Efeito da melatonina e do estrógeno sobre o crescimento do tumor de Ehrlich em camundongos swiss

Abstract

Breast tumors are estrogen-dependent and receptors are related to the first bitch death cause. The cancer cells spreading induced by estrogen, could be melatonin suppressed, that comes from the pineal gland. Knowing the proceeding importance of these hormones on the breast carcinomas development, the purpose of this study was assess the melatonin and estrogen effects on Ehrlich tumor in Swiss mice, through its interaction with the reproductive system. The experiments were carried out in 104 female Swiss mice (Mus musculus), 8 weeks old, obtained from the Pharmacology Laboratory from DMFA-UFRPE. The animals were maintained on a 12 hours light/dark cycle, at 22 ºC, and food and water were freely available. They were divided in the respective groups (n= 8 animals/group): A- Pinealectomized melatonin treated; B- Sham-Pinealectomized melatonin treated; C- Pinealectomized no treated; D- Sham-Pinealectomized no treated; E- Pinealectomized melatonin vehicle treated; F- Sham-Pinealectomized melatonin vehicle treated; G- Control; H- Pinealectomized melatonin and estrogen treated; I- Sham-Pinealectomized melatonin and estrogen treated; J- Pinealectomized estrogen treated; K- Sham-Pinealectomized estrogen treated; L- Pinealectomized estrogen vehicle treated; M- Sham-Pinealectomized estrogen vehicle treated. It could be noticed in the ovaries a higher follicle number in pinealectomized estrogen treated group, there was a corpus luteum increase compared to other groups in Sham-Pinealectomized melatonin treated group. The experiments showed a high tumor growth in the pinealectomized groups and in the estrogen treated groups, while it has observed a higher tumor inhibition percentage in the animals that received melatonin treatment. The estrogen treated animals presented a less cumulative survival relative to the other groups. Analysis of these results allows us to conclude that estrogen and melatonin, through its actions in the ovary interfere with regulatory mechanisms of the processes of Ehrlich tumor growth.