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Evaluating the relationship between social stress intensity and rapidity of carcinogenesis in an animal model

Zygmunt Steplewski, Katarzyna Steplewska-Mazur, Grzegorz Mazur, Henryk JaskoĊ‚ecki, Magdalena Elsner

Med Sci Monit 1997; 3(6): BR753-757

ID: 501723

Social stressors evolving from individual and population interactions produce stress reactions in many organisms (including humans), influencing homeostasis and altering the activity of the immunological system. Earlier reports showed that social stress, produced by altering social relations in breeding animals, accelerated the formation and growth of adenocarcinoma in rats. The objective of the present study was to identify relationships between intensity of the stress reaction, expressed as blood corticosterone concentrations, and the rapidity of adenocarcinoma growth in these rats. Sprague-Dawley rats were used for the studies. Stress reaction were induced through changes in g the roup relations of the rats' progeny after birth. The induction of adenocarcinoma was provoked chemically through DMBA administration or through inoculation of cultured neoplastic cells. Corticosterone concentrations were evaluated radioimmunologically. The rate of the neoplastic process was evaluated by weighing the dissected tumors. The results indicated that adenocarcinoma, induced chemically or through inoculation of tumor cells, develops faster in those animals which were separated from their mothers after termination of suckling and were then raised individually, than in those which remained with their mothers. The most rapid growth of adenocarcinoma was recorded in those animals which were separated from their mothers, kept in groups for a period of two weeks and then put into individual cages. Acceleration of carcinogenesis corresponded to the strength of the stress reaction, expressed as blood corticosterone concentrations. The results obtained imply a promoting effect of stress reactions upon carcinogenic processes. A possible responsible factor is the immunosuppresive effect of some components of the stress reaction, for instance corticosteroides.

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