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.
Glushkov
Andrew N
AN
Department of Cancer Immunology, Russian Academy of Sciences, Kemerovo, Russia. glushkov@ksma.kuzstu.ac.ru
D000818:Animals; D000906:Antibodies / Q000276:immunology* / Q000494:pharmacology; D000888:Antibodies, Anti-Idiotypic / Q000276:immunology; D016588:Anticarcinogenic Agents / Q000276:immunology; D001692:Biological Transport / Q000187:drug effects; D001711:Biotransformation / Q000276:immunology; D001940:Breast / Q000378:metabolism; D001980:Bronchi / Q000378:metabolism; D002274:Carcinogens, Environmental / Q000009:adverse effects* / Q000493:pharmacokinetics; D002471:Cell Transformation, Neoplastic / Q000139:chemically induced / Q000276:immunology*; D003577:Cytochrome P-450 Enzyme System / Q000276:immunology; D004848:Epithelium / Q000378:metabolism; D005260:Female; D006241:Haptens / Q000378:metabolism; D006728:Hormones / Q000009:adverse effects / Q000276:immunology; D006801:Humans; D007408:Intestinal Absorption; D008297:Male; D051379:Mice; D008954:Models, Biological; D011467:Prostate / Q000378:metabolism; D013256:Steroids / Q000009:adverse effects / Q000276:immunology
D000906:Antibodies; D000888:Antibodies, Anti-Idiotypic; D016588:Anticarcinogenic Agents; D002274:Carcinogens, Environmental; D006241:Haptens; D006728:Hormones; D013256:Steroids; D003577:Cytochrome P-450 Enzyme System