The PCBs constitute a series of 209 individual congeners, varying in the number and sites
of chlorine substitution. The biological effects caused by the various congeners differ, not
only in potency but also qualitatively. Our knowledge of the mechanisms of toxicity
indicates that some of the PCB congeners act by the same mechanisms as the chlorinated
dioxins, i.e. the toxicity is probably mediated through interaction with the Ah receptor,
and they are potent inducers of the P448 isoenzymes CYP1A1 and CYP1A2. Other PCB
congeners presumably act by different mechanisms and are potent inducers of a different
set of cytochromes, CYP2B1 and CYP2B2. In addition, there are PCB congeners that are
intermediate in this respect, i.e. they elicit a mixed spectrum of enzyme induction.
Some typical toxic effects of PCBs, such as tumour promotion, are caused by PCB
congeners of all these three classes (CYP1A1/2, CYP2B1/2 and mixed-type inducers), but
the underlying mechanisms are probably different. Our knowledge of possible interactions
between the various groups of PCBs is still very limited.