Abstract
Most carcinogens give rise to cytotoxic effects when administered in doses that are carcinogenic to animals in life time studies (1). There is also ample evidence to suggest that cytotoxicity may promote the carcinogenic process (2,3); in particular, a causal relationship has been discussed in connection with liver carcinogenesis (3). We have become interested in this carcinogenic factor because it tends to influence the risk assessment of many carcinogens (c.f. ref. 4), and a characterization of cytotoxic mechanisms of relevance for the carcinogenic process may lead to a more accurate classification and risk assessment. This mechanistic approach may also stimulate the development of more specific test systems.
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References
B.F. Trump, and I.K. Berezesky, Ion regulation, cell injury and carcinogenesis. Carcinogenesis. 8, 1027–1031 (1987).
R.W. Tennant, B.H. Margolin, M.D. Shelby, E. Zeiger, J.K. Haseman, J. Spalding, W. Caspary, M. Resnick, S. Stasiewicz, B. Anderson, and R. Minor, Prediction of chemical carcinogenicity in rodents from in vitro genetic toxicity assays. Science. 236,933–941 (1987).
E. Farber, Cellular biochemistry of the stepwise development of cancer with chemicals. Cancer Res. 44, 5463–5474 (1984).
F. Perera and C Petito, Formaldehyde: a question of cancer policy? Science. 216, 1285–1291 (1982).
U. Stenius and J. Hogberg, Gamma-glutamyltranspeptidase-conferred resistance to hydroquinone induced GSH depletion and toxicity in isolated hepatocytes. Carcinogenesis. 9, 1223–1227 (1988).
U. Stenius, K. Rubin, D. Gullberg, and J. Hogberg, Gamma-glutamyltranspeptidase-positive rat hepatocytes are protected from GSH depletion, oxidative stress and reversible alterations of collagen receptors. Carcinogenesis. 11, 69–73 (1990).
U. Stenius, M. Warholm, A. Rannug, S. Walles, I. Lundberg, and J. Hogberg, The role of GSH depletion and toxicity in hydroquinone-induced development of enzyme-altered foci. Carcinogenesis. 10, 593–599 (1989).
N. Ito, H. Tsuda, M. Tatematsu, T. Inoue, Y. Tagawa, T. Aoki, S. Uwagava, M. Kagawa, T. Ogiso, T. Masui, K. Imaida, S. Fukushima, and M. Asamoto, Enhancing effect of various hepatocarcinogens on induction of preneoplastic GSH-S-transferase placental form positive foci in rats-an approach for a new medium-term bioassay system. Carcinogenesis. 9, 387–394 (1988).
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© 1991 Springer Science+Business Media New York
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Högberg, J., Stenius, U. (1991). Selection of γ-Glutamyl Transpeptidase-Positive Hepatocytes as a Function of GSH Depletion, Oxidative Stress and Alterations of Integrins. In: Nygaard, O.F., Upton, A.C. (eds) Anticarcinogenesis and Radiation Protection 2. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-3850-9_24
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DOI: https://doi.org/10.1007/978-1-4615-3850-9_24
Publisher Name: Springer, Boston, MA
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