Molecular Mechanisms of Metal Toxicity and Carcinogenesis by Suwei Wang, Xianglin Shi (auth.), Xianglin Shi, Vince

By Suwei Wang, Xianglin Shi (auth.), Xianglin Shi, Vince Castranova, Val Vallyathan, William G. Perry (eds.)

During the final 20 years, chemical and mobile reviews have contributed vastly to our figuring out of metal-induced carcinogenesis, and lots of hypotheses at the function of metals in pathophysiological methods were investigated. furthermore, new thoughts can be found to make clear the mechanism of carcinogenesis in molecular phrases. This convention on Molecular Mechanisms of steel Toxicity and Carcinogenesis in September 2000 curious about the most recent study in molecular mechanisms of metal-induced toxicity and carcinogenesis. The convention promoted a multidisciplinary investigative process and integrated displays from foreign specialists on cutting-edge details during this field.

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Nucleic Acids Res 13: 7269--7288, 1985 49. Hankinson 0: The aryl hydrocarbon receptor complex. Annu Rev Pharmacol Toxicol35: 307~340, 1995 50. Whitlock JP Jr, Okino S, Dong L, Ko H, Clarke-Ktzenberg R, Ma Q, Li H: Induction of cytochrome P450lAl: A model for analyzing mammalian gene transcription. FASEB J 10: 809-818, 1996 51. Tchouwnou PB, Wilson BA, Schneider I, Ishaque AB: Cytogenetic assessment of arsenic trioxide in the Mutatox, Ames II and CAT-Tox (L) assays. A. Centeno, Ph. Collery, G. B.

Pb recovery was evaluated as described above for cellular Pb analysis. Pb release from plastic dishes Pb was detennined after filling the culture polystyrene dishes with 5% (v/v) HN0 3 at different contact times up to 72 h. Analytical detennination was carried out using the instrumental parameters described in the subsection 'Pb cell analysis', the only variation being that the samples were detennined calibrating against Pb standards prepared in 5%(v/v) HN03 • Cytosolic DNA fragments were quantified with a cell death detection ELISA assay (Boehringer Mannheim GmbH, Germany).

Huang C, Chen N, Ma W-Y, Dong Z: Vanadium induces AP-l and NFKB-dependent transcription activity. Int J Oncol13: 711-715. 19. Huang C, Ma W-Y, Young MR, Colburn N, Dong Z: Shortage ofmitogen-activated protein kinase is responsible for resistance to AP-l transactivation and transformation in mouse JB6 cells. Proc NatlAcad Sci USA 95: 156-161, 1998 20. Dong Z, Birrer MJ, Watts RG, Matrisian LM, Colburn NH: Blocking tumor promoter inducedAP-I activity inhibits induced transformation in JB6 cells. Proc Nat!

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