Embryonic Intermediary Metabolism under Normal and Pathological Conditions

Abstract

To elucidate the mode of action of drug-induced teratogenesis, the special susceptibility and sensitivity of the developing embryo to embryotoxic substances, compared to the toxicity seen in the adult organism, has to be considered. A number of parameters may be responsible for these toxicological differences including: (1) possible differences in drug metabolism and pharmacokinetics which may allow an accumulation of a given drug or its metabolites in embryonic cells; (2) the high rate of proliferation in certain stages of prenatal development; (3) typical induction and differentiation processes with characteristic transcriptional and translational regulations obligatory for a normal development; and (4) possible qualitative and quantitative differences in the intermediary metabolism of embryonic cells, for example, a metabolic pathway essential for normal prenatal development might produce little effect if inhibited in an adult organism.