CONICET | Buscador de Institutos y Recursos Humanos

A growing body of evidence indicates that stress is a key factor in the development of several pathologies. It has been reported that chronic, but not acute exposure to stress impairs the immune response. Thyroid hormones and zinc also participate in the control of the immune system. It is suggested that there is comorbidity between stress and cancer; however this hypothesis has not been further tested. The aim of this work was to study the effect of stress in the immune function and the evolution of tumors, and the participation of zinc mineral balance and thyroid axis in this effect. Female BALB/c mice were subjected to chronic restraint stress for three weeks. In order to evaluate the status of the immune response in normal and stressed animals, lymphocyte proliferation to both T and B selective mitogens was evaluated by [3H]-thymidine incorporation. A significant reduction in T cell proliferation was observed in stressed animals, whereas B cell proliferation was unchanged. Thyroid status was evaluated by measuring hormone levels in serum. Both T3 and T4 levels, determined by RIA, were reduced in stressed animals in comparison to controls. In order to evaluate the mineral balance in normal and stressed animals, zinc levels were measured by atomic absorption in mineralized femurs. Zinc levels were lower in femurs of stressed animals than in their normal counterparts. Stressed and normal syngeneic mice were injected subcutaneously with 1x106 LBC T lymphoma cells to generate a solid tumor. Measures of tumor volume indicated that growth is increased in chronically stressed mice as compared to control animals. Additionally, stressed mice displayed an accelerated death rate, indicating a worst prognosis of the neoplasic pathology. Taken together, these results suggest that chronic stress promotes tumor growth by depressing T-cell mediated immunity and that the zinc deficiency-related hypothyroidism would probably contribute to these effects.