ABSTRACT
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.
Subject(s)
Breast Neoplasms , Carcinogens, Environmental , Carcinogens , Estradiol , Female , Gonadal Steroid Hormones , Humans , ProgesteroneABSTRACT
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.
Subject(s)
Carcinogens, Environmental/toxicity , Neoplasms/prevention & control , Vaccination , Animals , Antibodies/blood , Antibody Specificity , Autoantibodies/immunology , Carcinogens/toxicity , Carcinogens, Environmental/pharmacokinetics , Cell Line, Tumor , Cocarcinogenesis , DNA Adducts/immunology , Female , Haptens/immunology , Humans , Immunization, Passive , Male , Mice , Mice, Inbred Strains , Neoplasms, Experimental/chemically induced , Neoplasms, Experimental/immunology , Neoplasms, Experimental/prevention & control , Neoplasms, Hormone-Dependent/chemically induced , Neoplasms, Hormone-Dependent/immunology , Neoplasms, Hormone-Dependent/prevention & control , Rats , Rats, Inbred Strains , Risk , Steroids/immunology , Vaccination/adverse effectsABSTRACT
AIM: To investigate the cross-reactivity of the hyperimmune antisera of animals (rabbits) and the sera of oncological patients to polycyclic aromatic hydrocarbons (PAHs) of a similar chemical structure. METHODS: Reactions of antibodies with haptens have been estimated by non-competitive and competitive ELISA with synthesized protein conjugates of PAHs as a coating antigene. RESULTS: All the model rabbit antisera have been stated to react with anthracene, chrysene, pyrene, benzo(a)pyrene and benz(a)anthracene irrespective of the hapten used to immunize animals. The cross-reactivity of serum antibodies to all five PAHs has been found in blood samples of oncological patients. CONCLUSION: It is recommended to use the conjugates of anthracene, chrysene and pyrene for detecting human antibodies to more dangerous environmental carcinogens--benzo(a)pyrene and benz(a)anthracene.
