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Measurements of the cytosolic Ah receptor among four strains of Drosophila melanogaster
Authors:Sanford W. Bigelow  Jakob A. Zijlstra  Ekkehart W. Vogel  Daniel W. Nebert
Affiliation:(1) Laboratory of Developmental Pharmacology, National Institute of Child Health and Human Development, National Institutes of Health, 20205 Bethesda, Maryland, USA;(2) Department of Radiation Genetics and Chemical Mutagenesis, State University of Leiden, Wassenaarseweg 72, 2333 Al Leiden, The Netherlands
Abstract:Four strains of Drosophila melanogaster exhibit differences in aryl hydrocarbon hydroxylase (AHH) inducibility by phenobarbital or Aroclor 1254, yet do not show the typical AHH induction response when exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) or benzo[a]anthracene. Adult flies were nevertheless examined for the presence of cytosolic TCDD-specific binding (Ah receptor). Berlin-K and Haag 79 exhibit AHH induction by Aroclor 1254 and possess detectable amounts of Ah receptor. Hikone-R has negligible AHH inducibility by Aroclor 1254, yet possesses measurable amounts of the receptor. Oregon-K displays AHH induction by Aroclor 1254 but has no detectable levels of the cytosolic receptor. Specific (high-affinity, low-capacity and saturable) binding of [3H-1,6]TCDD to the Ah receptor in D. melanogaster was shown to be similar to that observed in C57BL/6 mouse liver. Similar specific binding of generally labeled [3H]benzo[a]anthracene in D. melanogaster cytosol was not found. These data suggest that the presence of the Ah receptor per se, or quantity of receptor, does not guarantee AHH inducibility by TCDD or benzo[a]anthracene in adults of these four fruit fly strains.
Keywords:Ah locus  Aryl hydrocarbon hydroxylase inducibility  Cytochrome P1-450  Benzo[a]pyrene metabolism  Benzo[a]pyrene mutagenesis  Benzo[a]pyrene recessive lethal mutations    /content/j5455027t0ku4566/xxlarge946.gif"   alt="  beta"   align="  MIDDLE"   BORDER="  0"  >-Naphthoflavone  Aroclor 1254  Phenobarbital
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