Decabromodiphenyl ether (BDE 209), the major congener in the high volume industrial flame retardant mixture "DecaBDE", has recently been shown to be metabolized by carp. To further explore this phenomenon, juvenile rainbow trout were exposed to BDE 209 via the diet for a five month period. Analysis of the whole body homogenate, liver, serum, and intestinal tissues revealed that BDE 209 accumulated in rainbow trout tissues and was most concentrated in the liver. In addition to BDE 209, several hepta-, octa-, and nonaBDE congeners also accumulated in rainbow trout tissues over the same period as a result of BDE 209 debromination. Based on the total body burden of the hepta- through decaBDE congeners, uptake of BDE 209 was estimated at 3.2%. Congener profiles were different among whole body homogenate, liver, and serum, with the whole body homogenates having a greater contribution of the debrominated biotransformation products. Extracts of the rainbow trout whole body homogenates were compared with extracts from a previous experiment with common carp. This comparison revealed that BDE 202 (2,2',3,3',5,5',6,6'-octabromodiphenyl ether) was a dominant debromination product in both studies. To determine whether the observed debromination was metabolically driven, liver microsomal fractions were prepared from both common carp and rainbow trout. Analysis of the microsomal fractions following incubation with BDE 209 revealed that rainbow trout biotransformed as much as 22% of the BDE 209 mass, primarily to octa- and nonaBDE congeners. In contrast, carp liver microsomes biotransformed up to 65% of the BDE 209 mass, primarily down to hexaBDE congeners. These microsomal incubations confirm a metabolic pathway for BDE 209 debromination.

No abstract

No abstract