The aim of this work was to evaluate the effect of prolonged melatonin administration on chosen metabolic and hormonal variables in male and female Sprague-Dawley rats. Melatonin was administered in tap water (4 microg/ml) daily from the 6th month of age. Rats were fed a standard type of diet ad libitum and were kept in a light regimen L:D--12:12h. The experiment was terminated after 12 weeks of melatonin administration. Melatonin decreased body mass during the whole experiment in females and from the 42nd day of the experiment in males. Relative heart muscle weight in females and absolute/relative thymus weight in males were increased after melatonin administration. Melatonin decreased glycaemia, heart muscle glycogen concentration in females and liver glycogen concentration in both sexes. Serum insulin concentration in males was decreased; serum corticosterone concentration was increased in both males and females. Serum triacylglycerol and heart muscle cholesterol concentration in females were decreased, however in males serum and heart muscle cholesterol concentration was increased. Liver phospholipid concentration in females was decreased and heart muscle phospholipid concentration in males was increased. Melatonin increased malondialdehyde concentration in heart muscle in males and in liver in both sexes. Melatonin induced prominent sex-dependent changes in both carbohydrate and lipid metabolism.
Orendáš P., I. Ahlers, P. Kubatka, E. Ahlersová, B. Bojková, M. Kassayová, L. Friedmanová, J. Kisková, I. Ďatelinka, M. Starostová: Etoricoxib in the Prevention of Rat Mammary Carcinogenesis. Acta Vet. Brno 2007, 76: 613-618. Several experimental studies suggest that non-steroidal antiinflammatory drugs have chemopreventive effects in mammary carcinogenesis. In this study, tumour suppressive effects of a selective inhibitor of cyclooxygenase-2 (COX-2) etoricoxib in the prevention of N-methyl-Nnitrosourea (NMU)-induced mammary carcinogenesis in Sprague-Dawley rats were evaluated. Etoricoxib was administered in the diet, at two concentrations: 1) 0.01 mg/g (ETO 0.001%) and 2) 0.025 mg/g (ETO 0.0025%). Although the chemopreventive effects were not statistically significant, remarkable tumour suppressive effects with the concentration of ETO 0.0025% were recorded. The incidence decreased by 4.31% and tumour frequency per group decreased by 6.67% when compared to the control group. Latency (the period from carcinogen administration to the first tumour appearance) increased by 7.28% in dose-dependent manner. The results of our experiments point to dose-dependent tumour suppressive effects of a higher concentration of etoricoxib (ETO 0.0025%) when compared to the control group. They suggest that higher etoricoxib concentrations may enhance its tumour suppressive effects.
Chemopreventive effect of non-steroidal antiinflammatory drugs (NSAIDs) in mammary carcinogenesis was reported in several studies. In this study, the effect of a nonselective cyclooxygenase inhibitor diclofenac (DICLO) in the prevention of N-methyl-N-nitrosourea (NMU)-induced mammary carcinogenesis in Sprague-Dawley female rats was evaluated. NMU was administered to animals intraperitoneally in two doses of 50 mg kg −1 b.w. within postnatal days 42-48. In experiment A (short-term administration), DICLO was administrated intramuscularly (5 mg kg −1 b.w.) every other day, starting 3 days before and for subsequent 25 days after first NMU injection. In experiment B (long-term administration), DICLO was administered in tap water (0.01 mg ml −1 ) continually, starting 7 days before and for subsequent 22 weeks after first NMU dose. The study was terminated 22 weeks after the first dose of NMU in both experiments. After DICLO treatment, tumor frequency per group was reduced in both variants of drug administration: in experiment A by 38% and in experiment B by 39.5%. Moreover, DICLO decreased tumor incidence by 11.5% and delayed tumor latency by 14 days in experiment B. In our preventive-curative experiments DICLO decreased some parameters of NMU-induced rat mammary carcinogenesis, mainly the tumor frequency.
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