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• W1995749632 abstract "Estudis amb animals dexperimentacio han suggerit que lefecte promotor de la carcinogenesi pel greix dietetic no depen tan sols de la quantitat, sino del contingut especific dacids grassos (AG). En aquest sentit, lefecte dels AG de la serie n9, presents principalment en loli doliva, han sigut escassament estudiats.Objectius: i) Avaluar lefecte duna dieta amb un 5% doli doliva (n9), en comparacio a dues dietes isolipidiques a base doli de peix (n3) i oli de cartam (n6), a les fases de iniciacio i promocio tumoral en un model de carcinogenesi induida per azoximeta. ii) Estudiar el canvis en la composicio del contingut dAG de la mucosa colonica. iii) Quantificar la produccio deicosanoides a la fase inicial de la carcinogenesi colonica.Metodes: 108 rates Sprague-Dawley foren dividides en tres grups segons la font de greix emprada: n9, n3 i n6. El contingut de total greix fou normolipidic per a rates (5%). La meitat danimals de cada grup foren induits amb AOM (7.4 mg/kg/setmana, s.c.) durant 11 setmanes, a la resta danimals sels injecta un volum equivalent de sali. A la setmana 12, despres de la primera dosi dAOM o sali, es practica un dialisi intracolonica per valorar la produccio local deicosanoides (PGE2, PGE3, LTB4 i LTB5; HPLC i EIA); despres de la colectomia, savalua laparicio de lesions preneoplasiques (criptes aberrants i focus de criptes aberrants). A la setmana 19, despres del sacrifici, sestudia el nombre, incidencia (% de rates amb tumors), multiplicitat (numero de tumors/rata), localitzacio i grau de diferenciacio histologica dels tumors. A mes, tant a la setmana 12 com a la 19, es determina el patro dAG a la mucosa colonica (C16:0 a C24:0; CGL), aixi com la relacio acid araquidonic (AA): acid eicosapentaenoic (EPA).Resultats: Les rates tractades amb AOM del grup dietetic n6 mostraren un major nombre tant de criptes aberrants (p=0.004) com de focus de criptes aberrants (p=0.006) respecte als animals alimentats amb les dietes n3 i n9. La incidencia tumoral fou 58%, 45.5% i 83% (p=0.15) i la multiplicitat 0.8±0.2, 0.7±0.3 i 2.5±0.8 (p=0.03) per les dietes n9, n3 i n6, respectivament. No aparegue cap adenocarcinoma pobrament diferenciat en el grup n9, mentre que en el grup n3 i n6 les taxes foren un 25% i 60% (p=0.01, n9 vs n6), respectivament. Els tumors foren de localitzacio, preferentment, distal en els grups n3 i n6 (p=0.006, n9 vs n6). Daltra banda, la relacio AA:EPA no fou diferent entre les rates tractades amb AOM o sali, aixi, a la setmana 12, i de forma similar a la setmana 19, aquest quocient fou 69.4±7.4, 0.97±0.0 i 135±3.3 (p=0.001) per les rates amb AOM dels grups n9, n3 i n6, respectivament. El tractament amb carcinogen produi, en el grup n6, un significatiu augment en la produccio de PGE2 (p=0.004) i LTB4 (p=0.004) respecte a les tractades amb sali; aquest efecte no sobserva, o fou de menor magnitud, en les rates dels grups n3 i n9. A mes, en les rates amb AOM del grup n6 s'observa un augment de PGE2 (p=0.002), LTB4 (p=0.01) i LTB5 (p=0.01) respecte a n3 i n9. En el grup n3, les rates tractades amb AOm mostraren una reduccio dels nivells de PGE2 (p=0.025) i PGE3 (p=0.008) respecte a lesd tractades amb sali.Conclusions: L'oli d'oliva exerceix un efecte inhibidor del desenvolupament de lesions preneoplasiques i tumors similar a l'observat per l'oli de peix, pero amb un efecte addicional sobre el grau de diferenciacio. Aquests efectes poden esser deguts, en part, a la modulacio del metabolisme de l'AA i la sintesi de PGE2.Animal model studies have shown that the colon tumor promoting effect of dietary fat depend not only on the amount but on its fatty acid composition. With respect to this, the effect of n9 fatty acids, present in olive oil, on colon carcinogenesis has been scarcely investigated.Aims: i) To assess the effect of a 5% fat olive oil based diet (n9), in comparison with isolipidic fish (n3) and safflower oil (n6) baset diets, on the early and late phases of azoxymethane (AOM) induced colon carcinogenesis. ii) To examine the changes in mucosal fatty acid composition. iii) To determine the eicosanoid production on the precancer phase.Methods: 108 rats were divided into three groups to receive isocaloric diets (5% of the energy as fat) rich in n9, n3 and n6 fat, and were administered AOM subcutaneously once a week for 11 weeks at a dose rate of 7.4 mg/kg body weight. Vehicle treated groups received an equal volume of normal saline. Groups of animals were colectomised at weeks 12 and 19 after the first dose of AOM or saline. Mucosal fatty acids and the ratio araquidonic acid (AA): eicosapentaenoic acid (EPA) were assessed at 12 and 19 weeks (from C16:0 to C24:0; CGL). Aberrant crypt foci and local eicosanoid production were assessed at week 12 (PGE2, PGE3, LTB4 and LTB5; HPLC and EIA). Tumor formation, incidence (number of rats with colonic tumors), multiplicity (number of colonic tumors per rat), localisation and histological degree of differentation were studied at week 19.Results: Rats on the n6 diet showed more colonic aberrant crypts (p=0.004) and aberrant crypts foci (p=0.006) than those consuming either the n9 or n3 diet. The tumoral incidence was 58%, 45.5% and 83% (p=0.15) and the tumoral multiplicity was 0.8±0.2, 0.7±0.3 and 2.5±0.8 in n9, n3 and n6 diets, respectively. Animals fed with n3 and n6 diets had a predominance of colon tumors in the distal half of the colon as compared with those on the n9 diet (p= 0.006 n9 vs n6). Moreover, rats on the n9 diet showed a lower percentage of poorly differentiated adenocarcinomas than those fed n3 and n6 diets (0%, 25% and 60%; p=0.01 n9 vs n6). On the other hand, both at week 12 and 19, there were no differences in mucosal AA:EPA ratio between AOM and saline treated rats, but there were significant differences in AA:EPA ratio among diets (p<0.0005; n6 vs n3 and n9; n9 vs n3). Carcinogen treatment induced an appreciable increase in PGE2 (p=0.004) and LTB4 (p=0.004) formation in rats fed the n6 diet, but not in those fed the n3 and n9 diets. Additionally, AOM treated rats fed n6 fat released significantly higher amounts of PGE2 (p=0.002), LTB4 (p=0.01) and LTB5 (p=0.01) into the colonic lumen than both the other AOM treated groups and vehicle treated rats. In contrast, rats on the n3 diet treated with carcinogen showed a slight but significant decrease in the release of PGE2 (p=0.025) and PGE3 (p=0.008) as compared with saline treated rats.Conclusions: Dietary olive oil prevented the development of aberrant crypt foci and colon carcinomas in rats, suggesting that olive oil may have chemopreventive activity against colon carcinogenesis. These effects may be partly due to modulation of AA metabolism and local PGE2 synthesis." @default.
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• W1995749632 date "2002-07-12" @default.
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• W1995749632 title "Efecte de l'oli d'oliva sobre la carcinogènesi i la producció local d'eicosanoides en un model de càncer colorectal per azoximetà" @default.
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