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RE: mill effluent chloro-xanthene as toxic as tcdd; great lakes; cardiovascular

  I did reply to the entire list.
   I think that Safe was saying that they do not cause effects when binded
  to the Ah and hence the copetition for the binding site actually reduces
  effects of the TCDD.  He states" When coadministered, MCDF diminished
  the ability of 2,3,7,8-TCDD to induce these and other enzyme activities
  (aryl hydrocarbon hydroxylase, AHH, and 7-ethoxyresorufin
  O-dealkylation, EROD).  The 96 paper could have identified the xanthene
  correctly, but understanding the pulp mill process, the MCDF possibility
  is a better bet.  I have inquired with some folks at a research arm of
  the pulp industry and will keep you informed.
  Dennis Catalano
  From: ttweed@wildrockies.org
  To: Catalano, Dennis
  Subject: RE: mill effluent chloro-xanthene as toxic as tcdd; great
  lakes; cardiovascular
  Date: Thursday, July 17, 1997 7:08AM
  thanks.  i'll never understand why people who are motivatd to reply w/
  useful info don't reply to all interested parties, ie to the
  does safe believe that they are biologivally inert, as to Ah mediated
  effects, or only that they compete w/ other Ah binders?  also, it would
  seem reasonable to suppose that inc.'96, they may have identified the
  xanthene correctly...
  >A 1989 paper by Hans-Rudolf Buser, Lars-Owe Kjeller, Stephen Swanson,
  >and Christoffer Rappe states that errors were made when the initial
  >research was performed on pulp mill effluent and sediment down stream
  >from mills.  The compounds initially thought to be chloroxanthene was
  >actually methylated chlorofurans.  These compounds can not be
  >distinguished  by HRMS and some very good research was performed to
  >indicate that the latter compounds were the compounds found in effluent.
  > This paper states that the toxicalogical significance of the
  >alkyl-PCDFs is not known, but research by Safe and coworkers suggest
  >that they act as effective antagonists to TCDD.  They compete with the
  >TCDD for binding sites to the Ah receptor and thus block the TCDD
  >activity.  These compounds diminish the ability of TCDD to induce enzyme
  >Dennis Catalano
  tony tweedale