The 1990s: Cross-generational genetic damage evidenced

Independently of each other, EMA (1994) and Chang (1993), for instance, found out that the diverse capacities to bind to this receptor were caused by a mutation/genetic modification.

In plain language: Since the mid-nineties it is certain that the individual different effects of / sensitivities to hazardous substances are by no means fateful, but must always be ascribed to a prior genetic modification/mutation due to the contact with a ligand.

Thanks to researchers as Ema and Chang it has also been known since the mid-nineties that both cytochrome P450 1A1 and the glutathione-S-transferase expression as well as the genetic constitution undergo permanent, i.e., cross-generational modification after an accordingly high exposure to hazardous substances / ligand binding.

It is not least due to the analysis of the human genome that these pathological genetic modifications could be identified. The said analysis led to an improvement of the technical equipment of many medical scientific institutes and universities in the early to mid 1990s.

Over time, a clear picture emerged on the activities following to the bond of the hazardous substance (dioxin or a similar pollutant) to the dioxin receptor in the organism. Researchers around the world came to the same result: the activation of the Ah receptor through dioxin is always followed by the same reaction sequence globally referred to as “Ah receptor signalling pathway”.

It could be described as a fact that the findings of Nebert and Poland served as important leverage for the investigation and research work of the aryl hydrocarbon receptor . Year after year, thousands of doctoral theses in which PhD students describe the cause / pathogenesis of development damage in early childhood, diabetes or Alzheimer’s disease down to the last detail are composed on the basis of their work.