Distribution and metabolism of triamcinolone acetonide in inbred mice with different cleft palate sensitivities

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Abstract
The distribution and metabolism of labeled triamcinolone acetonide was compared in A/J, C3H, and CBA inbred mice. 3H‐Triamcinolone acetonide (5 mg/kg) administered at day 11.5 of gestation caused 100% cleft palate in A/J, 40% in C3H, and 0% in CBA. A half to 3 h later CBA maternal tissue (skeletal muscle) contained 60% as much radioactivity as did A/J and C3H tissue. CBA mice metabolized the drug faster than A/Js and C3Hs, although levels of unmetabolized drug and metabolites in livers of the three strains were not significantly different. As a consequence of the increased maternal metabolism of the drug in CBAs the level of unmetabolized drug in CBA embryos was 60% of that in A/J and C3H embryos. It is concluded that the cleft palate resistance of CBA embryos derives from the increased maternal metabolism of administered teratogen. However, the greater resistance of C3H than A/J is probably not due to increased metabolism, nor to altered distribution of drug.