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.

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.

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.

Arachidonic acid cytotoxicity in leukocytes: implications of oxidative stress and eicosanoid synthesis.

Arachidonic acid (AA)-induced cytotoxicity was evaluated in leukocytes: the human leukemia cell lines HL-60, Jurkat and Raji and in rat lymphocytes. Such cytotoxicity was dose- and time-dependent. At concentrations below 5 microM, AA was not toxic; at 10-400 microM, AA induced apoptosis and at concentrations beyond 400 microM, necrosis.