The effect of palm oil, a widely used vegetable oil, rich in tocotrienols, on peroxidation potential of rat liver was examined. Long-term feeding of rats with palm oil as one of the dietary components significantly reduced the peroxidation potential of hepatic mitochondria and microsomes. As compared to hepatic mitochondria isolated from rats fed control or corn oil-rich diet, those from palm oil-fed group showed significantly less susceptibility to peroxidation induced by ascorbate and NADPH. However, in microsomes, only NADPH-induced lipid peroxidation was significantly reduced in rats fed palm oil rich-diet. Though the accumulation of thiobarbituric acid reactive substances during ascorbate-induced lipid peroxidation in mitochondria from rats fed corn oil-rich diet supplemented with tocotrienol-rich fraction (TRF) of palm oil was similar to that of control rats, the initial rate of peroxidation was much slower than those from control or corn oil fed diets. Our in vitro studies as well as analyses of co-factors related to peroxidation potential indicated that the observed decrease in palm oil-fed rats may be due to increased amount of antioxidants in terms of tocotrienol as well as decrease in the availability of substrates for peroxidation.
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The effect of tocotrienol on the activities of glutathione S-transferases (GSTs), glutathione reductase (GR) and glutathione peroxidase (GPx) in rats given 2-acetylaminofluorene (AAF) was investigated over a 20 week period. Liver and kidney GST and liver GR activities were significantly increased after AAF administration. Kidney GPx activities were significantly affected; activity assayed with cumene hydroperoxide (cu-OOH) was increased but activity assayed with H2O2 was reduced. Supplementation of the diet with tocotrienol in the AAF-treated rats reduced the increase in enzyme activities. Tocotrienol on its own had no effect on the enzyme activities.
alpha-Tocopherol, the most active form of vitamin E, causes a dose-dependent inhibition of serum-induced proliferation of smooth muscle cells (A7r5) in culture. Some tocopherol-related compounds exhibiting various degrees of antioxidant potency have also been tested on cellular proliferation. No direct correlation between the antioxidant activity of these compounds and their effect on smooth muscle cell growth could be observed. While most of the derivatives employed were not effective in inhibiting protein kinase C, in the case of alpha-tocopherol the antiproliferative effect was found to be parallel to the inhibition of protein kinase C activity, as measured in streptolysin-O permeabilized cells.
Certain aspects of tocopherol and tocotrienol absorption, plasma transport, and tissue distribution were examined in humans and hamsters. Plasma transport differed in that tocopherols were found primarily in low density lipoprotein and high density lipoprotein in association with plasma surface components, whereas tocotrienols disappeared from plasma with chylomicron clearance. In keeping with transport by triglyceride-rich lipoproteins, tocotrienols were deposited in conjunction with triglycerides in the adipose tissue of hamsters. In hamsters, tocopherols were the only tocol readily detected in all tissues, except adipose during tocotrienol supplementation. In fasting humans, the plasma tocotrienol concentration was not significantly increased after tocotrienol supplementation, whereas the platelet concentration of delta-tocotrienol doubled. Furthermore, tocotrienol intake did not appear to modulate the plasma cholesterol concentration in normolipemic hamsters. Thus, the transport, tissue concentration, and relative biologic function of tocopherol and tocotrienol appear somewhat disparate and possibly unrelated.
Both alpha-tocopherol and a 1:1.7 mixture of alpha-tocopherol and tocotrienols at a 0.2% dietary level significantly depressed the age-related increase in the systolic blood pressure of spontaneously hypertensive rats (SHRs) after 3 weeks of feeding. The aortic production of prostacyclin was increased 1.5 times both by alpha-tocopherol and a tocotrienol mixture, suggesting a possible relevance to their hypotensive effect. These vitamins did not influence the delta 6- and delta 5-desaturase activities of liver microsomes, but fatty acid profiles of the liver phospholipids predicted a reduction of linoleic acid desaturation. These effects were in general more clear with tocotrienols than with alpha-tocopherol. Platelet aggregation by 5 microM ADP remained uninfluenced. Thus, tocotrienols may have effects on various lipid parameters somewhat different from those of alpha-tocopherol.
Individually and in combination with other oils, the tropical oils impart into manufactured foods functional properties that appeal to consumers. The use of and/or labeling in the ingredient lists give the impression that these oils are used extensively in commercially processed foods. The estimated daily intake of tropical oils by adult males is slightly more than one fourth of a tablespoon (3.8 g), 75% of which consists of saturated fatty acids. Dietary fats containing saturated fatty acids at the beta-position tend to raise plasma total and LDL-cholesterol, which, of course, contribute to atherosclerosis and coronary heart disease. Health professionals express concern that consumers who choose foods containing tropical oils unknowingly increase their intake of saturated fatty acids. The saturated fatty acid-rich tropical oils, coconut oil, hydrogenated coconut oil, and palm kernel oil, raise cholesterol levels; studies demonstrating this effect are often confounded by a developing essential fatty acid deficiency. Palm oil, an essential fatty acid-sufficient tropical oil, raises plasma cholesterol only when an excess of cholesterol is presented in the diet. The failure of palm oil to elevate blood cholesterol as predicted by the regression equations developed by Keys et al. and Hegsted et al. might be due to the dominant alpha-position location of its constituent saturated fatty acids. If so, the substitution of interesterified artificial fats for palm oil in food formulations, a recommendation of some health professionals, has the potential of raising cholesterol levels. A second rationale addresses prospective roles minor constituents of palm oil might play in health maintenance. This rationale is founded on the following observations. Dietary palm oil does not raise plasma cholesterol. Single fat studies suggests that oils richer in polyunsaturated fatty acid content tend to decrease thrombus formation. Anomalously, palm oil differs from other of the more saturated fats in tending to decrease thrombus formation. Finally, in studies comparing palm oil with other fats and oils, experimental carcinogenesis is enhanced both by vegetable oils richer in linoleic acid content and by more highly saturated animal fats. The carotenoid constituents of red palm oil are potent dietary anticarcinogens. A second group of antioxidants, the tocotrienols, are present in both palm olein and red palm oil. These vitamin E-active constituents are potent suppressors of cholesterol biosynthesis; emerging data point to their anticarcinogenic and antithrombotic activities. This review does not support claims that foods containing palm oil have no place in a prudent diet.
