By P. M. D. Foster (auth.), Philip L. Chambers, Claire M. Chambers, Helmut Greim (eds.)
This complement includes the papers submitted at EUROTOX 88, the joint Congress of the ecu Society of Toxicology and the Federation of the ecu Societies of Toxicology. The subject was once considered one of tracking and interpreting the results of poisonous components within the organic reaction on the subcellular point. Mechanisms of steel carcinogenicity are mentioned in addition to the biomonitoring of chemical publicity. experiences are supplied at the function of person modifications in guy and the influence of hazard review. Papers seem facing the genetic keep watch over of drug metabolizing enzymes. The function of metabolism in natural particular toxicity is mentioned. details is integrated at the toxicological influence of chemical compounds interfering with the endocrine process in addition to at the results of toxicants at the immune approach. shows take care of the present prestige of probability evaluation in environmental toxicology.
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Additional resources for Biological Monitoring of Exposure and the Response at the Subcellular Level to Toxic Substances: Proceedings of the European Society of Toxicology Meeting held in Munich, September 4–7, 1988
J Occup Med 29:762-768 Norseth T (1981) The carcinogenicity of chromium. Environ Health Perspect 40: 121-130 Oldiges H, Glaser U, Hochrainer D (1987) Long-term inhalation study with four different cadmium compounds in rats p. 337-339 Heavy metals in the Environment vol. 1 (Ed. ) CEP consuItants Ud, Edinburgh. Ott MG, Holder BB, Gordon HL (1974) Respiratory cancer and occupational exposure to arsenicals. Arch Environ HeaIth 29:250-255 Pershagen G (1981) The carcinogenicity of arsenic. Environ HeaIth Perspect 40:93-100 Pershagen G, Wall S, Taube A, Linnman L (1981) On the interaction between occupational arsenic exposure and smoking and its relationship to lung cancer.
Schaaper et al (1987) provided data that support the third hypothesis, showing that Ni + + interacts with DNA in vitro, promoting hydrolysis of deoxyadenosine by cleaving bonds between the purine base and deoxyribose, leading to release of adenine. The resulting apurinic sites of DNA are believed to induce mutations du ring subsequent replication by DNA polymerase, mediated by misincorporation of purines, particularly deoxyadenosine, in the daughter strand. Lipid Peroxidation Lipid peroxidation plays an important role in the pathogenesis of acute nickel toxicity (Sunderman 1987).
In: Chromate Symposium 80. Focus of a Standard, Industrial Health Foundation, Pittsburgh, PA, pp 76-99 Petrilli FL, De Flora S (1982) Interpretations on chromium mutagenicity and carcinogenicity. In: Sorsa M, Vainio H (eds) Mutagens in Our Environment, Alan R Liss Inc, New York, NY, pp 453-464 Petrilli FL, De Flora S (1988) Metabolie reduction of chromium as a threshold mechanism limiting its in vivo activity. Sci Total Environ 71 :357-364 Petrilli FL, Camoirano A, Bennicelli C, Zanacchi P, Astengo M, De Flora S (1985) Specificity and inducibility of the metabolie reduction of chromium (VI), mutagenicity by subcellular fractions ofrat tissues.
Biological Monitoring of Exposure and the Response at the Subcellular Level to Toxic Substances: Proceedings of the European Society of Toxicology Meeting held in Munich, September 4–7, 1988 by P. M. D. Foster (auth.), Philip L. Chambers, Claire M. Chambers, Helmut Greim (eds.)