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The apparent lack of As i III export in Hep G2 cells may be explained by considering the high arsenic biotransformation capacity of hepatocytes.
Efficient biotransformation of inorganic arsenic to methylarsenic species would remove the need for the extrusion of As i III as a significant resistance mechanism.
Kessel et al. Arsenic can either enhance or reduce nitric oxide NO production, depending on the type of cell, the arsenic species, and the concentration of the tested arsenical.
Suppression of NO production has been shown to reduce arsenite-induced oxidative DNA damage and micronucleus formation Gurr et al.
An elevated resistance to As-induced genotoxicity in Hep G2 cells was reported by Gebel et al. The authors did not find elevated numbers of induced micronuclei in Hep G2 cells after arsenic exposure.
A cell-cycle delay in arsenite-treated human leukaemia cells was reported by McCabe et al. Kligerman et al. In our study, a recovery period was instituted, i.
Hence, in contrast to the results of McCabe et al. Taken together, these data indicate that arsenic compounds are able to temporarily delay the cell cycle, but that this delay is reversible.
These results are in agreement with data of previous studies published by Dopp et al. After an extended exposure time of 24 h and a recovery period of 14 h in the present study, the DMA III -induced cell-cycle delay was still detectable.
In conclusion, the presented results reveal that the uptake capabilities of arsenic compounds are dependent upon both the cell type and the arsenic species: We noted a resistance to intracellular accumulation of arsenic, either due to increased resistance at the uptake level or an enhanced efflux mechanism by Hep G2 cells in comparison to CHO-9 cells.
The induced genotoxic effects were directly correlated to the increased intracellular arsenic concentrations. The authors thank Prof. Obe for instructive discussions.
We also thank Mrs. Gabriele Zimmer for excellent technical assistance. Conflict of interest: none declared. Aposhian, H.
Enzymatic methylation of arsenic species and other new approaches to arsenic toxicity. Occurrence of monomethylarsonous acid urine of humans exposed to inorganic arsenic.
A review of the enzymology of arsenic metabolism and a new potential role of hydrogen peroxide in the detoxication of the trivalent arsenic species.
Bau, D. Health Perspect. Basu, A. Micronuclei as biomarkers of carcinogen exposure in populations exposed to arsenic through drinking water in West Bengal, India: A comparative study in three cell types.
Cancer Epidemiol. Biomarkers Prev. Bernstam, L. Molecular aspects of arsenic stress. Health B. Bhattacharjee, H. Arsenic defence mechanisms.
Broome-Smith, S. Baumberg, C. Sterling, and F. Ward, Eds. Society for General Microbiology, Leeds. Bun-ya, M. Challenger, F. Biological methylation.
Chemical Reviews 36 , — Dopp, E. Uptake of inorganic and organic derivatives of arsenic associated with induced cytotoxic and genotoxic effects in Chinese hamster ovary CHO cells.
Interindividual variation in the metabolism of arsenic in cultured primary human hepatocytes. Gebel, T.
Low-level self tolerance to arsenite in human Hep G2 cells is associated with a depressed induction of micronuclei.
Goering, P. The enigma of arsenic carcinogenesis: Role of metabolism. Ghosh, M. Gong, Z. Unstable trivalent arsonic metabolites, monomethylarsonous acid and dimethylarsinous acid.
Atom Spectrom 16 , — Gradecka, D. Selected mechanisms of genotoxic effects of inorganic arsenic compounds.
Health 14 , — Gurr, J. Calcium-dependent nitric oxide production is involved in arsenite-induced micronuclei.
Nitric oxide production by arsenite. Hartwig, A. Carcinogenesis 18 , — Modulation of DNA repair processes by arsenic and selenium compounds.
Toxicology , — Hei, T. Mutagenicity of arsenic in mammalian cells: Role of reactive oxygen species. Huang, R.
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