Modulation by dietary factors of BHA-induced alterations in cell kinetics of gastro-intestinal tract tissues in rats.

To determine the effects of dietary ethanol or fibre on 2(3)-tert-butyl-4-hydroxyanisole (BHA)-induced alterations in cell kinetics in gastro-intestinal tract tissues, groups of six male Wistar rats were fed diets containing 0% (control) or 1.5% BHA for 2 wk. One group fed 1.5% BHA and one pair-fed control group received 10% ethanol in the drinking-water; two similarly fed groups received drinking-water only. Another group fed 1.5% BHA and a pair-fed control group received a diet supplemented with 20% cellulose; two similar groups received no fibre supplementation. Cell kinetics in the forestomach, glandular stomach and oesophageal tissue were determined, after 14 days, by bivariate 5-bromo-deoxyuridine/DNA analysis using immunocytochemistry and flow cytometry. In the fibre experiment, colorectal tissue was also examined. In both experiments the labelling indices in all the gastro-intestinal tract tissues were significantly altered in the BHA-fed groups compared with the corresponding control groups. In the ethanol experiment no statistically significant difference in the labelling indices was observed in the forestomach or glandular stomach between the two control groups or between the two BHA-fed groups. However, intake of ethanol-supplemented drinking-water induced increases in oesophageal labelling indices in rats fed a BHA-free diet. Thus 14 days of simultaneous ethanol administration has no effect on BHA-induced alterations in cell kinetics in the oesophagus, glandular stomach or forestomach of rats. In the forestomach and colorectal tissue, a high-cellulose diet resulted in a significant decrease in the BHA-induced elevation of labelling indices. Thus dietary cellulose provides a partial protection against the proliferation-enhancing effects of BHA in the rat gastro-intestinal tract.

Mutagenicity of deep-frying fat, and evaluation of urine mutagenicity after consumption of fried potatoes.

Mutagen formation during deep-frying was evaluated using standard frying conditions. Portions of pre-fried, sliced potatoes were fried in a commercial brand of hydrogenated vegetable frying fat, which was used repeatedly and for a prolonged period of time. Concentrations of polar oxidation and degradation products, and of dimeric and polymeric triglycerides, were found to increase in the frying fat as well as in fried potatoes with prolonged use of the fat. Thiobarbituric acid-reactive substances were detectable neither in the frying fat nor in the fried potatoes. Polar fractions of repeatedly used frying fat significantly increased the number of revertants in Salmonella typhimurium strain TA97 without S-9 mix. In the presence of S-9 mix mutagenic activity was reduced. As a consequence of ongoing formation of polar degradation and oxidation products, the mutagenicity of the fat increased after repeated use. Polar fractions of lipids extracted from commercially obtained pre-fried potatoes, as well as from fried potatoes, marginally increased the number of revertants in strain TA97 without S-9 mix. The mutagenicity of the lipid fractions of fried potatoes was not related to the heating time of the fat. Methanol extracts of fat-free residues of fried potatoes significantly increased numbers of revertants in strain TA97 after metabolic activation, which indicated that a different class of mutagens had been isolated. The mutagenicity of methanol extracts was not increased after either prolonged or repeated use of the fat. Urine samples of six healthy, non-smoking volunteers, collected during the 24 hr following consumption of portions of potatoes fried in repeatedly used fat, showed no increase in mutagenicity compared with control samples. Since the exact identity of mutagens formed during deep-frying, as well as their metabolic fate in man, is unclear at present, evaluation of possible adverse biological effects associated with consumption of fried foods will require strictly controlled metabolic studies.

Study on food intake and energy expenditure during extreme sustained exercise: the Tour de France.

Food intake and energy expenditure (EE) were studied in five cyclists during the 22-day race of the Tour de France. The course is about 4000 km including 30 mountain passages (up to 2700 m altitude) and can be considered as one of the most strenuous endurance endeavors. Nutritional intake was calculated from daily food records. EE was estimated from sleeping time and the low activity period. EE during cycling was predicted based on detailed information. Mean energy intake (EI) was 24.7 MJ with a highest mean daily EI of 32.4 MJ. Mean EE was 25.4 MJ with a highest mean daily EE of 32.7 MJ. Relative contribution of protein, CHO, and fat was 15, 62, and 23 En% resp. 49% of EI was taken during the race resulting in a CHO intake of 94 g.h-1 representing 69 en%. It is questioned whether this amount of CHO is optimal in relation to CHO oxidation and performance. About 30% from CHO intake came from CHO-rich liquids. High EI resulted in high Ca and Fe intake. For vitamins, especially B1, this relation was not found. Vitamin B1 nutrient density dropped to 0.25 mg/4.2 MJ during the race caused by a large intake of refined CHO-rich food items. However, vitamin supplementation was high. Daily water intake was 6.71 with extremes up to 11.81. Therefore, the strategy of intake of large quantities of CHO-rich liquids seems to be the appropriate answer to maintain energy and fluid balance under these extreme conditions.

Fish oil feeding lowers thromboxane- and prostacyclin production by rat platelets and aorta and does not result in the formation of prostaglandin I3.

It is demonstrated that feeding cod-liver oil to rats leads to a considerable reduction in the formation of platelet TxA2 and of vascular PGI2. No appreciable formation of TxA3 and PGI3 is observed, although arterial thrombosis is depressed and bleeding time is prolonged. These findings contradict the suggested role of prostaglandins of the 3-series in thromboregulation.

Influences of dietary fats on coronary flow rate and left ventricular work of the isolated rat heart: sunflower seed oil versus lard.

The influences of dietary sunflower seed oil and lard on coronary flow rate and external left ventricular work were studied in the isolated Langendorff-perfused and working rat heart. For 1, 4 or 6 weeks, rats were fed diets containing 25--50% of the total digestible energy as fat, 23% as casein an 52--27% as starch. The coronary flow rate and the maximum left ventricular work of hearts of rats fed sunflower seed oil were higher than those of hearts of rats fed lard (about 15 and 10%, respectively). The maximum left ventricular work was achieved at a left ventricular filling pressure of 10--12 mm Hg: this value was not affected by the type of dietary fat. The effect of dietary fat on coronary flow rare is already seen after 1 week of feeding, and on left ventricular work after 4 weeks of feeding. Analysis of variance shows a positive relationship between the maximum left ventricular work and the amount of sunflower seed oil. It is concluded that dietary fats affect coronary flow rate and left ventricular work in the isolated rat heart. The increase in left ventricular work may be caused by an increase in contractility.

Dietary manipulation of prostaglandin and thromboxane synthesis in heart, aorta and blood platelets of the rat.

We conclude that dietary changes can have a profound influence on prostaglandin and thromboxane synthesis of organ systems. A better insight into underlying mechanisms is necessary before more definite advice with respect to feeding a linolenic acid and very long-chain polyunsaturated fatty acids as found in fish oils can be given.