B16F10 was the most sensitive to all treatments and SK-MEL-1 the most resistant. Melphalan was the most active individual drug and 4-HA the least. Combinations of two drugs did not result in improved activity compared with drugs administered alone. Pretreatment with modulator seems to be a potential method for enhancing some treatments.

By means of optical and electron microscopy and by atomic absorption spectrophotometry in a graphite chamber, this study evaluated the effect of temperature (22-35 degrees C) on lesions in the kidney, liver, and brain, and on concentrations of lead caused by the administration of 2 and 5 mg/kg/IP of lead acetate to Swiss mice. The most pronounced effects were observed in the kidney and in groups of animals receiving the highest doses (5 mg/kg at 22 and 35 degrees C). These effects consisted of significantly higher (p < .05) lead concentrations in the tissues, a significant decrease (p < .05) in kidney weights, and progressive kidney atrophy and fibrosis with, at the ultrastructural level, constant intranuclear inclusions, which were also observed in the cytoplasm of renal and endothelial cells.

No abstract

Chemotherapy for melanoma results in low response and must be reinforced with sensitizer compounds. We believed that azelaic acid (AZA) could modulate melanomas' resistance to antineoplastics. Therefore we tried to compare in vitro treatment with antineoplastics alone versus AZA treatment followed by antineoplastics. We carried out MTT assays to evaluate the cytotoxicity of melphalan, lomustine (CCNU), fotemustine, and 4-Hydroxyanisole (4-HA) on three melanoma lines (B16F10, SK-MEL-28, and SK-MEL-1), and the modulating effect of pretreatment with AZA (1 mM). AZA showed a dose-dependent antineoplastic activity on the three lines. Melphalan was the most active drug followed by CCNU, fotemustine, and 4-HA. The most sensitive line was B16F10 and the least sensitive was SK-meL-1. Previous treatment with AZA of B16F10 reinforced the effect of melphalan (2.5 times), CCNU (10 times), and fotemustine (14 times); whereas for SK-MEL-28 and SK-MEL-1, only the cytotoxicity of CCNU and fotemustine increased. An antagonist effect was produced by 4-HA on all three lines. We concluded that AZA enhances in vitro cytotoxicity of CCNU and fotemustine.