Lipidomic and Antioxidant Response to Grape Seed, Corn and Coconut Oils in Healthy Wistar Rats.

Specialty oils differ in fatty acid, phytosterol and antioxidant content, impacting their benefits for cardiovascular health. The lipid (fatty acid, phytosterol) and antioxidant (total phenolics, radical scavenging capacity) profiles of grapeseed (GSO), corn (CO) and coconut (CNO) oils and their physiological (triacylglycerides, total and HDL-cholesterol and antioxidant capacity (FRAP) in serum and fatty acid and phytosterol hepatic deposition) and genomic (HL, LCAT, ApoA-1 and SR-BP1 mRNA hepatic levels) responses after their sub-chronic intake (10% diet for 28 days) was examined in healthy albino rats. Fatty acid, phytosterol and antioxidant profiles differed between oils (p ≤ 0.01). Serum and hepatic triacylglycerides and total cholesterol increased (p ≤ 0.01); serum HDL-Cholesterol decreased (p < 0.05); but serum FRAP did not differ (p > 0.05) in CNO-fed rats as compared to CO or GSO groups. Hepatic phytosterol deposition was higher (+2.2 mg/g; p ≤ 0.001) in CO- than GSO-fed rats, but their fatty acid deposition was similar. All but ApoA-1 mRNA level increased in GSO-fed rats as compared to other groups (p ≤ 0.01). Hepatic fatty acid handling, but not antioxidant response, nor hepatic phytosterol deposition, could be related to a more efficient reverse-cholesterol transport in GSO-fed rats as compared to CO or CNO.

Chemopreventive activity of systemically administered curcumin on oral cancer in the 4-nitroquinoline 1-oxide model.

Curcumin has therapeutic potential in preventing several types of cancer, including colon, liver, prostate, and breast. The goal of this study was to evaluate the chemopreventive activity of systemically administered curcumin on oral carcinogenesis induced by 4-nitroquinolone-1-oxide (4-NQO). A total of 50 male albino rats, Rattus norvegicus, (Holtzman), were divided into five groups (n = 10 per group). Four of these groups were exposed to 50 ppm 4-NQO in their drinking water ad libitum for 8 or 12 weeks, two groups were treated with curcumin by oral gavage at 30 or 100 mg/kg per day, and one group was treated with corn oil (vehicle) only. The negative control group was euthanized at baseline. Tongues of all animals were removed after euthanasia and used in the subsequent analysis because the tongue is the primary site of carcinogenesis in this model. Descriptive histological analysis and immunohistochemistry for PCNA, Bcl-2, SOCS1 e-3, and STAT3 were performed to assess the oncogenic process. The gene expression of Vimentin, E-cadherin, N-cadherin, or TWIST1 was assessed using RT-qPCR as a representative of epithelial-mesenchymal transition (EMT) events. The administration of curcumin at 100 mg/kg during the 12 weeks markedly decreased the expression of PCNA, Bcl-2, SOCS1 e -3, and STAT3. Curcumin also minimized the cellular atypia under microscopic analysis and diminished the expression of the genes associated with EMT. These findings demonstrate that the systemic administration of curcumin has chemopreventive activity during oral carcinogenesis induced by 4-NQO.

Attenuation of copaiba oil in hepatic damage in rats.

PURPOSE: To investigate the copaiba oil on the hepatic damage induced by acetaminophen, comparing against corn oil. METHODS: Fifty four rats were distributed into nine study groups (N=6): control group, that didn't receive the acetaminophen; Acetaminophen Group, that only received the acetaminophen; Prophylactic Copaiba Group 1, that received copaiba oil two hours before the acetaminophen; Prophylactic Copaiba Group 7, that received copaiba oil seven days, once by day, before the acetaminophen; Therapy Copaiba Group, that received the copaiba oil two hours after the acetaminophen, the corn's groups were similar than copaiba oil groups; and N-Acetyl-Cysteine Group, that received the N-Acetyl-Cysteine two hours after the acetaminophen. Euthanasia was performed after 24 hours. The serum levels transaminases, bilirubin and canalicular enzymes were analyzed. RESULTS: The prophylactic copaiba group 7, therapy copaiba group and N-Acetyl-Cysteine Group showed amounts of AST and ALT similar to the control group; and the prophylactic copaiba group 1 and corn's groups showed similar levels to the acetaminophen group. There was no significant difference between the groups regarding the amount of alkaline phosphatase and ɤ GT (p>0.05). The therapy copaiba group showed the highest levels of total bilirubin and was statistically different from the other groups (p<0.01). CONCLUSIONS: Copaiba oil administered prophylactically for seven days and therapeutically 2 hours after the acetaminophen acute intoxication offered a potential hepato protection against paracetamol-induced hepatic damage, normalizing the biochemical parameters similarly to N-Acetyl-Cysteine, and the treatment with corn oil shows no effect on the liver damage.

