Vanadium pentoxide


Genetic and related effects



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4.4

Genetic and related effects

4.4.1


Humans

Lener et al. (1998) studied children exposed to vanadium in air in an area close to a

plant processing vanadium-rich slag (see Section 4.2.3). Group A comprised 15 children

from the area potentially most affected by vanadium emissions; Group B, 28 children from

an area of medium exposure; and Group C, 32 children was the control group. No signi-

ficant induction of chromosomal aberrations was found in the lymphocytes of exposed

children (1.2 

± 1.2 in Group A; 1.3 ± 1.1 in Group B) compared with the control group

(0.95 

± 0.97). Sister chromatid exchange was analysed in exposed children (4.6 ± 1.0 in



Group A; 4.6 

± 0.87 in Group B) but no data were available from controls. However, the

authors concluded that these results revealed no genotoxic effects of vanadium exposure.

Only one in-vivo study of the genotoxic action of vanadium pentoxide in adult

humans has been reported. Ivancsigts et al. (2002) studied the effect of occupational expo-

sure to vanadium pentoxide by measuring DNA strand breaks using the single-cell gel

electrophoresis assay ‘Comet Assay’, formation of 8-hydroxy-2´-deoxyguanosine, and the

frequency of sister chromatid exchange in whole blood or lymphocytes of 49 male

workers in a vanadium-processing factory. Although there was significant vanadium

uptake (mean vanadium concentration in serum, 5.38 

µg/mL), no increase in cytogenetic

end-points nor in oxidative DNA damage was observed in the cells from these workers.

4.4.2

Experimental systems

(a)



Biochemical assays

Effects of vanadium compounds on DNA-metabolizing enzymes have been reported

by Sabbioni et al. (1983). Vanadate(V) ions (10

–7

–10



–3

M) inhibited calf thymus terminal

deoxynucleotidyl transferase (with an apparent Ki of 2.5 

µM) and the catalytic activity of

mammalian DNA polymerase 

α (at I


50

of 60 


µM), while bacterial DNA polymerase-I was

inhibited when the concentration was increased to about 0.5 mM.

(b)

Mutagenicity (see Table 7)

(i)


In-vitro studies

The mutagenicity of vanadium compounds has been reviewed (Graedel et al., 1986;

Léonard & Gerber, 1994; Altamirano-Lozano et al., 1998b; Léonard & Gerber, 1998;

National Toxicology Program, 2002).

The majority of the results of mutagenic activity of vanadium have been shown in

Escherichia coli and Salmonella typhimurium (Hansen & Stern, 1984; Graedel et al., 1986;

Leonard & Gerber, 1994); there is one study only with exogenous metabolic activation

(National Toxicology Program, 2002).

Early studies demonstrated that vanadium pentoxide was more genotoxic in recombi-

nation-repair-deficient (rec

) strains of Bacillus subtilis than in the wild-type rec



+

IARC MONOGRAPHS VOLUME 86

270

pp227-292.qxp  31/05/2006  09:49  Page 270




V

ANADIUM PENT

OXIDE

271


 

 

Table 7. Genetic and related effects of vanadium pentoxide 

Result

a

 



Test system 

Without 


exogenous 

metabolic 

system 

With 


exogenous 

metabolic 

system 

Dose


b

 

(LED/HID) 



Reference 

Escherichia coli, spot test B/r WP2try

, WP2hcr



try


 

– 



NT 

0.5 M 


Kanematsu et al. (1980) 

Escherichia coli, WP

2

, WP



2

uvrA, CM


891

, reversion assay 

NT 


1200 

µg/plate 

Si et al. (1982)

c

 



Escherichia coli, ND160 and MR102, frameshift mutation 

– 

 



1200 

µg/plate 

Si et al. (1988)

c

 



Bacillus subtilis, M45 recombination-repair-deficient (rec



NT 


0.5 M 

Kanematsu & Kada 

(1978); Kada et al. (1980); 

Kanematsu et al. (1980) 



Bacillus subtilis H17 (rec

+

) and M45 (rec



-

) recombination-repair- 

 deficient 

NT 



100 000 

Sun (1996) 



Salmonella typhimurium, TA100, TA1535, TA1537, TA1538, (his



– 

NT 


0.5 M 

Kanematsu et al. (1980) 



Salmonella typhimurium, TA100, TA98, TA102, TA1535 reverse 

 mutation 



 

– 

– 



333 

µg/plate 

National Toxicology 

Program (2002) 



Salmonella typhimurium, TA97, TA98, TA100, TA102 reverse 

 mutation 

– 

NT 


200 

µg/plate 

Zen et al. (1988)

c

 



Gene mutation, 6-thioguanine resistant mutation, Chinese hamster lung 

  fibroblast cell line (V79) in vitro 

– 

 



Zhong et al. (1994) 

Sister chromatid exchanges, Chinese hamster lung fibroblast cell line 

 (V79) 

in vitro 

– 

 



Zhong et al. (1994) 

Micronucleus formation in binucleated cells, cytochalasin-B assay, 

  Chinese hamster lung fibroblast cell line (V79) in vitro 

NT 


Zhong et al. (1994) 

Numerical chromosomal aberrations, endoreduplication, Chinese 

  hamster lung fibroblast cell line (V79) in vitro 

 



Zhong et al. (1994) 

pp227-292.qxp  31/05/2006  09:49  Page 271




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