Metformin reduces the stimulatory effect of obesity on in vivo Walker-256 tumor development and increases the area of tumor necrosis.

AIMS: The objective of this study was to analyze the influence of obesity and insulin resistance on tumor development and, in turn, the effect of insulin sensitizing agents. MAIN METHODS: Male offspring of Wistar rats received monosodium glutamate (400mg/kg) (obese) or saline (control) from the second to sixth day after birth. Sixteen-week-old control and obese rats received 5×10(5) Walker-256 tumor cells, subcutaneously injected into the right flank. Some of the obese and control rats received concomitant treatment with metformin (300mg/kg) by gavage. At the 18th week, obesity was characterized. The percentage of rats that developed tumors, the tumor relative weight and the percentage of cachexia incidence were analyzed. The tumor tissue was evaluated histologically by means of hematoxylin and eosin staining. KEY FINDINGS: Metformin did not correct the insulin resistance in obese rats. The tumor development was significantly higher in the obese group, whereas metformin treatment reduced it. After pathological analysis, we observed that the tumor tissues were similar in all groups except for adipocytes, which were found in greater quantity in the obese and metformin-treated obese groups. The area of tumor necrosis was higher in the group treated with metformin when compared with the untreated one. SIGNIFICANCE: Metformin reduced Walker-256 tumor development but not cachexia in obese rats. The reduction occurred independently of the correction of insulin resistance. Metformin increased the area of necrosis in tumor tissues, which may have contributed to the reduced tumor development.

Comparison of the anti-neoplastic effects of dirhodium(II) tetrapropionate and its adducts with nicotinate and isonicotinate anions in mice bearing Ehrlich tumors.

Rhodium(II) propionate, [Rh2(prop)4], and its adduct with nicotinate (nic-) and isonicotinate (isonic-) anions, [Rh2(prop)4(nic)2](2-) and [Rh2(prop)4(isonic)2](2-), respectively, were prepared for study. The compound effects on the survival rate of mice bearing Ehrlich ascites tumors were tested and presented in the form of a survival table, and analyzed by the Mantel-Haenszel chi-square test for N animals in each group. The survival rates of animals were significantly higher than that of control group (P<0.001) without distinguishing among the experimental groups. The estimated probability for an animal in the control group to survive up to the end of the observation period (30 days) was below 33%, whereas the animal groups in the treated group with complex, and its nicotinate and isonicotinate groups showed 85%, 85% and 90%, respectively, of surviving over the same period. The T/C values (survival average of the animals treated group/survival average of the animals control group) were obtained for each compounds being for the dirhodium propionate T/C=250, and for its adducts with nicotinate and isonicotinate anions, 267 and 264, respectively.

Apoptosis induced by metal complexes and interaction with dexamethasone.

Apoptosis induced by rhodium II amidate, rhodium II propionate, cisplatin and interactions with dexamethaxone were studied on some human leukemia cell lines Raji, Jurkat and U937. Apoptosis was studied by flow cytometry, agarose gel electrophoresis and morphological analysis. Rhodium II propionate induced apoptosis in all the three cell lines, Rhodium II amidate, in the lymphoid cell lines Jurkat and Raji, and cisplatin, only in the Jurkat, a T lymphoid cell line. It has also been observed that the addition of dexamethasone enhances the apoptosis index only in U937, a monocytic line with a glucocorticoid receptor bearing.

Estrógeno em tumor de Ehrlich: estudo da sobrevida e avaliaçäo da resposta imunológica / Estrogen in Ehrlich's tumor survival study and immune response evaluation

Estudou-se a sobrevida de camundongos inoculados com tumor de Ehrlich na vigência de tratamento estrogênico, e concomitantemente fêz-se uma avaliaçäo da atividade imunológica em um grupo paralelo. Concluiu-se que os estrógenos aceleram a mortalidade de camundongos machos portadores de tumor de Ehrlich e näo provocavam alteraçöes no número de macrófagos e atividade fagocitária em resposta à inflamaçäo. Os camundongos que receberam tumor de Ehrlich também näo apresentaram diferenças em relaçäo ao grupo de camundongos normais