Attenuation of copaiba oil in hepatic damage in rats

PURPOSE: To investigate the copaiba oil on the hepatic damage induced by acetaminophen, comparing against corn oil. METHODS: Fifty four rats were distributed into nine study groups (N=6): control group, that didn't receive the acetaminophen; Acetaminophen Group, that only received the acetaminophen; Prophylactic Copaiba Group 1, that received copaiba oil two hours before the acetaminophen; Prophylactic Copaiba Group 7, that received copaiba oil seven days, once by day, before the acetaminophen; Therapy Copaiba Group, that received the copaiba oil two hours after the acetaminophen, the corn's groups were similar than copaiba oil groups; and N-Acetyl-Cysteine Group, that received the N-Acetyl-Cysteine two hours after the acetaminophen. Euthanasia was performed after 24 hours. The serum levels transaminases, bilirubin and canalicular enzymes were analyzed. RESULTS: The prophylactic copaiba group 7, therapy copaiba group and N-Acetyl-Cysteine Group showed amounts of AST and ALT similar to the control group; and the prophylactic copaiba group 1 and corn's groups showed similar levels to the acetaminophen group. There was no significant difference between the groups regarding the amount of alkaline phosphatase and ɤ GT (p>0.05). The therapy copaiba group showed the highest levels of total bilirubin and was statistically different from the other groups (p<0.01). CONCLUSIONS: Copaiba oil administered prophylactically for seven days and therapeutically 2 hours after the acetaminophen acute intoxication offered a potential hepato protection against paracetamol-induced hepatic damage, normalizing the biochemical parameters similarly to N-Acetyl-Cysteine, and the treatment with corn oil shows no effect on the liver damage. .

Fibrates and fish oil, but not corn oil, up-regulate the expression of the cholesteryl ester transfer protein (CETP) gene.

Cholesteryl ester transfer protein (CETP) is a plasma protein that reduces high density lipoprotein (HDL)-cholesterol (chol) levels and may increase atherosclerosis risk. n-3 and n-6 polyunsaturated fatty acids (PUFAs) are natural ligands, and fibrates are synthetic ligands for peroxisome proliferator activated receptor-alpha (PPARα), a transcription factor that modulates lipid metabolism. In this study, we investigated the effects of PUFA oils and fibrates on CETP expression. Hypertriglyceridemic CETP transgenic mice were treated with gemfibrozil, fenofibrate, bezafibrate or vehicle (control), and normolipidemic CETP transgenic mice were treated with fenofibrate or with fish oil (FO; n-3 PUFA rich), corn oil (CO, n-6 PUFA rich) or saline. Compared with the control treatment, only fenofibrate significantly diminished triglyceridemia (50%), whereas all fibrates decreased the HDL-chol level. Elevation of the CETP liver mRNA levels and plasma activity was observed in the fenofibrate (53%) and gemfibrozil (75%) groups. Compared with saline, FO reduced the plasma levels of nonesterified fatty acid (26%), total chol (15%) and HDL-chol (20%). Neither of the oil treatments affected the plasma triglyceride levels. Compared with saline, FO increased the plasma adiponectin level and reduced plasma leptin levels, whereas CO increased the leptin levels. FO, but not CO, significantly increased the plasma CETP mass (90%) and activity (23%) as well as increased the liver level of CETP mRNA (28%). In conclusion, fibrates and FO, but not CO, up-regulated CETP expression at both the mRNA and protein levels. We propose that these effects are mediated by the activation of PPARα, which acts on a putative PPAR response element in the CETP gene.

Influencia de la administración a largo plazo de aceites de palma y maíz en la dieta sobre la vasoconstricción y vasodilatación arterial de la aorta del conejo / Influences of the long term administration of palm oils and corn in the dirt on the vasoconstrictor an arterial vasodilator of the aorta of the rabbit

Se evaluó el efecto de la administración en la dieta de aceite de palma o de maíz a largo plazo sobre los lípidos sanguíneos y la actividad arterial de anillos de aorta de conejo, agentes vasoconstrictores y vasodilatadores dependientes e independientes del endotelio. Los conejos albinos fueron divididos en tres grupos de 12 conejos cada uno, que recibieron: grupo I (control), dieta convencional de conejarina Grupo II, conejarina con aceite de palma (10 por ciento), Grupo III: conejarina con aceite de maíz (10 por ciento) por un período de 4 meses. Se tomaron muestras de sangre al inicio y al final del estudio, cuando fueron anestesiados, se extrajo la aorta y se cortó en anillos que fueron incubados en solución de Kerbs oxigenada para la evaluación de la reactividad a fenilefrina (FEN), acetilcolina (Ach) y niprotusiato de sodio (NPS). El aceite de palma aumentó el colesterol total plasmático de 20,4 a 35,1 mg/dL (p<0,05) y el de maíz de 27,0 a 44,5 mg/dL (p<0,05); el aceite de palma aumentó la HDLc de 12,2 a 24,0 mg/dL (p<0,015) y el aceite de maíz no modifico significativamente este parámetro, pero aumentó los triglicéridos de 21,5 a 46,0 mg/dL (p<0.004). La DE-50 de la curva dosis-respuesta (CDR) a la Ach en los anillos de la aorta control, fue 2,4 x 10 a la menos 7 mol/L y en el grupo que recibió aceite de palma, la CDR fue desplazada a la izquierda y la DE-50 disminuyó a 7,5 x 10 a la menos 8 mol/L (p<0,05); en el grupo que recibió aceite de maíz la De-50 disminuyó a 6,6 x 10 a la menos 8 mol/L (p<0,01). La reactividad a FEN en el grupo que recibió aceite de palma no cambió (p> 0,05) y desplazó significativamente la CDR a la derecha en los que recibieron aceite de maíz (p<0,05). La CDR al nitroprusiato de sodio no cambió en los conejos que recibieron aceite de palma y fue desplazada significativamente a la izquierda (p<0,01) en los que recibieron aceite de maíz. En conclusión los animales normocolesterolémicos, el suplemento de aceite de palma aumenta el colesterol a predominio de la fracción de HDL y sensibiliza la relajación dependiente del endotelio. El aceite de maíz aumenta la relajación arterial dependiente e independiente del endotelio adicionalmente atenúa la vasoconstricción mediana por el receptor adrenérgico &

