. 2010 Oct 20;119(1):189–208. doi: 10.1093/toxsci/kfq314

TABLE 2.

Genotypes of Mice Chosen for These Studies

AHR allele	AHR ligand affinity	CYP1A2	Genotype	Common name	Predicted phenotype^a
Ahr^b1	High affinity	Absent	Ahr^b1Cyp1a2(−/−)	Cyp1a2(−/−) knockout	Most vulnerable to PCB mixture
Ahr^d	Poor affinity	Absent	Ahr^dCyp1a2(−/−)		Almost as vulnerable
Ahr^d	Poor affinity	Present	Ahr^dCyp1a2(+/+)	B6.D2-Ahr^d	Almost as resistant
Ahr^b1	High affinity	Present	Ahr^b1Cyp1a2(+/+)	C57BL/6J (B6)	Most resistant

We predict that the most important factor—leading to PCB-induced poor growth rate—would be absence of maternal liver CYP1A2. Of less importance, but still to be reckoned with, is the high-affinity AHR maternal-fetal unit in which CYP1 enzymes are highly induced by the coplanar PCB ligands (and therefore PCBs are cleared from the tissues); alternatively, and competing with detoxication, more reactive PCB intermediates might be formed.