We observed the pathophysiological state of a colony of Wistar rats with a hereditary defect in vitamin C-synthesizing ability (the OD rat) in three kinds of experiments. In experiment 1. OD rats that were not supplemented with L-ascorbic acid (ASA) were killed 36 days after birth- In experiment 2, OD rats that were not supplemented with AsA were killed 63 days after birth. In experiment 3, OD rats that were supplemented with sufficient ASA (100mg/100g body weight/day) for 16 days from 47 days after birth were assayed 63 days after birth. From analyses of serum chemistry, platelet aggregability and counts of blood cells, some atherogenic risk factors were elucidated, that is, there was a decrease of high density lipoprotein in serum and an increase of platelet aggrega-bility. Furthermore, it was observed that OD rats have some charac-teristics different from latent vitamin C-deficient animals from the view-point of malnutrition.

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[³H]Pyridoxine or [³H]pyridoxal in physiological amounts was orally administered to mice and the distribution of isotope between the six recognized forms of vitamin B₆ and pyridoxic acid was determined at different times after the administration in the intestine, liver, blood, and brain. After 7 min about 50% of the radioactivity in pyridoxine and pyridoxal had been absorbed by the intestine and transported to the blood and other organs. When [³H]pyridoxine was administered, labeled pyridoxal, pyridoxal and pyridoxine-phosphate were found in the intestine and liver, and labeled pyridoxine could not be detected in the peripheral blood but substantial amounts of labeled pyridoxal and pyridoxalphosphate were found in the blood. The time course of the blood [³H]pyridoxal levels following the administration of [³H]pyridoxine was similar to that following the administration of [³H]pyridoxal. These results suggest that the intestine and/or liver play a major role. in converting dietary pyridoxine to circulating pyridoxal which is taken up and phosphorylated by other organs. Moreover, most of the blood [³H]pyridoxal was shown to be located in the plasma. This localization may facilitate utilization by the organs.

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The growth and DNA synthesis of L1210 mouse leukemia cells were examined under folate- and methionine-deficient conditions. Cell proliferation was dependent on methionine supplementation rather than on folate concentration. The UdR suppression value was abnormally high in the folate-deficient condition. However, it was also high when the methionine was low, despite folate supplementation. In accordance with this, UdR incorporation was significantly improved with various folates by cells grown in low-methionine conditions. Methionine depletion resulted in marked impairment of UdR incorporation regardless of folate concentration. These findings indicate close metabolic interrelations between folate and methionine, which may be relevant to the pathological biochemistry of human megaloblastic anemia.

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The intake of two milk protein-rich diets containing casein and whey protein attenuated the development of severe hypertension in stroke-prone spontaneously hypertensive rats (SHRSP), and extended their life span in comparison with SHRSP on a regular stock diet. Milk fat-rich diet intake reduced the incidence of cerebrovascular disease in SHRSP without a significant fall in blood pressure. These results suggest that certain milk components have a preventive effect on hypertension and cerebrovascular disease in SHRSP.

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Autoxidized linoleic acid (AL) having 800 meq/kg of peroxide value and 1, 700 meq/kg of carbonyl value was given in repeated oral doses for 1-15 days at a daily dose of 2.5 ml/kg to male Wistar rats. During the administration, the effect of AL on drug-metabolizing activity was investigated periodically in liver microsomes. The contents of cytochrome P-450 and b₅ were increased by consecutive oral doses for 3-7 days. Thereafter, the amount of cytochrome P-450 decreased gradually, but the b₅ decreased slightly. Thus, after administration for 11-15 days, the cytochrome P-450 content was significantly lower but the cytochrome b₅ content was rather high in comparison with the control group. The aminopyrin-N demethylase activity was not reduced even after repeated oral doses of AL for 15 days. The activation of 2-acetyl amino fluorene (2AAF), which the authors termed S-9 activity, gradually decreased during administration for more than 3 days, and completely disappeared after administration for 9 days.

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Winged beans were extracted with hexane and the extracted lipid was analyzed by HPLC for its triacylglycerol (triglyceride) compo-sition on a Lichrosorb RP-18 column with acetonitrile-tetrahydrofuran-dichloromethane (6:2:1) solvent mixtures. The chromatography yielded more than 21 peaks, and each triacylglycerol was analyzed for fatty acids by GLC.
The major triacylglycerols were found to be behenoyl-linoleoyl-oleoylglycerol (21.3%), trioleoylglycerol (10.5%) and behenoyl-diole-oylglycerol (15.6%). Winged bean oil was found to contain triacyl-glycerols of larger ECN (equivalent carbon number) than soybean oil.

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This study investigated the role of thyroxine on bone growth by injecting it into malnourished weaned and suckling rats. Weaned rats were fed a normal diet or a low-protein, low-energy diet, and injected with saline or thyroxine (5μg/100g BW) for 22 days. Suckling pups were injected with saline or 2μg of thyroxine, and reared by dams fed a normal diet or a low-protein diet for 15 days. Thyroxine injection decreased body weight gain in both growth stages. Bone length, width and weight were not affected by thyroxine injection in weaned rats. Thyroxine injection increased femur length and tail growth, but did not change bone width in suckling rats. The epiphyseal growth plate and zone of hypertrophic cartilage cells were thinner in malnourished rats than in normal rats at both growth stages, but the number of proliferating chondrocytes was greater in suckling rats that received thyroxine injections than in those that received saline injections. The disappearance of trabeculae was observed in both normal and malnourished weaned rats upon thyroxine injection. These results suggested that retarded bone growth due to malnutrition might be independent of thyroid function in both growth stages.

