Evidence suggests that differences in fatty acid composition among various fish species may be due to differences in diet or to environmental factors such as temperature, salinity, and depth at which the fish are caught. The beneficial effects of a diet containing fish on cardiovascular or other diseases have been associated with their high content of eicosapentaenoic (20:5n-3) and docosahexaenoic (22:6n-3) acids. In this study we analyzed the fatty acid composition of the flesh of 18 different species of marine fish and of cultured rainbow trout. The fish were obtained from the Black and the Marmara Seas, both of which have unique biological and ecological systems as well as eutrophication and pollution. The contents of 20:5n-3 and 22:6n-3 in the marine fish ranged from 4.2 to 13.3 wt% of total fatty acids, and from 6.6 to 40.8 wt%, respectively. The most important differences from other studies on oceanic fish were the tendencies toward higher percentages of 16:0 and 22:6n-3. The n-3 series of polyunsaturated fatty acids were present as 32.4+/-1.9% of the total fatty acids. The present study suggests that mature and immature Pomatomus saltator as well as Engraulis encrasicolus, Mullus surmuletus, Sardina pilchardus, Mugil cephalus, and Sarda sarda may be preferred for the Turkish diet as a result of their high 20:5n-3 and 22:6n-3 contents. The cultured rainbow trout Oncorhynchus mykiss is not as good a source of n-3 fatty acids as are the marine fish.

BackgroundVisceral fat deposition and its associated atherogenic complications are mediated by glucocorticoids. Cardiac visceral fat comprises mediastinal adipose tissue (MAT) and epicardial adipose tissue (EAT), and MAT is a potential biomarker of risk for obese patients.AimOur objective was to evaluate the role of EAT and MAT 11beta-hydroxysteroid dehydrogenase type 1 (11β-HSD-1) and glucocorticoid receptor (GCR) expression in comparison with subcutaneous adipose tissue (SAT) in the development of coronary atherosclerosis in obese patients with coronary artery disease (CAD), and to assess their correlations with CD68 and fatty acids from these tissues.Methods and resultsExpression of 11β-HSD-1 and GCR was measured by qRT-PCR in EAT, MAT and SAT of thirty-one obese patients undergoing coronary artery bypass grafting due to CAD (obese CAD group) and sixteen obese patients without CAD undergoing heart valve surgery (controls). 11β-HSD-1 and GCR expression in MAT were found to be significantly increased in the obese CAD group compared with controls (p < 0.05). In the obese CAD group, 11β-HSD-1 and GCR mRNA levels were strongly correlated in MAT. Stearidonic acid was significantly increased in EAT and MAT of the obese CAD group and arachidonic acid was significantly expressed in MAT of the obese male CAD group (p < 0.05).ConclusionsWe report for the first time the increased expression of 11β-HSD-1 and GCR in MAT compared with EAT and SAT, and also describe the interrelated effects of stearidonic acid, HOMA-IR, plasma cortisol and GCR mRNA levels, explaining 40.2% of the variance in 11β-HSD-1 mRNA levels in MAT of obese CAD patients. These findings support the hypothesis that MAT contributes locally to the development of coronary atherosclerosis via glucocorticoid action.

In this study we investigated the expression of COX-1, COX-2 and COX-3 mRNA in C6 glioblastoma and normal brain tissues and the effects of acetaminophen, indomethacin or metamizole treatments on the development of C6 glioblastoma in relation with COX inhibition. Glioblastoma cells were inoculated intracerebrally into frontal lobe of adult male Wistar albino rats. 10 days after inoculation, rats were treated with 150 mg/kg acetaminophen, 10 mg/kg indomethacin or 150 mg/kg metamizole. The tumor size was measured histologically and total RNA was isolated from tumor or normal brain tissue and mRNA levels of COX isoforms were determined by qRT-PCR. Our results showed the presence of COX-1, COX-2 and COX-3 expressions in both C6 glioblastoma and normal brain tissues. In tumor tissues COX-3 expression was significantly higher than normal brain tissue (p < 0.05) while there was no significant difference in COX-1 and COX-2 expressions. Acetaminophen and indomethacin decreased the tumor size by 71 and 43 % by inhibiting COX-3 mRNA expression around 87 and 91 % respectively. For the first time our study proposes a possible relationship between COX-3 mRNA expression and C6 glioblastoma development. We also suggested that the inhibition of COX-3 enzyme may be responsible for decrease in tumor size in part, the mechanism by which acetaminophen and indomethacin decreased rat C6 glioblastoma growth. However, the molecular events responsible for COX-3 effects on tumor development are still unresolved as these drugs exert their anti-cancer effect via both COX-3 dependent and independent mechanisms.

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