Toxicology of Industrial Compounds

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334 ANTIOXIDANTS AND LIGHT STABILISERS: TOXIC EFFECT Table 23.10 The effect of Compound F on selected biochemical dam and foetal liver parameters related to defence mechanisms against oxidative stress after treatment from day 6 through days 14, 17 and 20 of gestation Notes: Selenium-dependent and selenium-independent glutathione peroxidase activities were determined with cumene hydroperoxide and hydrogen per-oxide as substrate, respectively. Values are means±standard deviation from 6 dams per group and 6 pools of 2–9 foetuses per dam depending on the litter size. Asterisks indicate results significantly different (two-sided Dunnett’s test) from control: * p
compound is known to pass the liver and to be systemically distributed throughout the foetal body. Thus the endothelial cell injuries observed in the course of the Segment II study are regarded secondary to the effect of peroxisome proliferation and to have arisen as a consequence of oxidative damage which has been demonstrated to occur in various endothelial cell systems, for example as a result of iron-mediated oxygen free radical attack (Brieland et al., 1992; Barchowsky et al., 1994; Krautschick et al., 1995). Therefore, the observed foetotoxicity of Compound F in rats is regarded as occurring solely as a consequence of and secondary to peroxisome proliferation, and there is no evidence to assume that this effect as a result of exposure to benzotriazole based light stabilisers may occur in species that are non-responsive to the action of peroxisome proliferators as stated above, including humans. References H.THOMAS ET AL. 335 ABRAHAM, R., BENITZ, K.F., PATIL, G. and LYON, R., 1986, Rapid induction of forestomach tumors in partially hepatectomized Wistar rats given butylated hydroxyanisole, Experimental and Molecular Pathology, 44, 14–20. ANON., 1986, Butylated hydroxyanisole (BHA), IARC Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man, Vol. 40, pp. 123– 59. BARCHOWSKY, A., WILLIAMS, M.E., BINZ, C.C. and CHEPENIK, K.P., 1994, Oxidant-sensitive protein phosphorylation in endothelial cells, Free Radical Biology and Medicine, 16, 771–7. BARTER, R.A. and KLAASSEN, C.D., 1992, Rat liver microsomal UDPglucuronosyltransferase activity toward thyroxin: characterisation, induction and form specificity, Toxicology and Applied Pharmacology, 115, 261–7. BENSON, A.M., CHA, Y.-H., BUEDING, E., HEINE, H.S. and TALALAY, P., 1979, Elevation of extrahepatic glutathione S-transferase and epoxide hydratase activities by 2(3)-tert-butyl-4-hydroxyanisole, Cancer Research, 39, 2971–7. BENTLEY, P., CALDER, I., ELCOMBE, C., GRASSO, P., STRINGER, D. and WIEGAND, H.-J., 1993, Hepatic peroxisome proliferation in rodents and its significance for humans, Food and Chemical Toxicology, 31, 857–907. BRIELAND, J.K., CLARKE, S.J., KARMIOL, S., PHAN, S.H. and FANTONE, J. C., 1992, Transferrin: a potential source of iron for oxygen free radicalmediated endothelial cell injury, Archives of Biochemistry and Biophysics, 294, 265–70. CHOE, S.Y., KIM, H.M. and YANG, K.H., 1984, Effects of butylated hydroxytoluene (BHT) on biliary excretion of xenobiotics and bile flow in rats, Drug and Chemical Toxicology, 7, 149–65. CONNING, D.M. and PHILLIPS, J.C., 1986, Comparative metabolism of BHA, BHT and other phenolic antioxidants and its toxicological relevance, Food and Chemical Toxicology, 24, 1145–8.
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Toxicology of Industrial Compounds
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This edition published in the Taylo
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8. Pulmonary Toxicity Studies with
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Preface A large number of chemical
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Contributors May Akrawi Department
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Beverly M.Kulig TNO Toxicology, Dep
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Richard A.Versen Schuller MTC, Heal
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1 Biomonitoring and Absorption of I
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4 BIOMONITORING AND ABSORPTION OF I
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10 BIOMONITORING AND ABSORPTION OF
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2 Toxicokinetics and Biodisposition
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14 TOXICOKINETICS AND BIODISPOSITIO
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3 Metabolic Activation of Industria
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38 METABOLIC ACTIVATION OF INDUSTRI
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4 Sizing up the Problem of Exposure
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46 SIZING UP THE PROBLEM OF EXPOSUR
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5 Metabolism of Reactive Chemicals
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62 METABOLISM OF REACTIVE CHEMICALS
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6 Methods for the Determination of
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74 METHODS FOR THE DETERMINATION OF
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PART THREE Pulmonary toxicology of
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92 CARCINOGENIC POTENTIAL OF MAN-MA
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100 CARCINOGENIC POTENTIAL OF MAN-M
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118 PULMONARY TOXICITY STUDIES WITH
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130 PULMONARY HYPERREACTIVITY TO IN
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10 Mechanisms of Pulmonary Sensitiz
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140 MECHANISMS OF PULMONARY SENSITI
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150 OCCUPATIONAL ASTHMA INDUCED BY
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12 Biomarkers and Risk Assessment K
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160 BIOMARKERS AND RISK ASSESSMENT
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168 EXTRAPOLATION OF TOXICITY DATA
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14 Molecular Approaches to Assess C
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182 MOLECULAR APPROACHES TO ASSESS
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198 EVALUATION OF TOXICITY TO THE I
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208 USE OF LONG-TERM CULTURES OF HE
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PART FIVE Mechanisms of toxicity of
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224 PEROXISOME PROLIFERATION normal
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226 PEROXISOME PROLIFERATION demons
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228 PEROXISOME PROLIFERATION Specie
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230 PEROXISOME PROLIFERATION intend
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232 PEROXISOME PROLIFERATION BENTLE
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234 PEROXISOME PROLIFERATION KRAUPP
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236 PEROXISOME PROLIFERATION POPP,
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18 Neurotoxicity Testing of Industr
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240 NEUROTOXICITY TESTING OF INDUST
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256 ENDOCRINE TOXICOLOGY OF THE THY
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20 Testing and Evaluation for Repro
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282 TESTING AND EVALUATION FOR REPR
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Page 314 and 315: PART SIX Toxicity of selected class
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Page 370 and 371: 25 Low Dose of a Genotoxic Carcinog
Page 372 and 373: 358 CARCINOGENESIS AT LOW DOSE Tabl
Page 374 and 375: 360 CARCINOGENESIS AT LOW DOSE year
Page 376 and 377: 26 Controversial Mechanistic and Re
Page 378 and 379: 364 CONTROVERSIAL ISSUES IN SAFETY
Page 388 and 389: 374 INDEX 2-bromo-glutathionyl 64 B
Page 390 and 391: 376 INDEX Gas chromatography/mass s
Page 392 and 393: 378 INDEX mRNA analysis 211 Mutagen
Page 394 and 395: 380 INDEX Surfactants 338-55 acute
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