Effects of dietary n-3, n-6 and n-9 polyunsaturated fatty acids on benzo(a)pyrene-induced forestomach tumorigenesis in C57BL6J mice.

The modulating effect of dietary polyunsaturated fatty acids (PUFAs) on benzo(a)pyrene-induced forestomach tumorigenesis was assayed in mice fed with corn oil (CO), olein (O), Zizyphus mistol seed oil (MO), cod liver oil (CLO), and mixed fat (Stock diet). The fatty acid composition of liver lipids correlated well with the fatty acid composition of each diet. Only mice fed the O diet showed biochemical and clinical evidences of essential fatty acid deficiency (EFAD). Only 3 animals developed well-differentiated invading squamous cell carcinomas in the O group. The papilloma incidence was reduced in MO and CLO with respect to the O group. Forestomach papillomatosis was increased in mice fed an n-9 enriched diet in comparison to stock and CO groups. In comparison with stock mice, the frequency of multiple epidermoidal hyperplasia (MEH) was significantly decreased in the CLO group. Animals fed n-3 enriched diets (MO and CLO) showed significant antipromoting effect. These findings indicate that dietary fat can modulate tumorigenesis initiated in mouse forestomach by benzo(a)pyrene. In addition, the lack of action of an n-6 fatty acid-enriched diet in our experimental model suggests that the effect of PUFAs on tumorigenesis has target-tissue specificity. Mistol seed oil might be of potential value as a natural vegetable antipromoter nutrient.

Comparison of antioxidant status during recovery from malnutrition on a corn oil- or coconut oil-based diet - abstract

Children recovering from malnutrition are given a high-energy diet during the "catch-up" phase. Corn oil, a poly-unsaturated fatty acid (PUFA) rich vegetable oil, is used to supply 60 per cent of the energy in the recovery diets. Previous work suggests that this high intake of corn oil may be associated with a deterioration of antioxidant status. A normal antioxidant status is essential for protection against cell damage. We therefore compared indices of antioxidant status (whole blood gluthathione, GSH; plasma vitamen E; and urinary mercapturic acid outputs (UMCA) in two groups of malnourished children who had recovered on isocaloric diets containing either PUFA rich, corn oil (Control group) or coconut oil (test group), which is rich in saturated fatty acids. Both groups showed an initial normalisation of GSH and vitamin E levels; whereas the test group maintained normal levels, the control group showed a progressive decrease of both indices during recovery. At discharge the test group had GSH (2.7 ñ 0.08 vs 2.44 ñ 0.88 mmol/Lrbc, mean ñ SEM) and vitamen E (8.44 ñ 1.21 vs 7.38 ñ 1.01 mg/l), levels that were significantly higher (p< 0.05) that in the Control group. Several children in the Control group had vitamen E levels that were below the accepted normal range. At recovery, UMCA outputs of the Control group (4.85 ñ 0.55 umol/kg/24 hr) were further increased, and as such were significantly higher (p < 0.05) than the admission mean (3.32 ñ 0.54 umol/kg/24 hr). In the test group, mean discharge UMCA output (1.98 ñ 0.44 umol/kg/24 hr) was significantly lower than admission values, as well as the mean discharge UMCA output of the Control group. This suggests that the body's burden of compounds that require detoxification is significantly increased when malnourished children are rehabilitated on a diet rich in corn oil. Following recovery on the coconut oil diet, plasma cholesterol levels (2.30 ñ 0.15 mmol) were similar to the pre-treatment mean (2.15 ñ 0.11 mmol). However, plasma levels of triglycerides fell significantly (p < 0.05) with treatment (pre: 1.23ñ0.14; post 0.88ñ0.08 mmol). When given a diet that is not rich in PUFA, malnourished children are able to maintain their antioxidant status within the normal range. It is suggested that coconut oil be used routinely in the formulation of recovery diets for malnourished children (AU)