Abstract
The concept of ‘epigenetics’ was established by Waddington (1942) to explain the development and cellular differentiation of animals. Several processes, such as DNA methylation, histone modification, non-coding RNA transcription, and finally chromatin modification, control the cellular molecular mechanisms underlying epigenetics. Epigenetics was originally defined as the interaction between the genome and various environmental conditions. This scientific field is known as ‘Environmental Epigenetics’ and refers to the disruption of normal epigenetics by various environmental factors. Epigenetics comprises biochemical processes; therefore, epigenetics is easily disrupted by a variety of chemical substances in the environment. ‘Environmental Epigenetics’ is strongly correlated with toxicology, clinical medicine, and the psychosocial behaviour of humans. Furthermore, ‘The Developmental Origin of Health and Disease (DOHaD) Theory (Barker, 1968)’ has been accepted in various fields of clinical medicine. The main causes of DOHaD are attributable to epigenetics. Therefore, as in toxicology, the embryonic stages are very important from the standpoint of epigenetics as well.
We have been studying mutagenesis and epimutagenesis induced by chemical substances in mouse somatic and germ cells. We believe that ‘Epigenetic Toxicology’ is especially important during the embryonic stages. Herein, we propose the concept of ‘Embryonic Cells-originated Epigenetic Toxicology’. The test substance will be administered at the embryonic stage. The treated male mice will be mated with untreated female mice for 2 generations. We will test for somatic epigenetic toxicity in the F1 generation and for germinal epigenetic toxicity in the F2 generation . The various toxicological phenomena observed during this experiment could be considered from the viewpoint of ‘Environmental Epigenetics’.