The bioactivities of RRR-alpha-, beta-, gamma-, and delta-tocopherol (T) and R-alpha-tocotrienol (R-alpha-TT) were determined in rat resorption-gestation tests. The ranking order was RRR-alpha-T greater than RRR-beta-T greater than RRR-gamma-T greater than or equal to R-alpha-TT greater than RRE-delta-T. Accordingly, the biopotency of a palm-oil residue was assessed and expressed as alpha-tocopherol equivalents (alpha-TEs). The release of pyruvate kinase, a variable in the nutrition-linked necrotizing myopathy, into the plasma was dose-dependently inhibited by the RRR-alpha-T standard and the corresponding alpha-TE from this residue. Prostacyclin synthesis from aorta segments induced by thrombin or ionomycin was higher than the spontaneous release. However, there was no difference between the depleted group and groups treated with RRR-alpha-T or alpha-TEs from the palm-oil residue. Quantities of IgG in plasma of vitamin E-depleted rats were the highest. Upon supplementation with RRR-alpha-T or alpha-TEs from the palm-oil residue, reduced IgG concentrations were observed, similar to those of animals on a commercial diet containing adequate amounts of vitamin E.
The Finns average intake of tocopherols, tocotrienols, and vitamin E (alpha-tocopherol equivalents) was determined. The food consumption data were derived mainly from the national food balance sheets (for 1987). The average Finnish daily diet was composed and analyzed both in spring and in autumn in order to minimize the effect of seasonal variation. The four tocopherols and four tocotrienols were then determined using high-performance liquid chromatography (HPLC). For comparison, the intake of vitamin E compounds was also calculated using the most recent Finnish analytical data on tocopherols and tocotrienols in food. According to the analytical results, the average daily vitamin E intake in Finland was 10.7 mg alpha-tocopherol equivalents (alpha-TE) of which amount 85% is due to alpha-tocopherol. The analyzed values (10.8 mg alpha-TE in spring and 10.7 mg alpha-TE in autumn) of vitamin E intake did not markedly differ from the calculated value (10.3 mg alpha-TE), thus indicating that the Finnish food composition data upon tocopherols and tocotrienols is up-to-date and accurate. The best food sources of vitamin E were dietary fat (41% of the total amount), cereals (18%), and dairy products and eggs (13%). The average Finnish diet contained 9.5 g of polyunsaturated fatty acids (PUFA), which leads to the ratio of 0.9 between alpha-tocopherol (mg) and PUFA (g). According to these results, the dietary recommendations for vitamin E are met in Finland.
A major public health concern of affluent nations is the excessive consumption of dietary fats which are now closely linked to coronary heart disease. Against this scenario, the tropical oils and palm oil in particular, have been cast as major villains in the U.S.A., despite the fact that palm oil consumption there is negligible. The unsuspecting public may not realise that the call to avoid palm oil is nothing more than a trade ploy since in recent years palm oil has been very competitive and has gained a major share of the world’s edible oils and fats market. Many also lose sight of the fact that, palm oil, like other edible oils and fats, is an important component of the diet. The allegation that palm oil consumption leads to raised blood cholesterol levels and is therefore atherogenic is without scientific foundation. Examination of the chemical and fatty acid composition of palm oil or its liquid fraction should convince most nutritionists that the oil has little cholesterol-raising potential. The rationale for these are: it is considered cholesterol free. its major saturated fatty acid, palmitic acid (16:0) has recently been shown to be neutral in its cholesterolaemic effect, particularly in situations where the LDL receptors have not been down-regulated by dietary means or through a genetic effect. palm oil contains negligible amounts (less than 1.5%) of the hypercholesterolemic saturated fatty acids, namely lauric acid (12:0) and myristic acid (14:0). it has moderately rich amounts of the hypocholesterolaemic, monounsaturated oleic acid (18:1, omega-9) and adequate amounts of linoleic acid. (18:2, omega-6). It contains minor components such as the vitamin E tocotrienols which are not only powerful antioxidants but are also natural inhibitors of cholesterol synthesis. Feeding experiments in various animal species and humans also do not support the allegation that palm oil is atherogenic. On the contrary, palm oil consumption reduces blood cholesterol in comparison with the traditional sources of saturated fats such as coconut oil, dairy and animal fats. In addition, palm oil consumption may raise HDL levels and reduce platelet aggregability. As with all nutrients, there is a need to obtain a balance of different fatty acids found in fats in edible oils and other food sources. There is no single ideal source of fat that answers to the recent American Heart Association’s call to reflect a 1:1:1 ratio of saturated, monounsaturated and polyunsaturated fats in relation to the recommended dietary fat intake of 30% of calories or less.
The effect of sampling site and closeness of malignant tumor on the retinoid, carotenoid, tocopherol, and tocotrienol concentration of adipose tissue of human breast was studied in 10 cases of breast cancer. The four anatomic quadrants of breast did not differ from each other statistically significantly in relation to adipose tissue concentrations of the vitamins studied. Proximity of malignant tumor did not affect the vitamin concentrations when compared to the more distant sampling sites. Representative sample of breast adipose tissue for vitamin concentration analysis can be obtained from tissue adjacent to the tumor.