Endorphin Excess at Weaning Durably Influences Sexual Activity, Uterine Estrogen Receptor’s Binding Capacity and Brain Serotonin Level of Female Rats

2019

Hormonal imprinting takes place perinatally at the first encounter between the developing hormone receptor and its target hormone. This process is needed for the normal function of the receptor- hormone pair and its effect is life-long. However, in this critical period, when the developmental window is open, related molecules (members of the same hormone family, synthetic hormones and hormone-like molecules, endocrine disruptors) also can be bound by the receptor, causing life-long faulty imprinting. In this case, the receptors’ binding capacity changes and alterations are caused at adult age in the sexual and behavioral sphere, in the brain and bones, inclination to diseases and manifestation of diseases, etc. Hereby, faulty hormonal imprinting is the basis of metabolic and immunological imprinting as well as the developmental origin of health and disease (DOHaD). Although the perinatal period is the most critical for faulty imprinting, there are other critical periods as weaning and adolescence, when the original imprinting can be modified or new imprintings develop. Hormonal imprinting is an epigenetic process, without changing the base sequence of DNA, it is inherited in the cell line of the imprinted cells and also transgenerationally (up to 1000 generations in unicellulars and up to the 3rd generation in mammals are justified). Considering the enormously growing number and amount of faulty imprinters (endocrine disruptors) and the hereditary character of faulty imprinting, this latter is threatening the whole human endocrine system.

Section: The Late Hormonal Imprintingsmentioning

confidence: 99%

Hormonal Imprinting: The First Cellular-level Evidence of Epigenetic Inheritance and its Present State

2019

“…These materials change not only the receptors of their own, but related receptors, too. A single, minimal dose endorphin treatment at weaning life-long influences the endorphin and serotonin content of immune cells, cells of some brain regions, the binding capacity of uterine estrogen receptors, and sexual activity (Csaba et al 2004a, b, c). Treatment with the tricyclic antidepressant mianserin (Csaba et al 2003c) as well as H1 receptor blocker terfenadine (Csaba et al 2003b) durably influence the histamine content of white blood cells.…”

Section: The Late Imprintingmentioning

confidence: 99%

The biological basis and clinical significance of hormonal imprinting, an epigenetic process

2011

Clin Epigenet

The biological phenomenon, hormonal imprinting, was named and defined by us (Biol Rev, 1980, 55, 47-63) 30 years ago, after many experimental works and observations. Later, similar phenomena were also named to epigenetic imprinting or metabolic imprinting. In the case of hormonal imprinting, the first encounter between a hormone and its developing target cell receptor—usually at the perinatal period—determines the normal receptor-hormone connection for life. However, in this period, molecules similar to the target hormone (members of the same hormone family, synthetic drugs, environmental pollutants, etc), which are also able to bind to the receptor, provoke faulty imprinting also with lifelong—receptorial, behavioral, etc.,—consequences. Faulty hormonal imprinting could also be provoked later in life in continuously dividing cells and in the brain. Faulty hormonal imprinting is a disturbance of gene methylation pattern, which is epigenenetically inherited to the further generations (transgenerational imprinting). The absence of the normal or the presence of false hormonal imprinting predispose to or manifested in different diseases (e.g., malignant tumors, metabolic syndrome) long after the time of imprinting or in the progenies.

Hormonal imprinting: phylogeny, ontogeny, diseases and possible role in present‐day human evolution

Cell Biochemistry & Function

2007

Hormonal (chemical) imprinting which was first observed (and named) by us in the seventies of the last century, is a general biological phenomenon which takes place when the developing receptor meets its target hormone for the first time. Under the effect of imprinting, receptors mature and reach their maximal binding capacity. It also influences the cells' hormone production and different functions depending on receptors and hormones. Hormonal imprinting is present already at the unicellular level causing the development of specific receptors and helping the easier recognition of useful or harmful surrounding molecules. The phenomenon is an important factor in the survival of the species, as the effect of imprinting is transmitted to the progeny cell generations. At the same time it possibly helps the selection of molecules which are suitable for acting as hormones in higher ranked animals. In mammals, hormonal imprinting takes place perinatally and determines the function of receptor-signal-transduction systems as well as hormone production for life. However, there are other critical imprinting periods for continuously developing cells. Excess of the target hormones or presence of foreign molecules which are able to bind to the receptors, provoke faulty imprinting in the critical periods with life-long morphological, biochemical, functional or behavioural consequences. As many receptor-bound foreign molecules are used as medical treatments and many such molecules are present around us and inside us as environmental pollutants, they--causing faulty imprinting--are able to predispose the (human) organism to cardiovascular, endocrine, metabolic and cancerous diseases. It seems likely that this effect is connected with disturbance of DNA methylation process in the critical periods of life. There are some signs of the transgenerational effect of faulty imprinting and this could be manifested in the evolution of humans by an epigenetic route.