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The effect of enrichment of the branched chain amino acids (BCAAs) leucine, isoleucine and valine on total parenteral nutrition was studied in rats. Experimental infusion solutions with a sufficient, marginal or deficient level of glucose contained either the conventional, amino acid composition (22.6% BCAAs) or a BCAA-enriched amino acid composition (36% BCAAs). Rats were infused with experimental solutions for 4 days and several parameters of protein metabolism were evaluated in various tissues. Under conditions of sufficient energy supply, BCAAenriched and conventional groups showed similar body weight gains and muscle protein degradations as measured by urinary 3-methylhistidine excretion. Polysome profiles in the liver and gastrocnemius muscle of the BCAA-enriched group were more heavily aggregated than those of the conventional group. Under the conditions of marginal or deficient energy supply, beneficial effects of BCAA enrichment over the conventional amino acid composition became more evident in terms of better body weight retention, higher RNA/DNA ratio and heavier polysome profile in both liver and muscle, and reduced protein catabolism in muscle. The present study suggests that enrichment of BCAAs, particularly valine and isoleucine, may be useful for nutritional support under hypercatabolic or stressed conditions.

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The effects of “long-term” feeding of different lipid sup-plemented diets (12% added fat, w/w) on the incidence of lipidosis or the severity of necrosis was examined in the cardiac muscle of male Hooded Wistar rats, after at least 12 months on the diets. The effects of sup-plementation with either n-6 polyunsaturated fatty acids (PUFA's) added as sunflower seed oil (the SSO diet), or one enriched with n-3 PUFA's added as a low cholesterol, low vitamin (A & D) fish oil preparation obtained from eviscerated Southern Bluefin Tuna (the TFO diet) were compared to those found in the hearts of rats fed either a relatively low fat commercially available stock diet (REF) which contained 4% (w/w) of mixed fats of animal, vegetable and marine origin, or after this stock diet had been supplemented to the same extent by the addition of 12% (i.e. 12:88g) sheep kidney (perirenal) fat, the SF diet.
Extensive cardiac lipidosis was seen after feeding either the TFO or the SF diets, but was not observed in the hearts of experimental rats from either the SSO or REF fed groups. Conversely, in these mature animals, grade 1 necrotic lesions were uniformally found in the cardiac muscles of all rats examined, but neither their incidence nor severity could be attributed to any dietary effect. These necrotic lesions are therefore more probably a reflection of the age of the animals at the time of sacrifice, rather than to any of the dietary supplements employed.
Some evidence of “Yellow Fat” disease was found by the presence of lipofuscin pigmentation in the storage fat of rats receiving n-3 PUFA's (the TFO diet) but was not observed in any other dietary group nor in the livers or kidneys of any animals. This extent of storage fat pigmentationn was not associated with any retardation of growth in this dietary group.

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The acute effects of an intragastric administration of ethanol (2 g/kg body weight) (given as 13.3% w/v solution) on the in vivo gastrointestinal motility and gastrointestinal absorption and secretion of calcium were investigated in 20-h fasted rats. Gastric ethanol concentration remained high for 90 min while the concentration in the duodenum peaked at 30 min before declining to a range slightly higher than that in the mid and distal intestine. Plasma ethanol peaked at 60 min. From the polyethylene glycol (PEG) distribution, ethanol was found to delay gastric emptying, and at 60 min, 40% of PEG was still retained in the stomach of the ethanol-treated group while gastric emptying had been completed in the controls. However, ethanol placed directly into the duodenum was found to enhance intestinal motility.
Under control conditions, exogenous calcium was completely ab-sorbed by the time it reached the mid-small intestine (J₃) and calcium found in more distal segments was of endogenous origin. Ethanol suppressed calcium absorption while markedly stimulating calcium secretion in the stomach and the distal small intestine, resulting in a net 32% increase in the total gastrointestinal calcium content. This effect on the distal small intestine was from ethanol that had reached this area from the circulation, and not from ethanol transit along the gastrointestinal tract.

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This study was undertaken to examine the responsiveness of the sympathetic nervous system of chronic vitamin E-deficient rats to dietary changes. Rats receiving a vitamin E-deficient diet exhibited about 95% hemolysis after 4 weeks on the vitamin E-deficient diet and this value was maintained up to 18 months. α-Tocopherol in serum was not detectable in rats receiving the vitamin E-deficient diet for 18 months. Lipid peroxide concentration in serum of rats receiving the vitamin Edeficient diet for 18 months was 10-fold higher than that of control rats. Basal levels of urinary norepinephrine (NE) and epinephrine (E) excretion in chronic vitamin E-deficient rats was 2 to 3-fold higher than those of control rats. In control rats, urinary NE excretion declined during fasting and this decline was reversed upon refeeding. Urinary excretion of NE in control rats increased upon glucose feeding. However, in chronic vitamin E-deficient rats, no change was observed upon fasting and glucose feeding in either urinary NE or E excretion. These results suggest that the increase in basal levels of urinary NE excretion in chronic vitamin E-deficient rats was not influenced by dietary manipulation.

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