TY  - JOUR
  - O'Driscoll, D.a , Škrabáková, Z.a b , O'Halloran, J.b c , Van Pelt, F.N.A.M.b d , James, K.J.b
  - 2011
  - Environmental Science and Technology
  - Mussels increase xenobiotic (azaspiracid) toxicity using a unique bioconversion mechanism
  - Validated
  - ()
  - 45
  - 7
  - 3102
  - 3108
  - Azaspiracid Poisoning (AZP) is a human toxic syndrome which is associated with the consumption of bivalve shellfish. Unlike other shellfish, mussels contain a large array of azaspiracid analogs, many of which are suspected bioconversion products. These studies were conducted to elucidate the metabolic pathways of azaspiracid (AZA1) in the blue mussel (Mytilus edulis) and revealed that the main biotransformation product was the more toxic demethyl analog, AZA3. To elucidate the mechanism of this C-demethylation, an unprecedented xenobiotic bioconversion step in shellfish, AZA1 was fed to mussels that contained no detectable azaspiracids. Triple quadrupole mass spectrometry (MS) and high resolution Orbitrap MS were used to determine the uptake of AZA1 and the toxin profiles in three tissue compartments of mussels. The second most abundant bioconversion product was identified as AZA17, a carboxyl analog of AZA3, which is a key intermediate in the formation of AZA3. Also, two pairs of isomeric hydroxyl analogs, AZA4/AZA5 and AZA7/AZA8, have been confirmed as bioconversion products for the first time. Ultra high resolution (100 k) MS studies showed that the most probable structural assignment for AZA17 is 22-carboxy-AZA3 and a mechanism for its facile decarboxylation to form AZA3 has been proposed. © 2011 American Chemical Society.
  - http://www.scopus.com/inward/record.url?eid=2-s2.0-79953252748;partnerID=40;md5=f1472f32caa6308493e06cf705956743
DA  - 2011/NaN
ER  - 

@article{V153446286,
   = {O'Driscoll,  D.a  and  Škrabáková,  Z.a b  and  O'Halloran,  J.b c  and  Van Pelt,  F.N.A.M.b d  and  James,  K.J.b },
   = {2011},
   = {Environmental Science and Technology},
   = {Mussels increase xenobiotic (azaspiracid) toxicity using a unique bioconversion mechanism},
   = {Validated},
   = {()},
   = {45},
   = {7},
  pages = {3102--3108},
   = {{Azaspiracid Poisoning (AZP) is a human toxic syndrome which is associated with the consumption of bivalve shellfish. Unlike other shellfish, mussels contain a large array of azaspiracid analogs, many of which are suspected bioconversion products. These studies were conducted to elucidate the metabolic pathways of azaspiracid (AZA1) in the blue mussel (Mytilus edulis) and revealed that the main biotransformation product was the more toxic demethyl analog, AZA3. To elucidate the mechanism of this C-demethylation, an unprecedented xenobiotic bioconversion step in shellfish, AZA1 was fed to mussels that contained no detectable azaspiracids. Triple quadrupole mass spectrometry (MS) and high resolution Orbitrap MS were used to determine the uptake of AZA1 and the toxin profiles in three tissue compartments of mussels. The second most abundant bioconversion product was identified as AZA17, a carboxyl analog of AZA3, which is a key intermediate in the formation of AZA3. Also, two pairs of isomeric hydroxyl analogs, AZA4/AZA5 and AZA7/AZA8, have been confirmed as bioconversion products for the first time. Ultra high resolution (100 k) MS studies showed that the most probable structural assignment for AZA17 is 22-carboxy-AZA3 and a mechanism for its facile decarboxylation to form AZA3 has been proposed. © 2011 American Chemical Society.}},
   = {http://www.scopus.com/inward/record.url?eid=2-s2.0-79953252748;partnerID=40;md5=f1472f32caa6308493e06cf705956743},
  source = {IRIS}
}