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Ciba Foundation Symposium 76 - Environmental Chemicals,

Content:
Chapter 1 Chairman's advent (pages 1–2):
Chapter 2 The function of the Drug?Metabolizing Enzymes (pages 5–24): James W. Bridges
Chapter three The impact of Inducers on Drug?Metabolizing Enzyme job and on Formation of Reactive Drug Metabolites within the Liver (pages 25–42): Sten Orrenius, Hjordis Thor and Bengt Jernstrom
Chapter four results of Inducers and Inhibitors on Drug?Metabolizing Enzymes and on Drug Toxicity in Extrahepatic Tissues (pages 43–66): Michael R. Boyd
Chapter five Induction of Enzymes keen on DNA fix and Mutagenesis (pages 67–81): B. A. Bridges
Chapter 6 Induction of Drug?Metabolizing Enzymes via Polycyclic fragrant Hydrocarbons: Mechanisms, and a few Implications in Environmental wellbeing and fitness study (pages 83–99): John R. Bend
Chapter 7 Induction of Drug?Metabolizing Enzymes via Phenobarbitone: Structural and Biochemical elements (pages 101–118): Urs A. Meyer, Peter J. Meier, Hans Hirsiger, Urs Giger and Felix R. Althaus
Chapter eight Substrate?Dependent Irreversible Inactivation of Cytochrome P?450: Conversion of Its Haem Moiety into changed Porphyrins (pages 119–139): Francesco De Matteis, Anthony H. Gibbs, Lavinia Cantoni and Jean Francis
Chapter nine legislation of Human Drug Metabolism via nutritional components (pages 147–167): A.H. Conney, M.K. Buening, E.J. Pantuck, C.B. Pantuck, J.G. Fortner, K.E. Anderson and A. Kappas
Chapter 10 Infiuence of overseas Compounds on Formation and Disposition of Reactive Metabolites (pages 169–189): F. Oesch
Chapter eleven Pharmacokinetic components Governing the Steady?State Concentrations of international chemical substances and Their Metabolites (pages 191–217): James R. Gillette
Chapter 12 Toxicological Implications of Polymorphic Drug Metabolism (pages 219–244): J.C. Ritchie, T.P. Sloan, J.R. Idle and R.L. Smith
Chapter thirteen Immunologically Mediated Toxicity (pages 245–259): H.E. Amos
Chapter 14 Toxicological importance of Liver Hypertrophy Produced by way of Inducers of Drug?Metabolizing Enzymes (pages 261–274): Emmanuel Farber
Chapter 15 The impact of meals and Inducers on Mechanisms of Toxicity in people and Animals (pages 275–288): Andre E.M. McLean, David J. Wltts and Denise Tame
Chapter sixteen impression of Environmental chemical compounds on Drug treatment in people: reviews with Contraceptive Steroids (pages 289–306): A.M. Breckenridge, D.J. again, Karen go, Francesca Crawford, M. MacIver, M. L'E Orme, P.H. Rowe and Eileen Smith
Chapter 17 diet D Metabolism in sufferers taken care of with Phenytoin and Phenobarbitone (pages 315–330): J.O. Hunter and M. Davie
Chapter 18 Chemical disorder in people: difficulties in Comparative Toxicology (pages 331–347): Irving J. Selikoff
Chapter 19 Implications for destiny reviews in people (pages 349–358): John Higginson

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Extra info for Ciba Foundation Symposium 76 - Environmental Chemicals, Enzyme Function and Human Disease

Example text

It is unlikely that drug-metabolizing enzymes are randomly distributed throughout all cells in a particular extrahepatic organ; instead, they are more likely to be confined to relatively few types of cell which might therefore be especially susceptible to damage by compounds that require metabolic activation. Hybrid mechanisms. In reality, mechanisms A, B-I, and B-I1 represent extremes, and an actual case of chemical toxicity may not be described completely by one particular model. Thus, many types of extrahepatic toxicity may fall into ‘hybrid’ categories, such as A/B (in which both the parent compound and its metabolite(s) are toxic) or B-I/B-I1 (in which toxic metabolites in extrahepatic tissue are carried from the liver by the circulation, and are also formed in situ).

I also have a point about carbon tetrachloride. We have shown that if cysteine is given in vivo, protection against carbon tetrachloride does not occur (unpublished work). We found in liver cells that chelating agents will completely block lipid peroxidation, but the damage by paracetamol is not altered. O mM carbon tetrachloride and 20-90 FM benzo[a]pyrene. Further, I cannot claim that the isolated hepatocyte system represents the normal physiological situation. Our system for studying toxicity has, however, several advantages.

By definition, in mechanism I1 the toxic metabolites are sufficiently chemically stable to enter the circulation from the liver, and thereby to gain access to many extrahepatic tissues and cells where they may produce toxic responses. On the other hand, in mechanism I, ultimate toxic products might be generated more discretely, in specific extrahepatic tissues or cell types. It is unlikely that drug-metabolizing enzymes are randomly distributed throughout all cells in a particular extrahepatic organ; instead, they are more likely to be confined to relatively few types of cell which might therefore be especially susceptible to damage by compounds that require metabolic activation.

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