Perinatally, the developmental window for the adjustment of hormone receptors to their target hormones is open. The hormonal imprinting which determines the relationship of hormones and receptors for life takes place in this period. The recognition ability of developing receptors is not yet entirely specific, so they could be 'cheated' by false imprinters such as related hormones, drugs, environmental pollutants or certain food components and faulty imprinting may result. This causes a functional developmental abnormality, which is then manifested, at any later time in life, as the alteration of the binding capacity of hormone receptors. With or without the presence of other factors this could cause problems in hormone regulated functions or may result in diseases. So it may be stated that faulty hormonal imprinting, caused by a broad spectrum of receptor level molecules, is acting as a functional teratogen. This means that functional maldevelopment is not restricted to intrauterine life, but can also occur after birth, in the perinatal period. The inclusion of faulty imprinting as maldevelopment widens both the list of functional teratogens and the period of teratogenicity. The importance and danger of faulty imprinting is high, especially considering its heritable (transgenerational) character. Considering the facts, the attitudes in the present-day perinatal treatments and medical training must be changed.
Female rats were treated with beta-endorphin on the 19th day of pregnancy. Serotonin content of immune cells (peritoneal lymphocytes, monocyte-macrophage-granulocyte group (mo-gran), mast cells, blood lymphocytes, granulocytes and monocytes, thymus lymphocytes) were studied in the mothers (P-generation four weeks after delivery), in the male offspring (F1) generation (at seven weeks), in the female offspring (four weeks after their own delivery) and in their offspring (F2 generation, at seven weeks). P-mother cells' serotonin content was not influenced by endorphin treatment, while F1 generation's mo-gran and blood lymphocyte serotonin content was reduced (in contrast, histamine content of mo-gran increased). Four weeks after delivery, an increase in serotonin content was observed in the F1 generation in the peritoneal lymphocytes and mast cells as well as in blood lymphocytes. In contrast, serotonin content was reduced in blood granulocytes and monocytes. In the F2 (grandson) generation, a reduction in mast cell serotonin content and sensitization of blood and thymic lymphocytes to repeated endorphin treatment was provoked. The significant changes were more expressed in the F2 generation compared to F1, also appearing earlier. The results unequivocally suggest that the increase in endorphin levels during late pregnancy can cause permanent changes in the F1 and F2 generations, which means that the imprinting effect can be transgenerationally transmitted.
The effect of histamine in 10 -9 , 10 -12 , 10 -15 and 10 -18 molar concentrations was studied on the beta-endorphin and triiodothyronine (T 3 ) content of peritoneal immune cells (lymphocytes, monocyte-granulocyte group and mast cells), using immunocytochemical flow cytometric method. The lower concentrations (10 -15 and 10 -18 M) were effective, where endorphin content was significantly lowered and T 3 content was significantly elevated. The results call attention to the extreme sensitivity of histamine receptors in this hormonal index and to the specific response by hormone production to histamine, in the immune cells. The new data support the earlier hypothesis, that there is a hormonal network inside the immune system.
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