By Ciba Foundation Symposium 26
Chapter 1 Chairman's creation (pages 1–3): Alan S. Curry
Chapter 2 The Clinician's standards from the Laboratory within the therapy of the Acutely Poisoned sufferer (pages 5–15): R. W. Newton
Chapter three The position of the Laboratory within the therapy of Narcotic Poisoning (pages 17–28): Vincent P. Dole
Chapter four Formation of Reactive Metabolites as a explanation for Drug Toxicity (pages 29–55): James R. Gillette
Chapter five Separation and Detection of risky Metabolites of Amphetamines, Analgesics and Phenothiazines (pages 57–82): A. H. Beckett
Chapter 6 overview of Chromatographic and Spectroscopic methods (pages 83–103): A. C. Moffat
Chapter 7 Use of fuel Chromatography?Mass Spectrometry in Toxicological research (pages 105–124): Bo Holmstedt and Jan?Erik Lindgren
Chapter eight decision of hashish elements in Blood (pages 125–137): Stig Agurell
Chapter nine Drug Assay by means of Radioactive Reagents (pages 139–154): W. Riess
Chapter 10 An On?Line Liquid Chromatograph?Mass Spectrometer method (pages 155–169): R. P. W. Scott, C. G. Scott, M. Munroe and J. Hess
Chapter eleven Luminescence equipment in Drug research (pages 171–192): J. W. Bridges
Chapter 12 Immunoassay of substances (pages 193–200): Irving Sunshine
Chapter thirteen Immunological tools for Detecting medications: their software within the Detection of Digitoxin, Digoxin and Morphine (pages 201–217): Charles W. Parker
Chapter 14 Drug research within the Overdosed sufferer (pages 219–238): B. Widdop
Chapter 15 The Morbid Anatomist's position in Drug Detection (pages 239–251): D. J. Gee
Chapter sixteen Drug?Induced Iatrogenic affliction: the chance of its Detection (pages 253–268): Henry Leach
Chapter 17 obstacles of Haemodialysis and compelled Diuresis (pages 269–289): L. F. Prescott
Chapter 18 The Poisoned sufferer: The Clinician and the Laboratory (pages 291–314): Roy Goulding
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Extra resources for Ciba Foundation Symposium 26 - The Poisoned Patient: The Role of the Laboratory
1971). Although these h t studies indicated that the toxicity was not mediated by bromobenzene but by one of its metabolites, they did not indicate whether 40 JAMES R. GILLETTE the active metabolite was chemically reactive or inert. Nevertheless, autoradiographic studies after the administration of radiolabelled bromobenzene revealed that a reactive metabolite combined preferentially with macromolecules in the centrilobular necrotic areas of liver (Brodie et al. 1971). Moreover, subsequent studies showed that pretreatment of rats with phenobarbitone increased the rate and the maximum amount of covalent binding of radiolabelled bromobenzene to liver macromolecules, whereas prior administration of SKF 525-A decreased it (Reid et al.
Although the decrease in glutathione might by itself lead to the liver necrosis caused by bromobenzene, other substances such as diethyl maleate bring glutathione concentrations in liver (Boyland & Chasseaud 1970) down to about the same extent as does bromobenzene, but do not cause necrosis. However, the severity of necrosis and the magnitude of the covalent binding can be markedly increased by the prior administration of diethyl maleate (Reid & Krishna 1973; Reid 1973), which depletes liver glutathione without causing necrosis.
But glutathione is rapidly synthesized in liver and thus much of the bromobenzene epoxide is still inactivated by its conjugation with glutathione (about 50% in rats), even after the concentrations of glutathione in liver have decreased to very low levels (Zampaglione et al. 1973). However, the rate of synthesis of the glutathione conjugate is now limited by the rate of synthesis of glutathione, and therefore is no longer directly proportional to the bromobenzene epoxide concentration ; thus the proportion of the bromobenzene epoxide that is inactivated by formation of the glutathione conjugate can be altered by changing the rate of formation of the epoxide.