[Co-genotoxic potential of PCB mixtures from pediatric fatty tissue].

In the present study a mixture containing the 11 PCB major components identified in fatty tissues of children was examined for its potency to enhance the toxification of pregenotoxicants (cogenotoxicity) in the liver. As a basis for the study GC/MS PCB analyses of 207 fatty tissue samples of children were used. The PCB mixture was produced on this basis. As a model for the identification of the cogenotoxic potency of the PCB mixtures an in vivo/in vitro enzyme induction assay was developed. The goal of the study was to clarify the question, whether the in vivo pretreatment of rats with a complex PCB pattern derived from children led to a synergism of cogenotoxicants and pregenotoxicants with regard to the enhancement of the in vitro toxification of benzo[a]pyrene (B[a]P) and 2-aminoanthracene (2-AA) to DNA reactive metabolites. Using the SOS-Chromotest as the in vitro part of the induction assay, all liver enzyme fractions of PCB pretreated rats (S9PCB) showed an increase of the toxification of the pregenotoxicants B[a]P and 2-AA in comparison to enzyme factions of untreated animals (S9(0)). With regard to the reactivity pattern it may be supposed that the PCB mixture probably induced cytochrome P450-dependent oxigenases of the subclasses CYP1A1 and CYP1A2. Additionally, it seems to be of interest that the use of S9(0) fractions did not lead to any or only to weak toxification of B[a]P and 2-AA. Thus, a synergism of cogenotoxicants and pregenotoxicants could be confirmed. PCB could be identified in fatty tissues of children in amounts up to 1 mg/kg. Additionally, pregenotoxicants like polycyclic aromates, mycotoxins and/or aminocontaining compounds, are available in almost all environmental sources. Therefore, from the present point of view, a genetic risk caused by PCB in humans (children) cannot be excluded.