Abstract
e14052 Background: Along with tumor itself, mechanisms of regulation of homeostasis are the target for tumor progression inhibition. The brain, various organs and tumor have different resources of energetic and metabolic substrates. Involvement of cyclic adenosine monophosphate (cAMP) into intimate mechanisms of proliferation, hormonal and energetic homeostasis indicates the possibility to use this factor in chemotherapy of tumors to improve the resistance of the organism. The purpose of the study was to analyze levels of endogenous cAMP in tumor and in organs as a criterium of systemic body response to chemotherapy with cAMP application. Methods: The study included 56 male Wistar rats with Heren’s carcinoma receiving peritumoral injections of cyclophosphan (CP) 50 mcg/kg (Baxter Oncology GmbH, Germany) alone and in combination with cAMP (Sigma-Aldrich, USA), P.O. at a concentration of 0.01%. cAMP levels in homogenates of organs and tumors were measured by immunoradiometric assay (Immunotech, Czech Republic) using Arian radiometer (Vitaco, Russia). Data were processed using Statistica 6. Results: cAMP levels in growing tumors in rats without treatment (the control) were maximal (7.03±1.5 nmol/L). CP injections alone during inhibition of carcinoma growth allowed the reduction of tumor cAMP level by 3.3 times. Combination of CP and cAMP resulted in tumor regression, and endogenous cAMP levels in tumor decreased by 10 times compared with the control. Similar dynamics of cAMP reductions was noted in the adrenal glands. The lungs, thymus, lymph nodes and especially the testes and the brain, on the contrary, showed accumulation of cAMP to the normal levels and higher. Conclusions: The range of cAMP levels in organs and tumors of rats receiving combination of CP and cAMP demonstrated the development of adaptive and regenerative processes in organs responsible for the neuroendocrine regulation, suppression of stimulation of stress-realizing systems and metabolic support of the processes of increasing non-specific antitumor resistance along with inhibited proliferative activity of tumors.
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