Inversion of natural immuno-hormonal interactions under influence of antibodies against environmental chemical carcinogens.

In this article we present a hypothesis that interactions between sex hormones and specific antibodies change inversely in presence of antibodies against environmental carcinogens. Natural occurrence antibodies to estradiol (E2) and progesterone (Pg) do not influence on E2 concentration, but antibodies to Pg increase Pg concentration in blood serum of postmenopausal healthy women with low levels of antibodies against benzo[a]pyrene (Bp). Thereby natural occurrence antibodies to Pg inhibit the promotion of breast carcinogenesis. Antibodies to E2 and Pg increase E2 concentration but decrease Pg concentration when the levels of antibodies to Bp are high. Therefore, antibodies against Bp switch hormonal effects of antibodies to E2 and Pg from the increase of Pg concentration to the increase of E2, thus stimulating breast cancer promotion. These immuno-hormonal interactions are weaker in breast cancer patients, probably due to corresponding anti-idiotypic antibodies.

Immunomodulation of carcinogens-induced steroids-dependent human diseases.

The experimental and clinical data about antibodies against environmental chemical carcinogens and endogenous steroids are represented. The conception of immunomodulation of carcinogens- and steroids-dependent human diseases is proposed. It is postulated that antibodies to polycyclic aromatic hydrocarbons and heterocyclic amines in cooperation with antibodies to cholesterol, sex hormones, mineralo- and glucocorticoids stimulate or inhibit cancer, malformation, cardiovascular and autoimmune diseases depending on their personal combination. It is recommended to use immunoassay of these antibodies for the human diseases prediction. The alternative approaches for prevention using the probiotics transformed by anti-carcinogen antibodies are substantiated.

Immunization against environmental chemical carcinogens: Pro and contra.

The problems of immunoprotection from the environmental chemical carcinogens are discussed. The main experimental argument pro active immunization against carcinogens is a possibility of specific mucosal antibodies (Abs) to inhibit the penetration of carcinogens from environment and to stimulate its excretion with the following decreasing of carcinogen-DNA adducts levels. Hypothesis of cancer immunostimulation after active immunization against carcinogens is based on a high cancer risk in persons with high levels of serum Abs specific to environmental carcinogens coupled with high levels of Abs to endogenous steroids stimulating the proliferation of target cells, for example, Abs to benzo[a]pyrene together with Abs to estradiol. The active immunization could increase the cancer risk much more in those persons. The passive immunization could be an alternative safe approach to avoid this problem.

Immunostimulation of the chemical-induced carcinogenesis in the phase of initiation MH-G 0166.

It is postulated that the immune reaction on chemical carcinogens can inhibit or stimulate the chemical-induced carcinogenesis depending on the individual peculiarities of the synthesis of antibodies. Critical events take place on the barriers between external and internal media. Antibodies to chemical carcinogens, which are secreted into the digestive or bronchial tract, bind the environmental carcinogens and prevent them from penetrating into the blood through the epithelium and thereby inhibit the beginning of the tumour growth in any organs. On the contrary, the serum antibodies promote the penetration of carcinogens through the digestive and bronchial epithelia and thereby stimulate carcinogenesis in the proper organs. The other events take place in the organs such as breast and prostate where carcinogens are transported from the blood. Secretory antibodies bind carcinogens in the blood and transport them through the epithelium of these glands and thereby stimulate the tumour origin in these organs. Antibodies, which are not secreted into the ducts of breast and prostate, hold carcinogens in the blood and thereby inhibit carcinogenesis in these organs. Antibodies to steroid hormones function in the same way, i.e., secretory antibodies stimulate, while the serum antibodies inhibit the genetoxic action of the hormones on breast and prostate. The stimulation of carcinogenesis in the lymphoid cells is realized owing to hapten-specific binding of carcinogens by the membrane receptors of the corresponding clones. Antibodies to the natural inhibitors of carcinogenesis (retinoids, tocopherole, etc.) stimulate the beginning of the tumour growth. Antibodies to carcinogens and antiidiotypic antibodies to the cytochromes p-450 may act as abzymes, i.e., as cytochromes p-450 and thereby increase the level of the carcinogen metabolites.