L, OC, UC: MN
61
West Bengal, India
exposed: 368.1
µ
g/l
95 (59, 36)
controls: 6.4
µ
g/l
L: SCE
, CA
62
West Bengal, India
exposed: 211.7
µ
g/l
317 (163, 154)
controls: 9.2
µ
g/l
L,OC,UC: MN
63
West Bengal, India
exposed: 214.7
µ
g/l
320 (165, 155)
controls: 9.1
µ
g/l
L: CA
, SCE
64
West Bengal, India
exposed: 215
µ
g/l
217 (106, 111)
controls: 2.0
µ
g/l
L: MN
65
North Chile
exposed: 750
µ
g/l
206 (105, 102)
controls: 2.0
µ
g/l
OC: MN (
)
66
North Chile
exposed: 750
µ
g/l
306 (204, 102)
controls: 7.2
µ
g/l
L,OC,UC: MN
67
L: CA
West Bengal, India
exposed: 220
µ
g/l
CA, chromosomal aberrations; L, lymphocytes; MN, micronuclei; OC, oral mucosa cells; SCE, sister chromatid
exchanges; UC, urothelial cells;
, signifi cant increase; (
), increase but not signifi cant, (-), no effect
benzo[a]pyrene and alkylating agents, 46 - 51 which may be explained by the interfer-
ence with DNA repair processes. 52 This is consistent with the comutagenic effect
of arsenic, resulting in arsenic cocarcinogenesis, which has been shown in vivo
(see below).
18.4.2 Involvement of Reactive Oxygen (ROS) and Nitrogen Species (RNS) in
Arsenic Response
Numerous studies provide strong evidence that oxidative stress mediated by
increased levels of ROS and RNS is an important molecular mechanism contribut-
ing to arsenic-induced genotoxicity and carcinogenicity (reviewed in references
 
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